Phenotypes associated with this allele

• Allele Symbol: Tg(Adipoq-cre)1Evdr
• Allele Name: transgene insertion 1, Evan Rosen
• Allele ID: MGI:4836360
• Summary: 31 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Senp1^tm1Wami/Senp1^tm1Wami Tg(Adipoq-cre)1Evdr/0	B6.Cg-Senp1^tm1Wami Tg(Adipoq-cre)1Evdr	MGI:5707796
cn2	Snrk^tm1.1Hxu/Snrk^tm1.1Hxu Tg(Adipoq-cre)1Evdr/0	B6.Cg-Snrk^tm1.1Hxu Tg(Adipoq-cre)1Evdr	MGI:6284773
cn3	Lrrc8a^em1Uia/Lrrc8a^em1Uia Tg(Adipoq-cre)1Evdr/0	involves: 129 * C57BL/6 * FVB/NJ	MGI:6467523
cn4	Tle3^tm1.1Pton/Tle3^tm1.1Pton Tg(Adipoq-cre)1Evdr/0	involves: 129P2/OlaHsd * C57BL/6J * FVB/NJ	MGI:5505584
cn5	Ehmt1^tm1.1Tara/Ehmt1^tm1.1Tara Tg(Adipoq-cre)1Evdr/0	involves: 129P2/OlaHsd * FVB/NJ	MGI:5910281
cn6	Gt(ROSA)26Sor^tm1(Notch1)Dam/Gt(ROSA)26Sor^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/NJ	MGI:5816455
cn7	Pten^tm1Hwu/Pten^tm1Hwu Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJae * C57BL/6J * FVB/NJ	MGI:5816458
cn8	Lztfl1^tm1.2Zpl/Lztfl1^tm1.2Zpl Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6N * FVB/NJ	MGI:7435344
cn9	Zdhhc5^tm1.1Smoc/Zdhhc5^tm1.1Smoc Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJaeSor * C57BL/6 * FVB/NJ	MGI:6363198
cn10	Gt(ROSA)26Sor^tm1(Notch1)Dam/Gt(ROSA)26Sor^+ Lep^ob/Lep^ob Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJaeSor * C57BL/6J * FVB/NJ	MGI:5816452
cn11	Gt(ROSA)26Sor^tm1(Notch1)Dam/Gt(ROSA)26Sor^+ Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJaeSor * C57BL/6J * FVB/NJ	MGI:5816451
cn12	Lep^tm1.1Gvcao/Lep^tm1.1Gvcao Tg(Adipoq-cre)1Evdr/0	involves: 129S4/SvJaeSor * C57BL/6J * FVB/NTac	MGI:5881975
cn13	Sik1^tm1.1Berd/Sik1^tm1.1Berd Tg(Adipoq-cre)1Evdr/0	involves: 129S7/SvEvBrd * C57BL/6J * FVB/NJ * SJL	MGI:5805515
cn14	Prdm16^tm1.1Brsp/Prdm16^tm1.1Brsp Tg(Adipoq-cre)1Evdr/0	involves: 129/Sv * C57BL/6 * FVB/N	MGI:5564786
cn15	Bola3^tm1a(EUCOMM)Wtsi/Bola3^tm1a(EUCOMM)Wtsi Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6 * C57BL/6N * FVB/NJ	MGI:6696118
cn16	Hdac3^tm1.1Laz/Hdac3^tm1.1Laz Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6 * FVB	MGI:5515398
cn17	Tg(Adipoq-cre)1Evdr/0 Tg(CAG-Jmjd8)#Kaso/0	involves: C57BL/6 * FVB/NJ	MGI:7386885
cn18	Crls1^tm1Geno/Crls1^tm1Geno Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6 * FVB/NJ	MGI:6720820
cn19	Pwwp2b^tm1.1Bcgen/Pwwp2b^tm1.1Bcgen Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6 * FVB/NJ	MGI:6867797
cn20	Bcl6^tm1Gdba/Bcl6^tm1Gdba Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6 * FVB/NJ	MGI:6294151
cn21	Rab10^tm1c(KOMP)Wtsi/Rab10^tm1c(KOMP)Wtsi Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6J * C57BL/6N * FVB/NJ	MGI:6282048
cn22	Med19^tm1c(EUCOMM)Wtsi/Med19^tm1c(EUCOMM)Wtsi Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6J * C57BL/6N * FVB/NJ	MGI:6505535
cn23	Adissp^tm1c(EUCOMM)Hmgu/Adissp^tm1c(EUCOMM)Hmgu Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6J * C57BL/6N * FVB/NJ	MGI:7432563
cn24	Gpbar1^em1Gpt/Gpbar1^em1Gpt Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6JGpt * FVB/NJ	MGI:7310209
cn25	Bscl2^tm1c(EUCOMM)Hmgu/Bscl2^tm1c(EUCOMM)Hmgu Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6N * FVB/NJ	MGI:6159704
cn26	Opn3^tm2c(EUCOMM)Wtsi/Opn3^tm2c(EUCOMM)Wtsi Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6N * FVB/NJ	MGI:6457282
cn27	H6pd^tm1c(EUCOMM)Wtsi/H6pd^tm1c(EUCOMM)Wtsi Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6N * FVB/NJ	MGI:6449844
cn28	Pex16^tm1c(EUCOMM)Hmgu/Pex16^tm1c(EUCOMM)Hmgu Tg(Adipoq-cre)1Evdr/0	involves: C57BL/6N * FVB/NJ * SJL	MGI:6682105
cn29	Atp6v0d1^em1Nju/Atp6v0d1^em1Nju Tg(Adipoq-cre)1Evdr/0	involves: FVB/NJ	MGI:7616527
cn30	Acox1^em1Wum/Acox1^em1Wum Tg(Adipoq-cre)1Evdr/0	involves: FVB/NJ	MGI:6682106
tg31	Tg(Adipoq-cre)1Evdr/0	involves: FVB/NJ	MGI:6358596

Genotype
MGI:5707796

cn1

• Allelic Composition: Senp1^tm1Wami/Senp1^tm1Wami; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: B6.Cg-Senp1^tm1Wami Tg(Adipoq-cre)1Evdr

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cellular

increased pancreatic beta cell apoptosis ( J:228009 )

• increase in apoptosis of beta cells

endocrine/exocrine glands

increased pancreatic beta cell apoptosis ( J:228009 )

• increase in apoptosis of beta cells

abnormal pancreatic islet morphology ( J:228009 )

• structures of pancreatic islets are disrupted, with increased apoptosis of beta cells after onset of diabetes and more severe at later stages

decreased insulin secretion ( J:228009 )

• insulin secretion declines after 8 weeks of age

growth/size/body

decreased body weight ( J:228009 )

• lower body weight after onset of diabetes

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:228009 )

N • mice exhibit normal lipid profiles up to the age of 14 weeks, including total cholesterol, low-density lipoprotein, high-density lipoprotein, triglyceride and free fatty acid

decreased insulin secretion ( J:228009 )

• insulin secretion declines after 8 weeks of age

hyperglycemia ( J:228009 )

• age-dependent increase in glucose levels

• level of hyperglycemia seen with glucose tolerance test is prolonged compared to controls

Genotype
MGI:6284773

cn2

• Allelic Composition: Snrk^tm1.1Hxu/Snrk^tm1.1Hxu; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: B6.Cg-Snrk^tm1.1Hxu Tg(Adipoq-cre)1Evdr

adipose tissue

abnormal adipose tissue distribution ( J:257980 )

• infiltration of adipocytes between muscle fibers

decreased fat cell size ( J:257980 )

brown adipose tissue inflammation ( J:257980 )

• macrophage accumulation in BAT

white adipose tissue inflammation ( J:257980 )

• macrophage accumulation in WAT

growth/size/body

increased body weight ( J:257980 )

homeostasis/metabolism

increased circulating free fatty acids level ( J:257980 )

• plasma FFA and triglyceride levels are elevated

increased circulating triglyceride level ( J:257980 )

• plasma FFA and triglyceride levels are elevated

abnormal circulating chemokine level ( J:257980 )

• plasma levels of cytokines and chemokines are increased - TNF, IL6, MCP1, MCP2, MCP3

increased circulating interleukin-6 level ( J:257980 )

increased circulating tumor necrosis factor level ( J:257980 )

decreased core body temperature ( J:257980 )

decreased energy expenditure ( J:257980 )

impaired glucose tolerance ( J:257980 )

insulin resistance ( J:257980 )

liver/biliary system

hepatic steatosis ( J:257980 )

• increased lipid accumulation in liver

immune system

brown adipose tissue inflammation ( J:257980 )

• macrophage accumulation in BAT

white adipose tissue inflammation ( J:257980 )

• macrophage accumulation in WAT

abnormal circulating chemokine level ( J:257980 )

• plasma levels of cytokines and chemokines are increased - TNF, IL6, MCP1, MCP2, MCP3

increased circulating interleukin-6 level ( J:257980 )

increased circulating tumor necrosis factor level ( J:257980 )

Genotype
MGI:6467523

cn3

• Allelic Composition: Lrrc8a^em1Uia/Lrrc8a^em1Uia; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129 * C57BL/6 * FVB/NJ

adipose tissue

adipose tissue phenotype ( J:246515 )

N • mice exhibit normal adipocyte development

decreased total body fat amount ( J:246515 )

• when fed a high-fat diet

abnormal fat cell morphology ( J:246515 )

• when fed a high-fat diet, adipocyte size is shifted toward a lean phenotype compared with wild-type cells

decreased epididymal fat pad weight ( J:246515 )

• when fed a high-fat diet

decreased inguinal fat pad weight ( J:246515 )

• when fed a high-fat diet

homeostasis/metabolism

increased susceptibility to diet-induced obesity ( J:246515 )

• when fed a high-fat diet despite normal daily food consumption

increased energy expenditure ( J:246515 )

• when fed a high-fat diet

• however, mice fed standard chow exhibit normal energy expenditure

impaired glucose tolerance ( J:246515 )

• whether mice are fed a high-fat diet or standard chow

insulin resistance ( J:246515 )

• whether mice are fed a high-fat diet or standard chow

behavior/neurological

hyperactivity ( J:246515 )

• when fed a high-fat diet

growth/size/body

increased susceptibility to diet-induced obesity ( J:246515 )

• when fed a high-fat diet despite normal daily food consumption

Genotype
MGI:5505584

cn4

• Allelic Composition: Tle3^tm1.1Pton/Tle3^tm1.1Pton; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * FVB/NJ

adipose tissue

abnormal brown adipose tissue morphology ( J:198134 )

• browner in color than in control mice

abnormal brown fat cell morphology ( J:198134 )

• increase in cells with multilocular lipid droplets characteristic of young brown adipose tissue

abnormal inguinal fat pad morphology ( J:198134 )

• evidence of browning with increased numbers of cells with multilocular lipid droplets

homeostasis/metabolism

decreased susceptibility to induced hypothermia ( J:198134 )

• improved ability to respond to cold exposure

increased core body temperature ( J:198134 )

• in respond to cold exposure

increased energy expenditure ( J:198134 )

• when housed in metabolic cages

behavior/neurological

behavior/neurological phenotype ( J:198134 )

N • mice exhibit normal activity level and food intake

Genotype
MGI:5910281

cn5

• Allelic Composition: Ehmt1^tm1.1Tara/Ehmt1^tm1.1Tara; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129P2/OlaHsd * FVB/NJ

homeostasis/metabolism

decreased fatty acid oxidation ( J:207678 )

• reduced fatty-acid oxidation capacity in brown adipose tissue

impaired adaptive thermogenesis ( J:207678 )

• temperature drop in cold-exposed mice

increased circulating glucose level ( J:207678 )

increased circulating insulin level ( J:207678 )

• at fasted and glucose-stimulated states

increased circulating free fatty acids level ( J:207678 )

decreased body temperature ( J:207678 )

• temperature drop in cold-exposed mice

abnormal oxygen consumption ( J:207678 )

• loss of induced increase in oxygen consumption after administering CL316,243

impaired glucose tolerance ( J:207678 )

insulin resistance ( J:207678 )

increased liver triglyceride level ( J:207678 )

adipose tissue

increased brown fat cell lipid droplet size ( J:207678 )

increased white fat cell lipid droplet size ( J:207678 )

increased epididymal fat pad weight ( J:207678 )

increased interscapular fat pad weight ( J:207678 )

abnormal brown adipose tissue physiology ( J:207678 )

• reduced fatty-acid oxidation capacity and fatty acid uptake in brown adipose tissue

growth/size/body

increased body weight ( J:207678 )

• without a change in food intake

liver/biliary system

abnormal liver morphology ( J:207678 )

• higher amounts of lipids

increased liver triglyceride level ( J:207678 )

cellular

decreased fatty acid oxidation ( J:207678 )

• reduced fatty-acid oxidation capacity in brown adipose tissue

Genotype
MGI:5816455

cn6

• Allelic Composition: Gt(ROSA)26Sor^{tm1(Notch1)Dam}/Gt(ROSA)26Sor⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/NJ

adipose tissue

abnormal brown adipose tissue morphology ( J:237232 )

• brown adipose tissue shows hypertrophy, accompanied by presence of large unilocular adipocytes

lipodystrophy ( J:237232 )

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:237232 )

N • mice shown normal glucose metabolism, with reversal of hyperglycemia to a level that is lower than in wild-type mice and normalized response to glucose challenge

neoplasm

increased liposarcoma incidence ( J:237232 )

• mice develop malignant sarcomas by 3 months of age at various locations of the body, including diaphragm, limb, spine, retroperitoneum, subcutaneous regions, and in the thoracic cavity

• multiple tumors of various sizes are seen in all mice

• tumors show classical biphasic neoplasm with one component of atypical lipomatous tumors and a second component of high-grade sarcoma indicating dedifferentiated liposarcoma

• tumors show heavy infiltration of inflammatory cells which are Cd45+/Ki67-

• treatment with rosigliatazone starting from 3 weeks of age prevents liposarcoma formation at 5 months of age

Genotype
MGI:5816458

cn7

• Allelic Composition: Pten^tm1Hwu/Pten^tm1Hwu; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * FVB/NJ

neoplasm

neoplasm ( J:237232 )

N • mice do not develop liposarcomas

Genotype
MGI:7435344

cn8

• Allelic Composition: Lztfl1^tm1.2Zpl/Lztfl1^tm1.2Zpl; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6N * FVB/NJ

normal phenotype

no abnormal phenotype detected ( J:287261 )

• mice are born normal and indistinguishable from wild-type mice and do not become obese

Genotype
MGI:6363198

cn9

• Allelic Composition: Zdhhc5^tm1.1Smoc/Zdhhc5^tm1.1Smoc; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6 * FVB/NJ

homeostasis/metabolism

decreased circulating glucose level ( J:270120 )

• in cold-exposed mice

abnormal lipid homeostasis ( J:270120 )

• reduced fatty acid uptake in brown and white adipose tissue

• however, uptake in heart and muscle are normal

increased circulating free fatty acids level ( J:270120 )

• after gavage of olive oil indicating slow clearance that is not as profound as in Zdhhc4^em1Smoc homozygotes

• in cold-exposed mice

increased circulating triglyceride level ( J:270120 )

• after gavage of olive oil indicating slow clearance that is not as profound as in Zdhhc4^em1Smoc homozygotes

adipose tissue

adipose tissue phenotype ( J:270120 )

N • whether fed standard chow or a high-fat diet, mice exhibit normal white adipose tissue

growth/size/body

growth/size/body region phenotype ( J:270120 )

N • whether fed standard chow or a high-fat diet, mice exhibit normal body weight

Genotype
MGI:5816452

cn10

• Allelic Composition: Gt(ROSA)26Sor^{tm1(Notch1)Dam}/Gt(ROSA)26Sor⁺; Lep^ob/Lep^ob; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6J * FVB/NJ

adipose tissue

adipose tissue phenotype ( J:237232 )

N • mice show normalization of obesity phenotype seen in single Lep^ob homozygotes

homeostasis/metabolism

hyperglycemia ( J:237232 )

• mice exhibit very high blood glucose levels

Genotype
MGI:5816451

cn11

• Allelic Composition: Gt(ROSA)26Sor^{tm1(Notch1)Dam}/Gt(ROSA)26Sor⁺; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6J * FVB/NJ

neoplasm

increased liposarcoma incidence ( J:237232 )

• mice develop solid tumors starting at 8 months of age at various locations of the body, including diaphragm, limb, spine, retroperitoneum, and subcutaneous regions

• by 13 months of age, all mice develop tumors

• tumors are identified as dedifferentiated liposarcomas

• treatment with rosigliatazone starting at 7 months of age prevents liposarcoma formation at 15 months of age

adipose tissue

absent epididymal fat pad ( J:237232 )

• epididymal white adipose tissue is not visible in mice older than 5 months of age

abnormal white fat cell differentation ( J:237232 )

• adipose tissues of adults, but not 3 week old mice, express lower levels of mature adipocyte markers, indicating dedifferentiation of white adipocytes

• mice treated with rosiglitazone, show reactivation of mature adipocyte marker expression

lipodystrophy ( J:237232 )

• adults gradually develop lipodystrophy, resulting in an approximate 90% reduction of adipose tissue weights

• mice treated with rosiglitazone, a synthetic Ppar-gamma ligand and antidiabetic drug, show increased size and weight of adipose tissues

cellular

abnormal white fat cell differentation ( J:237232 )

• adipose tissues of adults, but not 3 week old mice, express lower levels of mature adipocyte markers, indicating dedifferentiation of white adipocytes

• mice treated with rosiglitazone, show reactivation of mature adipocyte marker expression

growth/size/body

decreased susceptibility to diet-induced obesity ( J:237232 )

• mice are resistant to high-fat diet-induced body weight gain

increased liver weight ( J:237232 )

homeostasis/metabolism

decreased susceptibility to diet-induced obesity ( J:237232 )

• mice are resistant to high-fat diet-induced body weight gain

hyperglycemia ( J:237232 )

increased circulating insulin level ( J:237232 )

• 15-fold and 40-fold increase in circulating insulin levels under fasted and re-fed conditions, respectively

• treatment with rosigliatazone rescues the diabetes

insulin resistance ( J:237232 )

• 15-fold and 40-fold increase in circulating insulin levels under fasted and re-fed conditions, respectively, indicating severe insulin resistance

• mice fail to respond to insulin in all time points during the 2-hour insulin tolerance tests on both a chow diet and high-fat diet

liver/biliary system

increased liver weight ( J:237232 )

hepatic steatosis ( J:237232 )

• livers show very high fat content accompanied by elevated expression levels of genes involved in lipid metabolism

Genotype
MGI:5881975

cn12

• Allelic Composition: Lep^tm1.1Gvcao/Lep^tm1.1Gvcao; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6J * FVB/NTac

reproductive system

infertility ( J:218720 )

• both male and female mutant mice are infertile

female infertility ( J:218720 )

♀

male infertility ( J:218720 )

♂

growth/size/body

obese ( J:218720 )

• male and female mutant mice weigh significantly more than controls by postnatal day 21 and continue to gain weight into adulthood

homeostasis/metabolism

decreased circulating follicle stimulating hormone level ( J:218720 )

♂ • adult male, but not female, mutants exhibit significantly decreased circulating FSH levels relative to controls

decreased circulating luteinizing hormone level ( J:218720 )

♀ • adult female, but not male, mutants show significantly decreased circulating LH levels relative to controls

decreased circulating prolactin level ( J:218720 )

♀ • adult female, but not male, mutants show significantly decreased circulating prolactin levels relative to controls

decreased circulating leptin level ( J:218720 )

• male and female mutant mice lack adipose leptin protein and do not produce any detectable circulating serum leptin levels, indicating that circulating leptin is mainly or completely produced by adipocytes with no contribution from the pituitary

decreased circulating growth hormone level ( J:218720 )

♂ • adult male, but not female, mutants show a trend toward a reduction in serum GH levels, although the result is not significant relative to controls

increased pituitary hormone level ( J:218720 )

♂ • primary pituitary cells derived from adult male mutant mice show an increased % of cells immunolabeled for leptin relative to control pituitary cells

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:218720 )

N • primary pituitary cells derived from adult male and female mutant mice show no significant difference in the % of cells immunolabeled for growth hormone (GH) relative to control pituitary cells

Genotype
MGI:5805515

cn13

• Allelic Composition: Sik1^tm1.1Berd/Sik1^tm1.1Berd; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J * FVB/NJ * SJL

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:236223 )

N • mice fed chow or a high-fat diet exhibit normal glucose homeostasis

Genotype
MGI:5564786

cn14

• Allelic Composition: Prdm16^tm1.1Brsp/Prdm16^tm1.1Brsp; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: 129/Sv * C57BL/6 * FVB/N

adipose tissue

abnormal adipose tissue morphology ( J:208683 )

• subcutaneous adipose tissue contains larger adipocytes and fewer smaller multiocular UCP1+ adipocytes relative to control mice following cold exposure

• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of crown like structures, however, there are no changes in visceral (abdominal) fat

• subcutaneous adipose tisse from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages

increased subcutaneous adipose tissue amount ( J:208683 )

♂ • subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged

increased total body fat amount ( J:208683 )

♂ • body composition analysis after 16 weeks on high fat diet indicates increased fat mass with no change in lean body mass

abnormal adipose tissue distribution ( J:208683 )

• subcutaneous fat mass is doubled as compared to controls after 16 weeks on high fat diet; epididymal and BAT masses are unchanged

increased fat cell size ( J:208683 )

♂ • subcutaneous adipocytes from male mice after 18 weeks on high fat diet exhibit a 33% increase in mean adipocyte area

abnormal adipose tissue physiology ( J:208683 )

• O₂ consumption is reduced in subcutaneous adipose pads, but not in brown adipose pads, at baseline (36% reduced) and following stimulation with a beta-adrenergic agonist (49% reduced)

decreased adipocyte glucose uptake ( J:208683 )

• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls

abnormal brown adipose tissue thermogenesis ( J:208683 )

• subcutaneous adipocytes exhibit a blunted response to stimuli such as isoproterenol that induce a thermogenic gene program (beige adipocytes)

growth/size/body

increased susceptibility to weight gain ( J:208683 )

• mice exhibit increased weight gain after 16 weeks on high-fat, high-carbohydrate diet relative to control mice

hematopoietic system

increased macrophage cell number ( J:208683 )

• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged

homeostasis/metabolism

increased circulating insulin level ( J:208683 )

• increased fasting plasma insulin levels (55%) in mice after 6 weeks on high fat diet

abnormal oxygen consumption ( J:208683 )

• unlike controls, mutant mice do not exhibit increased O₂ consumption following stimulation with a beta-adrenergic agonist

increased respiratory quotient ( J:208683 )

• mice exhibit an increased respiratory exchange ratio (RER), but no increase in O₂ consumption

insulin resistance ( J:208683 )

• a reduced glucose infusion rate (64% of controls) is observed in mice after 6 weeks on high fat diet

• decreased whole body glucose uptake is observed in mice after 6 weeks on high fat diet

• clamped insulin levels do not increase as much as controls in mice after 6 weeks on high fat diet

increased liver triglyceride level ( J:208683 )

• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls

immune system

increased macrophage cell number ( J:208683 )

• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged

integument

increased subcutaneous adipose tissue amount ( J:208683 )

♂ • subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged

liver/biliary system

increased liver triglyceride level ( J:208683 )

• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls

hepatic steatosis ( J:208683 )

• after 6 weeks on high fat diet

cellular

decreased adipocyte glucose uptake ( J:208683 )

• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls

Genotype
MGI:6696118

cn15

• Allelic Composition: Bola3^{tm1a(EUCOMM)Wtsi}/Bola3^{tm1a(EUCOMM)Wtsi}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6 * C57BL/6N * FVB/NJ

adipose tissue

increased white adipose tissue mass ( J:287367 )

• the increase in body weight at 30 degrees C is due to increased tissue mass of epididymal white adipose tissue and liver

decreased adipocyte glucose uptake ( J:287367 )

• brown adipose tissue glucose uptake is lower

• however, glucose uptake in other metabolic organs, including skeletal muscle, liver, and brain, is not different

• alpha-lipoic acid supplementation fails to increase glucose uptake in the brown adipose tissue of mutant mice as it does in controls

abnormal brown adipose tissue physiology ( J:287367 )

• lipoylation in brown adipose tissue is reduced

• brown adipose tissue glucose uptake is lower

• brown adipose tissue shows reduced glucose oxidation and valine oxidation

• pyruvate dehydrogenase activity in interscapular brown adipose tissue (iBAT), but not white adipose tissue, is lower

• supplementation with alpha-lipoic acid fails to increase lipoylation in the iBAT of old mice, fails to enhance pyruvate dehydrogenase activity in BAT, and fails to increase glucose oxidation in aged BAT as in control

abnormal brown adipose tissue thermogenesis ( J:287367 )

• norepinephrine-induced iBAT thermogenesis is impaired

• alpha-lipoic acid supplementation does not restore norepinephrine-stimulated BAT thermogenesis in old mutant mice as it does is old controls

growth/size/body

increased susceptibility to weight gain ( J:287367 )

• mice gain more weight than controls at 30 degrees C but not at ambient temperature of 22 degrees C

homeostasis/metabolism

decreased energy expenditure ( J:287367 )

• mice exhibit lower whole-body energy expenditure than controls following beta-adrenergic receptor activation

decreased oxygen consumption ( J:287367 )

• oxygen consumption rate in the iBAT is lower than in controls following beta3- adrenergic receptor activation

• the increase in oxygen consumption rate maintained at thermoneutrality (30 degrees C) in response to beta3- adrenergic receptor agonist treatment that is seen in wild-type mice is blunted in mutant mice

impaired glucose tolerance ( J:287367 )

• mice show glucose intolerance in the glucose tolerance test, even at ambient temperature

• however, systemic insulin tolerance and glucose-stimulated insulin secretion are not altered

• alpha-lipoic acid supplementation fails to improve systemic glucose tolerance of aged mutant mice as it does in controls

abnormal enzyme/coenzyme activity ( J:287367 )

• pyruvate dehydrogenase activity in interscapular brown adipose tissue (iBAT), but not white adipose tissue, is lower

• mice chronically treated with beta3-adrenergic receptor agonist to stimulate beige fat biogenesis in the inguinal white adipose tissue show lower pyruvate dehydrogenase activity

cellular

decreased adipocyte glucose uptake ( J:287367 )

• brown adipose tissue glucose uptake is lower

• however, glucose uptake in other metabolic organs, including skeletal muscle, liver, and brain, is not different

• alpha-lipoic acid supplementation fails to increase glucose uptake in the brown adipose tissue of mutant mice as it does in controls

abnormal mitochondrial physiology ( J:287367 )

• mitochondrial Complex I and II activities are reduced in brown adipose tissue mitochondria

Genotype
MGI:5515398

cn16

• Allelic Composition: Hdac3^tm1.1Laz/Hdac3^tm1.1Laz; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6 * FVB

mortality/aging

mortality/aging ( J:199860 )

N • mice show no reduction in survival to at least 6 months

Genotype
MGI:7386885

cn17

• Allelic Composition: Tg(Adipoq-cre)1Evdr/0; Tg(CAG-Jmjd8)#Kaso/0
• Genetic Background: involves: C57BL/6 * FVB/NJ

homeostasis/metabolism

increased circulating insulin level ( J:319518 )

• mice fed a high fat diet (HFD) exhibit higher insulin levels

impaired glucose tolerance ( J:319518 )

• mice fed a HFD exhibit worsened glucose tolerance

• however, mice fed a chow diet show no difference in glucose tolerance

insulin resistance ( J:319518 )

• mice fed a HFD exhibit worsened insulin sensitivity

• however, mice fed a chow diet show no difference in the insulin tolerance test

• mice fed a HFD exhibit a higher Homeostatic Model Assessment (HOMA) of insulin resistance compared to control mice

adipose tissue

white adipose tissue inflammation ( J:319518 )

• HFD-fed mice show increased macrophage infiltration in epididymal white adipose tissue (eWAT)

immune system

white adipose tissue inflammation ( J:319518 )

• HFD-fed mice show increased macrophage infiltration in epididymal white adipose tissue (eWAT)

growth/size/body

growth/size/body region phenotype ( J:319518 )

N • mice fed a chow diet show no differences in body weight, body composition, or tissue mass

N • mice fed a high fat diet (HFD) show no changes in body weight or body composition or in energy homeostasis compared with controls

Genotype
MGI:6720820

cn18

• Allelic Composition: Crls1^tm1Geno/Crls1^tm1Geno; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6 * FVB/NJ

adipose tissue

decreased subcutaneous adipose tissue amount ( J:266083 )

• chow-fed mice show a significant reduction in subcutaneous white adipose tissue (scWAT) weight, and this phenotype is exacerbated on a HFD

abnormal brown adipose tissue morphology ( J:266083 )

• interscapular brown adipose tissue (iBAT) is distinctly paler than that in control mice, due to a virtual ablation of all cardiolipin species

abnormal brown fat cell morphology ( J:266083 )

• brown adipocytes exhibit distorted cellular and lipid droplet morphology in iBAT, as a result of mitochondrial dysfunction

• however, white adipose depots are not severely affected

increased brown fat cell lipid droplet size ( J:266083 )

decreased fat cell mitochondrial DNA content ( J:266083 )

• mtDNA content is markedly decreased in iBAT

• however, mtDNA levels in epididymal white adipose tissue (eWAT) are normal

decreased epididymal fat pad weight ( J:266083 )

• chow-fed mice show a significant reduction in epididymal white adipose tissue (eWAT) weight, and this phenotype is exacerbated on a HFD

decreased interscapular fat pad weight ( J:266083 )

• chow-fed mice show a significant reduction in iBAT weight

decreased adipocyte glucose uptake ( J:266083 )

• following i.p. injection with the beta3 agonist CL-316,243 to specifically stimulate glucose uptake into thermogenic fat, mice exhibit significantly lower glucose uptake into iBAT than controls

abnormal brown adipose tissue physiology ( J:266083 )

• in interscapular brown adipose tissue (iBAT), expression profile of genes linked to thermogenesis, adipogenesis, and mitochondrial respiration more closely resemble that of white fat than brown fat

abnormal brown adipose tissue thermogenesis ( J:266083 )

• mice show a marked reduction in norepinephrine (NE)-induced uncoupled respiration and heat production relative to controls

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:266083 )

N • chow-fed mice show no significant alterations in energy expenditure relative to control mice

decreased susceptibility to diet-induced obesity ( J:266083 )

• mice fed a 60% high-fat diet (HFD) gain significantly less weight and have more lean mass but less fat mass than HFD-fed controls

impaired adaptive thermogenesis ( J:266083 )

• mice show a significantly greater drop in core body temperature than controls in response to acute cold exposure (a 22 to 4 degrees Celsius challenge for 1.5 h), indicating reduced cold tolerance

• cold exposure fails to induce Ucp1 transcription in iBAT or subcutaneous white adipose tissue (scWAT), unlike in control mice

increased fasting circulating glucose level ( J:266083 )

• mice fed a HFD show increased fasting blood glucose levels

decreased oxygen consumption ( J:266083 )

• mice show a marked reduction in norepinephrine (NE)-induced uncoupled respiration relative to controls

decreased respiratory quotient ( J:266083 )

• mice housed in metabolic cages show a marked reduction in the daily respiratory quotient (RQ) biorhythm relative to controls, indicating decreased metabolic flexibility

insulin resistance ( J:266083 )

• chow-fed mice show decreased insulin sensitivity relative to control mice

• mice fed a 60% high-fat diet (HFD) are completely refractory to insulin

cellular

decreased fat cell mitochondrial DNA content ( J:266083 )

• mtDNA content is markedly decreased in iBAT

• however, mtDNA levels in epididymal white adipose tissue (eWAT) are normal

decreased adipocyte glucose uptake ( J:266083 )

• following i.p. injection with the beta3 agonist CL-316,243 to specifically stimulate glucose uptake into thermogenic fat, mice exhibit significantly lower glucose uptake into iBAT than controls

disorganized mitochondrial cristae ( J:266083 )

• mitochondria isolated from iBAT show disrupted cristae structure

decreased mitochondrial size ( J:266083 )

• mitochondria isolated from iBAT show reduced mitochondrial mass (as measured by citrate synthase activity)

abnormal respiratory electron transport chain ( J:266083 )

• mitochondria isolated from iBAT show altered respiratory chain complex and super complex formation and reduced GDP-inhibitable (UCP1-linked) respiration

growth/size/body

growth/size/body region phenotype ( J:266083 )

N • chow-fed mice show no significant alterations in body weight or composition relative to control mice

decreased susceptibility to diet-induced obesity ( J:266083 )

• mice fed a 60% high-fat diet (HFD) gain significantly less weight and have more lean mass but less fat mass than HFD-fed controls

increased liver weight ( J:266083 )

• chow-fed mice show increased liver weight relative to control mice, and this phenotype is exacerbated on a HFD

• however, liver triglyceride levels are normal

liver/biliary system

increased liver weight ( J:266083 )

• chow-fed mice show increased liver weight relative to control mice, and this phenotype is exacerbated on a HFD

• however, liver triglyceride levels are normal

integument

decreased subcutaneous adipose tissue amount ( J:266083 )

• chow-fed mice show a significant reduction in subcutaneous white adipose tissue (scWAT) weight, and this phenotype is exacerbated on a HFD

behavior/neurological

behavior/neurological phenotype ( J:266083 )

N • chow-fed mice show no significant alterations in food intake or physical activity relative to control mice

Genotype
MGI:6867797

cn19

• Allelic Composition: Pwwp2b^tm1.1Bcgen/Pwwp2b^tm1.1Bcgen; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6 * FVB/NJ

homeostasis/metabolism

abnormal adaptive thermogenesis ( J:319940 )

• enhanced adaptive thermogenesis with increased temperature following cold exposure compared with control mice

increased oxygen consumption ( J:319940 )

• at night in mice fed a high-fat diet compared with control mice

• however, carbon dioxide production is normal

improved glucose tolerance ( J:319940 )

• in mice fed a high-fat diet compared with control mice

increased insulin sensitivity ( J:319940 )

• in mice fed a high-fat diet compared with control mice

increased basal metabolism ( J:319940 )

• in mice fed a high-fat diet compared with control mice

adipose tissue

decreased body fat mass ( J:319940 )

• in mice fed a high-fat diet compared with control mice

decreased brown fat cell lipid droplet size ( J:319940 )

• in mice fed a high-fat diet compared with control mice

whitened brown adipose tissue morphology ( J:319940 )

decreased white fat cell lipid droplet size ( J:319940 )

• in mice fed a high-fat diet compared with control mice

decreased inguinal fat pad weight ( J:319940 )

• in mice fed a high-fat diet compared with control mice

growth/size/body

decreased body fat mass ( J:319940 )

• in mice fed a high-fat diet compared with control mice

decreased susceptibility to weight gain ( J:319940 )

• in mice fed a high-fat diet compared with control mice

liver/biliary system

abnormal liver morphology ( J:319940 )

• fewer vacuoles in the liver of mice fed a high-fat diet compared with control mice

respiratory system

decreased pulmonary respiratory rate ( J:319940 )

• during the day and night in mice fed a high-fat diet compared with control mice

Genotype
MGI:6294151

cn20

• Allelic Composition: Bcl6^tm1Gdba/Bcl6^tm1Gdba; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6 * FVB/NJ

growth/size/body

increased body fat mass ( J:271078 )

• mice fed a regular chow exhibit increased mass and percentage of fat

• however, body weight of regular chow fed mice is normal

increased susceptibility to diet-induced obesity ( J:271078 )

• mice fed a high-fat diet exhibit a greater increase in total fat mass than controls fed the same diet

• adiposity in high-fat diet fed mice is due to increased subcutaneous adipose tissue

adipose tissue

increased subcutaneous adipose tissue amount ( J:271078 )

• expanded fat mass in regular chow-fed mice is due to a 2-fold increase in subcutaneous, but not perigonadal or brown, adipose tissue

• adiposity in high-fat diet fed mice is due to increased subcutaneous adipose tissue

increased body fat mass ( J:271078 )

• mice fed a regular chow exhibit increased mass and percentage of fat

• however, body weight of regular chow fed mice is normal

increased white fat cell size ( J:271078 )

• subcutaneous adipocyte diameters are larger, with this size difference limited to subcutaneous and not perigonadal adipose tissue

• subcutaneous adipocytes of high-fat fed mice exhibit larger size, with nearly 50% of cells having greater than 60 micron diameters compared to 25% of adipocytes in controls

• however, there is no evidence of hypercellularity in adipose tissues

abnormal gonadal fat pad morphology ( J:271078 )

• perigonadal adipose tissue is reduced by 30% compared to controls in high-fat diet fed mice

• perigonadal adipose tissue of high-fat diet fed mice has increased interstitial cell infiltration and crown-like structures

decreased adipocyte glucose uptake ( J:271078 )

• mice exhibit decreased insulin-stimulated glucose uptake into brown adipose tissue

increased adipocyte glucose uptake ( J:271078 )

• mice exhibit increased insulin-stimulated glucose uptake into perigonadal adipose tissue

white adipose tissue inflammation ( J:271078 )

• perigonadal adipose tissue of high-fat diet fed mice has increased interstitial cell infiltration and crown-like structures

cellular

decreased adipocyte glucose uptake ( J:271078 )

• mice exhibit decreased insulin-stimulated glucose uptake into brown adipose tissue

increased adipocyte glucose uptake ( J:271078 )

• mice exhibit increased insulin-stimulated glucose uptake into perigonadal adipose tissue

increased muscle cell glucose uptake ( J:271078 )

• mice exhibit increased insulin-stimulated glucose uptake in gastrocnemius and vastus lateralis muscles

homeostasis/metabolism

increased susceptibility to diet-induced obesity ( J:271078 )

• mice fed a high-fat diet exhibit a greater increase in total fat mass than controls fed the same diet

• adiposity in high-fat diet fed mice is due to increased subcutaneous adipose tissue

decreased fasting circulating glucose level ( J:271078 )

• both regular chow and high-fat diet fed mice exhibit reduced fasting glucose levels

decreased circulating insulin level ( J:271078 )

• both regular chow and high-fat diet fed mice exhibit reduced fasting insulin levels

• both pre-clamp and clamped plasma insulin levels are lower

increased circulating leptin level ( J:271078 )

• levels of leptin are higher in chow-fed, but not high-fat diet fed, mice

decreased respiratory quotient ( J:271078 )

• mice exhibit no differences in energy expenditure although respiratory exchange ratio is lower at some time points

impaired gluconeogenesis ( J:271078 )

• rate of endogenous glucose production is reduced during hyperinsulinemic-euglycemic clamp, indicating that gluconeogenesis is more sensitive to insulin-mediated suppression

increased insulin sensitivity ( J:271078 )

• insulin resistance is reduced in both regular diet and high-fat diet fed mice, indicating improved glucose metabolism

• high-fat diet fed mice require glucose infusion rates nearly double those of controls to maintain steady-state glucose levels, indicating enhanced insulin sensitivity

increased circulating adiponectin level ( J:271078 )

• about 30% increase in serum levels of adiponectin in regular chow-fed or high-fat diet fed mice

abnormal lipid level ( J:271078 )

• 2.5-fold elevation of fatty acid esters of hydroxy fatty acid (FAHFAs) levels in serum, including the 16:0H18:0 form (PAHSA)

• levels of many other lipids, including triglyceride-associated fatty acyl chains, total triglycerides, ceramides, and several glycerophospholipids are reduced in serum

• subcutaneous adipose tissue shows twice as high levels of insulin-sensitizing lipokines known as FAHFs and C16:1n7-palmitoleate and increased levels of other triglyceride-associated fatty acyl chains and total triglycerides, various membrane-associated and signaling glycerophospholipids, and sphingomyelin

decreased circulating free fatty acids level ( J:271078 )

• fasting plasma free fatty acid levels are normal, but clamped levels are lower, indicating enhanced insulin-mediated suppression of lipolysis

decreased circulating triglyceride level ( J:271078 )

• total triglyceride levels are reduced in serum

decreased ceramide level ( J:271078 )

• serum ceramide levels are reduced

decreased liver triglyceride level ( J:271078 )

• liver triglyceride content is reduced by 48% in chow-fed and 44% in high-fat fed mice

increased lipogenesis ( J:271078 )

• mice exhibit a 2-fold increase in rates of de novo synthesis of triglyceride-bound palmitate and triglyceride-bound glycerol in the subcutaneous adipose tissue indicating increase in de novo lipogenesis

• however, mice exhibit normal fatty acid oxidation and acute lipolytic responses to beta adrenergic agonists

immune system

white adipose tissue inflammation ( J:271078 )

• perigonadal adipose tissue of high-fat diet fed mice has increased interstitial cell infiltration and crown-like structures

integument

increased subcutaneous adipose tissue amount ( J:271078 )

• expanded fat mass in regular chow-fed mice is due to a 2-fold increase in subcutaneous, but not perigonadal or brown, adipose tissue

• adiposity in high-fat diet fed mice is due to increased subcutaneous adipose tissue

liver/biliary system

decreased liver triglyceride level ( J:271078 )

• liver triglyceride content is reduced by 48% in chow-fed and 44% in high-fat fed mice

decreased liver weight ( J:271078 )

• liver weight is reduced by 13% in chow-fed and 20% in high-fat fed mice

decreased susceptibility to diet-induced hepatic steatosis ( J:271078 )

• mice fed a high-fat diet show a reduction in steatosis compared to wild-type mice fed the same diet

muscle

increased muscle cell glucose uptake ( J:271078 )

• mice exhibit increased insulin-stimulated glucose uptake in gastrocnemius and vastus lateralis muscles

Genotype
MGI:6282048

cn21

• Allelic Composition: Rab10^{tm1c(KOMP)Wtsi}/Rab10^{tm1c(KOMP)Wtsi}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * FVB/NJ

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:249843 )

N • mice exhibit normal fasting plasma glycerol and NEFA levels and normal insulin-mediated suppression of plasma NEFA

increased circulating insulin level ( J:249843 )

• following glucose challenge

• however, levels after overnight fast are normal

increased hepatic glucose production ( J:249843 )

• lack of insulin suppression

insulin resistance ( J:249843 )

• when fed a low- or high-fat diet

adipose tissue

adipose tissue phenotype ( J:249843 )

N • mice exhibit normal visceral white adipose tissue with normal lipid droplet size

decreased adipocyte glucose uptake ( J:249843 )

• reduced insulin-stimulated glucose uptake

cellular

decreased adipocyte glucose uptake ( J:249843 )

• reduced insulin-stimulated glucose uptake

Genotype
MGI:6505535

cn22

• Allelic Composition: Med19^{tm1c(EUCOMM)Wtsi}/Med19^{tm1c(EUCOMM)Wtsi}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * FVB/NJ

growth/size/body

decreased body fat mass ( J:298822 )

• reduced fat mass in both sexes at 12 weeks of age, as revealed by body composition analysis (EchoMRI)

increased lean body mass ( J:298822 )

• slightly increased lean mass in both sexes at 12 weeks of age, as revealed by EchoMRI

increased body weight ( J:298822 )

• increased body weight in both sexes at 9 and 12 weeks of age, but not at 3 or 6 weeks of age

• however, food intake is not significantly altered

enlarged liver ( J:298822 )

• enlarged liver at 12 weeks of age

increased liver weight ( J:298822 )

• markedly increased liver weight at 12 weeks of age

adipose tissue

decreased body fat mass ( J:298822 )

• reduced fat mass in both sexes at 12 weeks of age, as revealed by body composition analysis (EchoMRI)

whitened brown adipose tissue morphology ( J:298822 )

• brown adipose tissue (BAT) contains many white-adipocyte-like unilocular cells, indicating whitening of brown fat

• however, no change in brown adipose tissue (BAT) mass at 3 or 12 weeks of age

decreased gonadal fat pad weight ( J:298822 )

• severely reduced gonadal white fat depot (gWAT) weight in males as early as 3 weeks of age

decreased inguinal fat pad weight ( J:298822 )

• severely reduced inguinal white fat depot (iWAT) weight in males as early as 3 weeks of age

decreased mesenteric fat pad weight ( J:298822 )

• reduction in mesenteric WAT (mWAT) weight at 12 weeks of age

decreased retroperitoneal fat pad weight ( J:298822 )

• reduction in retroperitoneal WAT (rWAT) weight at 12 weeks of age

abnormal interscapular fat pad morphology ( J:298822 )

• interscapular BAT is much paler at 12 weeks of age, resembling WAT

abnormal white adipose tissue morphology ( J:298822 )

• small amount of residual WAT appears unhealthy with sparse, irregularly sized adipocytes among a fibrous extracellular matrix

decreased subcutaneous adipose tissue amount ( J:298822 )

• reduction in anterior subcutaneous WAT (asWAT) weight at 12 weeks of age

decreased white fat cell number ( J:298822 )

• sparse white adipocytes

abnormal white fat cell size ( J:298822 )

• irregularly sized white adipocytes

decreased white adipose tissue mass ( J:298822 )

• dramatic reduction in white adipose tissue mass at 12 weeks of age

• however, no change in brown adipose tissue (BAT) mass at 3 or 12 weeks of age

abnormal brown adipose tissue physiology ( J:298822 )

• mRNA expression of BAT genes, including Ucp1, is reduced

abnormal white adipose tissue physiology ( J:298822 )

• gene expression analysis of gWAT and iWAT revealed reduced mRNA levels of the adipocyte genes aP2, C/EBPalpha, and PPARgamma; mRNA expression of C/EBPbeta and KLF5 is either unchanged or elevated

homeostasis/metabolism

hyperglycemia ( J:298822 )

• both sexes are hyperglycemic

increased circulating insulin level ( J:298822 )

• markedly increased fasting serum insulin levels

impaired glucose tolerance ( J:298822 )

• both sexes are glucose intolerant

insulin resistance ( J:298822 )

• impaired response to insulin in insulin tolerance test

increased liver triglyceride level ( J:298822 )

• 4-fold increase in liver triglyceride content

liver/biliary system

enlarged liver ( J:298822 )

• enlarged liver at 12 weeks of age

increased liver weight ( J:298822 )

• markedly increased liver weight at 12 weeks of age

increased liver triglyceride level ( J:298822 )

• 4-fold increase in liver triglyceride content

hepatic steatosis ( J:298822 )

• massive accumulation of lipid droplets in liver at 12 weeks of age

pale liver ( J:298822 )

• pale liver at 12 weeks of age

abnormal liver physiology ( J:298822 )

• impaired hepatic insulin signaling, as assessed by phosphorylation of Akt in response to insulin

integument

decreased subcutaneous adipose tissue amount ( J:298822 )

• reduction in anterior subcutaneous WAT (asWAT) weight at 12 weeks of age

Genotype
MGI:7432563

cn23

• Allelic Composition: Adissp^{tm1c(EUCOMM)Hmgu}/Adissp^{tm1c(EUCOMM)Hmgu}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * FVB/NJ

adipose tissue

abnormal fat cell morphology ( J:332979 )

• mice housed at 30 degrees Celsius and fed a normal chow diet for 2 months show differences in inguinal white adipose tissue (WAT) and brown adipose tissue (BAT) adipocyte morphology

abnormal white adipose tissue morphology ( J:332979 )

• intracellular cAMP content is decreased in inguinal WAT depot in mice housed at 30 degrees Celsius and fed a normal chow diet for 2 months

increased white fat cell size ( J:332979 )

• mice fed a high-fat diet show larger adipocytes

increased white adipose tissue mass ( J:332979 )

• mice housed at 30 degrees Celsius and fed a normal chow diet for 2 months show an increase in WAT mass

• mice contain more inguinal WAT mass after acute cold exposure than controls, indicating decreased fat burning

abnormal adipose tissue physiology ( J:332979 )

• inguinal WAT browning is compromised after cold exposure

• administration of CL-316,243, a beta3-adrenergic agonist, does not lead to inguinal WAT browning as in controls or a decrease in inguinal WAT mass loss

decreased adipocyte glucose uptake ( J:332979 )

• decrease in glucose uptake by inguinal WAT after cold exposure

abnormal beige fat cell physiology ( J:332979 )

• beige fat formation is impaired upon cold exposure

growth/size/body

increased susceptibility to diet-induced obesity ( J:332979 )

• mice show increased susceptibility to high-fat diet-induced obesity, with mice gaining more weight despite consuming similar amount of food as controls; body weight increase is due to fat mass and not lean mass

• however, mice have normal body weight on normal chow diet at room temperature

homeostasis/metabolism

increased susceptibility to diet-induced obesity ( J:332979 )

• mice show increased susceptibility to high-fat diet-induced obesity, with mice gaining more weight despite consuming similar amount of food as controls; body weight increase is due to fat mass and not lean mass

• however, mice have normal body weight on normal chow diet at room temperature

impaired adaptive thermogenesis ( J:332979 )

• body temperature is lower than in controls upon cold exposure

increased circulating glucose level ( J:332979 )

• both steady-state and fasting glucose levels are higher in mice fed a high-fat diet for 18 and 19 weeks

increased fasting circulating glucose level ( J:332979 )

• fasting glucose levels are higher in mice fed a high-fat diet for 18 and 19 weeks

impaired glucose tolerance ( J:332979 )

• glucose tolerance is deteriorated in mice fed a high-fat diet for 5-6 weeks and for 18 and 19 weeks

insulin resistance ( J:332979 )

• insulin sensitivity is deteriorated in mice fed a high-fat diet for 5-6 weeks and for 18 and 19 weeks

cellular

decreased adipocyte glucose uptake ( J:332979 )

• decrease in glucose uptake by inguinal WAT after cold exposure

behavior/neurological

behavior/neurological phenotype ( J:332979 )

N • mice have normal food intake as controls on normal chow diet at room temperature

Genotype
MGI:7310209

cn24

• Allelic Composition: Gpbar1^em1Gpt/Gpbar1^em1Gpt; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6JGpt * FVB/NJ

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:325395 )

• mice fed a high-fat diet and transplanted with fecal microbiota (FMT) from Hif1a^tm1Stom/Hif1a^tm1Stom Tg(Vil1-cre)20Syr mice exhibit no change in food intake, body weight, body fat composition, insulin sensitivity, normal adaptive thermogenesis, and mitochondrial CF activity unlike wild-type mice receiving the FMT, which phenocopy Hif1a^tm1Stom/Hif1a^tm1Stom Tg(Vil1-cre)20Syr mice

• mice fed a high-fat diet and treated with TCA or DCA exhibit no attenuation of body wight gain and body fat content or restored glucose intolerance and insulin resistance or increased adaptive thermogenesis, respiratory exchange ratio, or oxygen consumption unlike control mice

Genotype
MGI:6159704

cn25

• Allelic Composition: Bscl2^{tm1c(EUCOMM)Hmgu}/Bscl2^{tm1c(EUCOMM)Hmgu}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6N * FVB/NJ

adipose tissue

decreased body fat mass ( J:260853 )

♂ • mice exhibit decreased fat mass levels at 6 and 12 weeks of age

decreased bone marrow adipose tissue amount ( J:260853 )

♂ • 16 week old mice exhibit severe depletion of total tibial bone marrow adipose tissue, resulting from loss of both constitutive bone marrow adipose tissue of the distal tibia and regulated bone marrow adipose tissue in the mid-to-proximal tibia

♂ • however, caudal vertebrae constitutive bone marrow adipose tissue appears normal

abnormal brown adipose tissue morphology ( J:260853 )

♂ • brown adipose tissues shows altered triglyceride accumulation, with numerous large droplets rather than the normal multilocular morphology

decreased brown adipose tissue mass ( J:260853 )

♂ • brown adipose tissue shows only a modest reduction in total mass

abnormal infrapatellar fat pad morphology ( J:260853 )

♂ • mice show a reduction in total number of infrapatellar fat pad adipocytes

abnormal white adipose tissue morphology ( J:260853 )

♂ • the residual epididymal white adipose tissue and subcutaneous white adipose tissue have a disorganized mixture of hypertrophic and smaller adipocytes

decreased subcutaneous adipose tissue amount ( J:260853 )

♂ • mice exhibit only residual subcutaneous white adipose tissue

decreased white adipose tissue amount ( J:260853 )

♂ • mice exhibit only residual epididymal white adipose tissue

browned white adipose tissue morphology ( J:260853 )

♂ • marker analysis show increased expression of brown adipocyte markers suggesting that browing occurs in residual epididymal white adipose tissues

lipodystrophy ( J:260853 )

♂ • mice exhibit early-onset generalized loss of adipose tissue

♂ • mice are unable to expand adipose tissue stores in response to a high-fat diet challenge

behavior/neurological

decreased locomotor activity ( J:260853 )

♂ • 14 week old mice are less active during the day than controls

♂ • however, mice show normal activity levels during the night

growth/size/body

decreased body fat mass ( J:260853 )

♂ • mice exhibit decreased fat mass levels at 6 and 12 weeks of age

increased lean body mass ( J:260853 )

♂ • lean mass is increased at 6 and 12 weeks of age

decreased susceptibility to diet-induced obesity ( J:260853 )

♂ • 8 week old mice fed a high-fat diet do not gain as much weight as controls and are unable to increase fat mass in response to the diet, with lean mass remaining elevated during high-fat diet feeding

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:260853 )

♂N • mice do not exhibit severe metabolic dysfunction, with normal food and water intake and normal energy expenditure and no differences in serum triglyceride, insulin or glucose levels in mice fasted for 5 hours, and no impairment of glucose tolerance

decreased susceptibility to diet-induced obesity ( J:260853 )

♂ • 8 week old mice fed a high-fat diet do not gain as much weight as controls and are unable to increase fat mass in response to the diet, with lean mass remaining elevated during high-fat diet feeding

decreased respiratory quotient ( J:260853 )

♂ • mice exhibit decreased respiratory exchange ratio during the active phase, indicating an increased propensity towards lipid oxidation

♂ • although mice exhibit elevated respiratory exchange ratio during a 9 hour fast, upon re-feeding, mice fail to increase their respiratory exchange ratio to the same level as controls, leading to lower mean values

increased respiratory quotient ( J:260853 )

♂ • during a 9 hour fast, mice show elevated starting respiratory exchange ratio and their mean respiratory exchange ratio levels remain higher during much of the fasting period

decreased circulating adiponectin level ( J:260853 )

♂ • fasted mice exhibit decreased circulating adiponectin levels

♂ • however, circulating leptin levels are normal

abnormal triglyceride level ( J:260853 )

♂ • brown adipose tissues shows altered triglyceride accumulation, with numerous large droplets rather than the normal multilocular morphology

increased liver triglyceride level ( J:260853 )

♂ • mice exhibit elevated liver triglyceride levels

♂ • liver triglyceride levels are not further increased by a high-fat diet

♂ • however, generalized organomegaly or hepatic steatosis are not seen

integument

decreased subcutaneous adipose tissue amount ( J:260853 )

♂ • mice exhibit only residual subcutaneous white adipose tissue

liver/biliary system

increased liver triglyceride level ( J:260853 )

♂ • mice exhibit elevated liver triglyceride levels

♂ • liver triglyceride levels are not further increased by a high-fat diet

♂ • however, generalized organomegaly or hepatic steatosis are not seen

skeleton

decreased bone marrow adipose tissue amount ( J:260853 )

♂ • 16 week old mice exhibit severe depletion of total tibial bone marrow adipose tissue, resulting from loss of both constitutive bone marrow adipose tissue of the distal tibia and regulated bone marrow adipose tissue in the mid-to-proximal tibia

♂ • however, caudal vertebrae constitutive bone marrow adipose tissue appears normal

Genotype
MGI:6457282

cn26

• Allelic Composition: Opn3^{tm2c(EUCOMM)Wtsi}/Opn3^{tm2c(EUCOMM)Wtsi}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6N * FVB/NJ

adipose tissue

abnormal beige fat cell morphology ( J:287419 )

• low beige content in inguinal white adipose tissue

abnormal white fat cell size ( J:287419 )

• larger size distribution

abnormal adipose tissue physiology ( J:287419 )

• fed and fasted, cold-exposed mice impaired fat mobilization compared with control mice

homeostasis/metabolism

impaired adaptive thermogenesis ( J:287419 )

• reduced core body temperature following cold-exposure under full spectrum lighting

• however, mice raised without 480 nm light exhibit normal cold exposure response and tail temperatures are normal

abnormal circulating glycerol level ( J:287419 )

• unlike wild-type mice, fasted mice exhibit reduced elevation of serum glycerol compared with fed mice

decreased core body temperature ( J:287419 )

• following cold-exposure

Genotype
MGI:6449844

cn27

• Allelic Composition: H6pd^{tm1c(EUCOMM)Wtsi}/H6pd^{tm1c(EUCOMM)Wtsi}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6N * FVB/NJ

adipose tissue

decreased subcutaneous adipose tissue amount ( J:292236 )

• 34% reduction

decreased fat cell size ( J:292236 )

• 20% reduction

decreased epididymal fat pad weight ( J:292236 )

• 53% reduction; also reduced under fasting conditions

decreased mesenteric fat pad weight ( J:292236 )

• 62% reduction

homeostasis/metabolism

decreased fasting circulating glucose level ( J:292236 )

decreased circulating insulin level ( J:292236 )

• during GTT and under fasting conditions

decreased circulating free fatty acids level ( J:292236 )

• under both fed and fasting states

improved glucose tolerance ( J:292236 )

• decreased glucose levels during GTT

increased insulin sensitivity ( J:292236 )

• improved glucose clearance during ITT

abnormal corticosterone level ( J:292236 )

• decreased in epididymal and subcutaneous fat

• normal plasma levels

impaired lipolysis ( J:292236 )

• in epididymal fat under both fed and fasting states

decreased lipogenesis ( J:292236 )

• in epididymal and subcutaneous fat

integument

decreased subcutaneous adipose tissue amount ( J:292236 )

• 34% reduction

growth/size/body

growth/size/body region phenotype ( J:292236 )

N • normal weight gain

cardiovascular system

cardiovascular system phenotype ( J:292236 )

N • normal mean systolic blood pressure

behavior/neurological

behavior/neurological phenotype ( J:292236 )

N • normal food intake

Genotype
MGI:6682105

cn28

• Allelic Composition: Pex16^{tm1c(EUCOMM)Hmgu}/Pex16^{tm1c(EUCOMM)Hmgu}; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: C57BL/6N * FVB/NJ * SJL

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:270463 )

• in cold exposed mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:270463 )

N • mice fed a high-fat diet exhibit normal resting energy metabolism

increased susceptibility to diet-induced obesity ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

• cold exposed mice exhibit whitening of brown adipose tissue and increased lethality unlike control mice

• however, diet-induced obesity is normal at 30 degrees Celcius

impaired adaptive thermogenesis ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

• however, diet-induced obesity is normal at 30 degrees Celcius and thermogenesis is recused by a diet containing alkylglycerols

decreased oxygen consumption ( J:270463 )

• reduced oxygen consumption after treatment with norepinephrine

impaired glucose tolerance ( J:270463 )

• in mice fed standard chow

• however, no difference is observed when mice are fed a high-fat diet

abnormal response/metabolism to endogenous compounds ( J:270463 )

• reduced oxygen consumption after treatment with norepinephrine

adipose tissue

increased total body fat amount ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

increased brown fat cell lipid droplet size ( J:270463 )

• in cold exposed mice

whitened brown adipose tissue morphology ( J:270463 )

• after cold treatment, brown adipose tissue is paler with higher levels of triglyceride content compared with control mice

• however, mitochondria cristae are normal

decreased fat cell mitochondrial DNA content ( J:270463 )

• in brown adipose tissue at 22 and 4 degrees Celsius

• in white adipose tissue at 4 degrees Celsius

• however, mitochondrial DNA content is recused by a diet containing alkylglycerols

increased white fat cell size ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

increased gonadal fat pad weight ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

growth/size/body

increased susceptibility to diet-induced obesity ( J:270463 )

• in mice fed a high-fat diet at 22 degrees Celcius

• cold exposed mice exhibit whitening of brown adipose tissue and increased lethality unlike control mice

• however, diet-induced obesity is normal at 30 degrees Celcius

behavior/neurological

behavior/neurological phenotype ( J:270463 )

N • mice fed a high-fat diet exhibit normal food intake and physical activity

cellular

decreased fat cell mitochondrial DNA content ( J:270463 )

• in brown adipose tissue at 22 and 4 degrees Celsius

• in white adipose tissue at 4 degrees Celsius

• however, mitochondrial DNA content is recused by a diet containing alkylglycerols

abnormal mitochondrial physiology ( J:270463 )

• impaired mitochondrial fatty acid oxidation and modest reduction in citrate synthase activity

• however, mitochondrial function is improved by a diet containing alkylglycerols

Genotype
MGI:7616527

cn29

• Allelic Composition: Atp6v0d1^em1Nju/Atp6v0d1^em1Nju; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: FVB/NJ

adipose tissue

decreased brown adipose tissue amount ( J:346448 )

• brown adipose tissue weight is reduced at 24 weeks of age

decreased total body fat amount ( J:346448 )

• mice exhibit diminished adipose depots at both 8 and 24 weeks of age

decreased epididymal fat pad weight ( J:346448 )

• at 24 weeks of age, mice have no visible epididymal white adipose depots

decreased inguinal fat pad weight ( J:346448 )

• inguinal white adipose tissue weight is largely reduced at both 8 and 24 weeks of age

decreased retroperitoneal fat pad weight ( J:346448 )

• at 24 weeks of age, mice have no visible retroperitoneal white adipose depots

lipodystrophy ( J:346448 )

• mice exhibit reduced and diminished adipose depots at 8 and 24 weeks of age, respectively

cardiovascular system

abnormal heart morphology ( J:346448 )

• excessive lipid accumulation is seen in the heart

increased myocardial fiber size ( J:346448 )

• increase in size of cardiomyocytes

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age show reduced cardiomyocyte size

enlarged heart ( J:346448 )

• hearts are visibly larger in 36-week-old mice and the heart weight to tibia length ratio is increased

• however, no difference in the heart weight to body weight ratio is seen but this may be due to increase in liver weight

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age show attenuation of the increased heart weight to tibial weight ratio

cardiac hypertrophy ( J:346448 )

• cardiac hypertrophy is not accompanied by activation of fetal genes, Nppa and Myh7, even when contractile function is impaired

• mice develop cardiac hypertrophy with preserved contractile function by 24 weeks of age but by 28 weeks of age, mice show apparent cardiac contractile dysfunction

• mice injected with AAV9-cTNT-myocardin show amelioration of cardiac hypertrophy but it is not completely corrected

cardiac fibrosis ( J:346448 )

• mice exhibit cardiac fibrosis

• mice injected with an adeno-associated virus 9 that expresses myocardin under the control of the Tnnt2 promoter (AAV9-cTNT-myocardin) at 16 weeks of age show reduced cardiac fibrosis

abnormal cardiovascular system physiology ( J:346448 )

• mice develop cardiac insulin resistance as indicated by decreased insulin receptor substrate (IRS)-1 and IRS-2 expression in hearts

• expression of genes associated with fatty acid uptake and oxidation is upregulated indicating that energy expenditure is reprogrammed in hearts so that is it is shifted preferentially to fatty acid oxidation

• while basal oxygen consumption rate of isolated cardiomyocytes is normal, FCCP (Trifluoromethoxy carbonylcyanide phenylhydrazone)-induced maximal respiration of isolated cardiomyocytes is reduced, despite comparable abundance of the mitochondrial respiratory complexes in hearts

• following application of etomoxir, an inhibitor for carnitine palmitoyl-transferase (CPT1), the reduction in FCCP-induced maximal respiration is greater in cardiomyocytes than in controls

• treatment with Rosiglitazone, a systemic insulin sensitizer, improves cardiac metabolism and function

decreased cardiac muscle contractility ( J:346448 )

• at 28 weeks of age, percent ejection fraction and percent fractional shortening are reduced by 59.4% and 31.2%, respectively, compared to 84.3% and 52.6% in controls and there is only a minor decrease in percent ejection fraction and percent fractional shorting in mice aged 36 weeks compared to those at 26 week of age, indicating slow progression of congestive heart failure

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age increases percent ejection fraction and percent fractional shortening to levels comparable to controls

• treatment with Rosiglitazone, a systemic insulin sensitizer, improves cardiac metabolism and function

abnormal heart echocardiography feature ( J:346448 )

• echocardiography shows that the anterior and posterior wall thickness of the left ventricle at systole and diastole are larger, the internal left ventricle diameter at diastole is smaller at 12 weeks of age, but not 8 weeks of age, and the percent ejection fraction and fractional shortening are comparable to controls until 24 weeks and reduced at 28 weeks of age

growth/size/body

growth/size/body region phenotype ( J:346448 )

N • body weight is unaltered

enlarged heart ( J:346448 )

• hearts are visibly larger in 36-week-old mice and the heart weight to tibia length ratio is increased

• however, no difference in the heart weight to body weight ratio is seen but this may be due to increase in liver weight

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age show attenuation of the increased heart weight to tibial weight ratio

cardiac hypertrophy ( J:346448 )

• mice develop cardiac hypertrophy with preserved contractile function by 24 weeks of age but by 28 weeks of age, mice show apparent cardiac contractile dysfunction

• mice injected with AAV9-cTNT-myocardin show amelioration of cardiac hypertrophy but it is not completely corrected

• cardiac hypertrophy is not accompanied by activation of fetal genes, Nppa and Myh7, even when contractile function is impaired

increased liver weight ( J:346448 )

homeostasis/metabolism

decreased circulating leptin level ( J:346448 )

• plasma leptin levels are reduced at 24 weeks of age

increased circulating cholesterol level ( J:346448 )

• plasma cholesterol levels are increased at 24 weeks of age and plasma cholesterol remains high at 36 weeks of age

increased circulating free fatty acids level ( J:346448 )

• non-esterified fatty acid (NEFA) levels are high at 36 weeks of age

decreased circulating triglyceride level ( J:346448 )

• triglyceride levels are reduced at 24 weeks of age

increased circulating aspartate transaminase level ( J:346448 )

• the aspartate aminotransferase (AST) to alanine aminotransferase (ALT) level ratio is increased at 24 weeks of age, indicating liver injury

improved glucose tolerance ( J:346448 )

• mice show increased glucose tolerance at 24 weeks of age

insulin resistance ( J:346448 )

• mice show reduced insulin sensitivity at 24 weeks of age and systemic insulin resistance is seen in 36-week-old mice

• mice develop cardiac insulin resistance as indicated by decreased IRS-1/2 expression in hearts

• injection with AAV9-cTNT-myocardin at 16 weeks of age increases IRS-1 expression but does not restore IRS-2 expression

decreased circulating adiponectin level ( J:346448 )

• plasma adiponectin levels are reduced at 24 weeks of age

increased liver cholesterol level ( J:346448 )

• at 24 weeks of age

increased liver free fatty acids level ( J:346448 )

• at 24 weeks of age

increased liver triglyceride level ( J:346448 )

• at 8 and 24 weeks of age

liver/biliary system

increased liver weight ( J:346448 )

increased liver cholesterol level ( J:346448 )

• at 24 weeks of age

increased liver free fatty acids level ( J:346448 )

• at 24 weeks of age

increased liver triglyceride level ( J:346448 )

• at 8 and 24 weeks of age

hepatic steatosis ( J:346448 )

• hepatic steatosis is evident at 8 weeks of age

muscle

increased myocardial fiber size ( J:346448 )

• increase in size of cardiomyocytes

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age show reduced cardiomyocyte size

decreased cardiac muscle contractility ( J:346448 )

• at 28 weeks of age, percent ejection fraction and percent fractional shortening are reduced by 59.4% and 31.2%, respectively, compared to 84.3% and 52.6% in controls and there is only a minor decrease in percent ejection fraction and percent fractional shorting in mice aged 36 weeks compared to those at 26 week of age, indicating slow progression of congestive heart failure

• mice injected with AAV9-cTNT-myocardin at 16 weeks of age increases percent ejection fraction and percent fractional shortening to levels comparable to controls

• treatment with Rosiglitazone, a systemic insulin sensitizer, improves cardiac metabolism and function

cellular

increased fibroblast proliferation ( J:346448 )

• staining for FSP, a biomarker for fibroblasts, is increased in hearts, suggesting enhanced proliferation of cardiac fibroblasts

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
cardiomyopathy		DOID:0050700		J:346448
lipodystrophy		DOID:811		J:346448

Genotype
MGI:6682106

cn30

• Allelic Composition: Acox1^em1Wum/Acox1^em1Wum; Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: FVB/NJ

adipose tissue

adipose tissue phenotype ( J:270463 )

N • mice exhibit normal diet-induced obesity

growth/size/body

growth/size/body region phenotype ( J:270463 )

N • mice exhibit normal diet-induced obesity

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:270463 )

N • mice exhibit normal cold tolerance

Genotype
MGI:6358596

tg31

• Allelic Composition: Tg(Adipoq-cre)1Evdr/0
• Genetic Background: involves: FVB/NJ

homeostasis/metabolism

decreased fasting circulating glucose level ( J:249843 )

• in mice fasted mice fed a high-fat diet

improved glucose tolerance ( J:249843 )

• in mice fed a high-fat diet