About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Pomc1-cre)16Lowl
transgene insertion 16, Bradford B Lowell
MGI:3640616
Summary 24 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Htr2ctm1Jke/Y
Tg(Pomc1-cre)16Lowl/0
B6.Cg-Htr2ctm1Jke Tg(Pomc1-cre)16Lowl MGI:3841490
cn2
Insrtm1Khn/Insrtm1Khn
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
involves: 129 * 129S4/SvJae * 129S6/SvEvTac * C57BL/6J * FVB/N MGI:5471586
cn3
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Nr5a1-cre)2Lowl/0
Tg(Pomc1-cre)16Lowl/0
involves: 129 * C57BL/6J * FVB MGI:3663493
cn4
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
involves: 129 * C57BL/6J * FVB MGI:3640618
cn5
Gt(ROSA)26Sortm2(Sirt1)Ktm/Gt(ROSA)26Sor+
Tg(Pomc1-cre)16Lowl/0
involves: 129 * C57BL/6J * FVB/N MGI:5586726
cn6
Gt(ROSA)26Sortm1(Sirt1)Ktm/Gt(ROSA)26Sor+
Tg(Pomc1-cre)16Lowl/0
involves: 129 * C57BL/6J * FVB/N MGI:5586724
cn7
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
involves: 129 * FVB MGI:5142227
cn8
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
Tg(Pomc1-hrGFP)1Lowl/0
involves: 129 * FVB MGI:5142226
cn9
Glp2rtm1.1Xfg/Glp2rtm1.1Xfg
Tg(Pomc1-cre)16Lowl/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5446804
cn10
Gt(ROSA)26Sortm1(Foxo1)Jnk/Gt(ROSA)26Sor+
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:4820871
cn11
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:4820873
cn12
Gt(ROSA)26Sortm2(Foxo1)Jnk/Gt(ROSA)26Sor+
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:4820872
cn13
Rock1tm1.1Itl/Rock1tm1.1Itl
Tg(Npy-hrGFP)1Lowl/0
Tg(Pomc1-cre)16Lowl/0
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:5543677
cn14
Rock1tm1.1Itl/Rock1tm1.1Itl
Tg(Pomc1-cre)16Lowl/0
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:5543676
cn15
Htr2ctm2Jke/Y
Tg(Pomc1-cre)16Lowl/0
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N MGI:5569627
cn16
Nhlh2tm2Thbr/Nhlh2tm2Thbr
Tg(Pomc-EGFP)1Low/0
Tg(Pomc1-cre)16Lowl/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * FVB/N MGI:5524040
cn17
Htr2ctm2Jke/Htr2ctm2Jke
Tg(Pomc1-cre)16Lowl/0
involves: 129X1/SvJ * C57BL/6J * FVB/N MGI:5569624
cn18
Leprtm1Jke/Leprtm1Jke
Tg(Pomc1-cre)16Lowl/0
involves: 129X1/SvJ * C57BL/6J * FVB/N MGI:5426233
cn19
Htr2ctm2Jke/Y
Tg(Pomc1-cre)16Lowl/0
involves: 129X1/SvJ * C57BL/6J * FVB/N MGI:5569623
cn20
Gt(ROSA)26Sortm1(CAG-Foxo1*)Jcbr/Gt(ROSA)26Sor+
Pdpk1tm1Jcbr/Pdpk1tm1Jcbr
Tg(Pomc1-cre)16Lowl/0
involves: C57BL/6 * FVB/N MGI:3804312
cn21
Pdpk1tm1Jcbr/Pdpk1tm1Jcbr
Tg(Pomc1-cre)16Lowl/0
involves: C57BL/6 * FVB/N MGI:3804310
cn22
Tg(CAG-PPARG,-tdTomato)#Sig/0
Tg(Pomc1-cre)16Lowl/0
involves: C57BL/6 * FVB/N * SJL MGI:5912228
cn23
Tg(CAG-PPARG*,-tdTomato)#Sig/0
Tg(Pomc1-cre)16Lowl/0
involves: C57BL/6 * FVB/N * SJL MGI:5912229
tg24
Tg(Pomc1-cre)16Lowl/0 involves: 129 * C57BL/6J * FVB/N MGI:3655815


Genotype
MGI:3841490
cn1
Allelic
Composition
Htr2ctm1Jke/Y
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
B6.Cg-Htr2ctm1Jke Tg(Pomc1-cre)16Lowl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2ctm1Jke mutation (1 available); any Htr2c mutation (9 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice exhibit a decreased survival rate compared to wild-type mice
• mice fed a regular diet exhibit decreased survival compared to mice fed a high fat diet

nervous system

behavior/neurological
N
• mice exhibit normal food intake and locomotor activity levels

homeostasis/metabolism
N
• mice exhibit normal leptin levels and anorexigenic responses to d-Fen and metachlorophenylpiperazine

adipose tissue
N
• mice exhibit normal adiposity in response to a high fat diet

growth/size/body
N
• mice exhibit normal weight gain in response to a high fat diet




Genotype
MGI:5471586
cn2
Allelic
Composition
Insrtm1Khn/Insrtm1Khn
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * 129S4/SvJae * 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Insrtm1Khn mutation (1 available); any Insr mutation (30 available)
Leprtm1.1Chua mutation (0 available); any Lepr mutation (83 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• trend towards increased intra-abdominal adiposity at 4 months of age
• perigonadal adipocyte hypertrophy at 4 months of age
• perigonadal adipocyte hypertrophy at 4 months of age
• an increase in macrophage accumulation is seen in the perigonadal fat indicating inflammation
• percent body fat is increased in females at 4 months of age, however absolute body weight is not increased at this time
• an increase in macrophage accumulation is seen in the perigonadal fat, and macrophage marker analysis and cytokine expression indicates low-grade inflammation in adipose tissue

endocrine/exocrine glands
• 45% of mice lack either corpora lutea or preovulatory follicles
• 45% of mice lack either corpora lutea or preovulatory follicles
• low-grade inflammation as indicated by increased IL-6 expression in the ovary

growth/size/body
• percent lean body mass is decreased at 4 months of age

homeostasis/metabolism
• females are hyperglycemic before (at 3 months of age) and during pregnancy (at gestational days 12 and 15), without evidence of gestational glucose intolerance
• circulating levels of adipokine leptin are increased at 4 months of age

immune system
• an increase in macrophage accumulation is seen in the perigonadal fat, and macrophage marker analysis and cytokine expression indicates low-grade inflammation in adipose tissue
• low-grade inflammation as indicated by increased IL-6 expression in the ovary
• low-grade inflammation as indicated by increased IL-1beta expression in the liver

liver/biliary system
• low-grade inflammation as indicated by increased IL-1beta expression in the liver

reproductive system
• 45% of mice lack either corpora lutea or preovulatory follicles
• 45% of mice lack either corpora lutea or preovulatory follicles
• low-grade inflammation as indicated by increased IL-6 expression in the ovary
• females exhibit reduced ovulation but show normal cycling suppression from fasting

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
polycystic ovary syndrome DOID:11612 OMIM:184700
J:192274




Genotype
MGI:3663493
cn3
Allelic
Composition
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Nr5a1-cre)2Lowl/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * C57BL/6J * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprtm1.1Chua mutation (0 available); any Lepr mutation (83 available)
Tg(Nr5a1-cre)2Lowl mutation (1 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increase in fat mass
• size of fat pads (perigonadal, perirenal, and mesenteric) is increased

growth/size/body
• weigh significantly more than mice lacking Lepr only in SF1 neurons or POM1 neurons

homeostasis/metabolism




Genotype
MGI:3640618
cn4
Allelic
Composition
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * C57BL/6J * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprtm1.1Chua mutation (0 available); any Lepr mutation (83 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• exhibit mild obesity with an increase in body weight at 10 weeks of age that is 18.2% that of homozygous Leprtm1.2Chua mice

adipose tissue
• increase in fat mass (J:105327)
• exhibit increased body fat but no differences in food intake or energy expenditure (J:106354)
• epididymal fat pads are at least twice as large as in controls
• size of perigonadal fat pads is increased
• size of mesenteric fat pads is increased (J:105327)
• mesenteric fat pads are at least twice as large as in controls (J:106354)
• size of perirenal fat pads is increased (J:105327)
• perirenal fat pads are at least twice as large as in controls (J:106354)

homeostasis/metabolism




Genotype
MGI:5586726
cn5
Allelic
Composition
Gt(ROSA)26Sortm2(Sirt1)Ktm/Gt(ROSA)26Sor+
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Sirt1)Ktm mutation (0 available); any Gt(ROSA)26Sor mutation (534 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
N
• mice fed normal chow exhibit normal epididymal white adipose tissue weight

behavior/neurological
N
• mice fed normal chow exhibit normal food intake and locomotor activity

growth/size/body
N
• mice fed normal chow exhibit normal susceptibility to age-associated weight gain and body length

homeostasis/metabolism
N
• mice fed normal chow exhibit normal oxygen consumption




Genotype
MGI:5586724
cn6
Allelic
Composition
Gt(ROSA)26Sortm1(Sirt1)Ktm/Gt(ROSA)26Sor+
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Sirt1)Ktm mutation (0 available); any Gt(ROSA)26Sor mutation (534 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• noradrenaline turnover in the white adipose tissue is increased in male mice compared to in control mice
• however, turnover in skeletal muscle is normal

homeostasis/metabolism
N
• mice exhibit normal hypothalamus-pituitary-adrenal and hypothalamus-pituitary-thyroid axes
• mice exhibit improved leptin sensitivity compared with control mice
• mice tend to be cold-resistant for short-term exposure compared with control mice
• however, mice fed a high fat high sugar diet exhibit normal cold resistance
• noradrenaline turnover in the white adipose tissue is increased in male mice compared to in control mice
• however, turnover in skeletal muscle is normal
• male mice fed normal chow exhibit increased energy expenditure suggested by a tend toward higher oxygen consumption and lower locomotor activity compared with control mice
• however, mice fed a high fat high sugar diet exhibit normal energy expenditure
• trend in male mice fed normal chow

growth/size/body
N
• male and female mice fed normal chow exhibit normal body length
• mice fed a high fat high sugar diet exhibit normal weight gain
• in male, but not female, mice fed normal chow

adipose tissue
• in male, but not female, mice fed normal chow
• however, mice fed a high fat high sugar diet exhibit normal adiposity
• in male mice fed normal chow

behavior/neurological
N
• female and male mice exhibit normal food intake
• trend in male mice fed normal chow
• however, mice fed a high fat high sugar diet exhibit normal locomotion




Genotype
MGI:5142227
cn7
Allelic
Composition
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprtm1.1Chua mutation (0 available); any Lepr mutation (83 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• no change in spontaneous IPSC amplitude or frequency in Pomc1 neurons in slices is observed, indicating that Lepr deletion from postsynaptic Pomc1 neurons does not affect inhibitory tone




Genotype
MGI:5142226
cn8
Allelic
Composition
Leprtm1.1Chua/Leprtm1.1Chua
Tg(Pomc1-cre)16Lowl/0
Tg(Pomc1-hrGFP)1Lowl/0
Genetic
Background
involves: 129 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprtm1.1Chua mutation (0 available); any Lepr mutation (83 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
Tg(Pomc1-hrGFP)1Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• addtion of leptin to neurons reduces the frequency of spontaneous (s)IPSCs in Pomc1 neurons by about 40%, similar to the inhibition observed in control neurons




Genotype
MGI:5446804
cn9
Allelic
Composition
Glp2rtm1.1Xfg/Glp2rtm1.1Xfg
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glp2rtm1.1Xfg mutation (0 available); any Glp2r mutation (4 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• accelerated gastric emptying with a dramatic shortening of half-excretion time and lag phase for a liquid meal

behavior/neurological
• increase in meal frequency but not meal size
• higher food intake during the dark cycle
• during the dark cycle

growth/size/body
• lean mass as a percent of body weight is decreased by 32 weeks of age
• late onset obesity develops after 33 weeks of age

adipose tissue

homeostasis/metabolism
• in fed mice during the dark cycle
• increase in heat production by fed mice during the dark cycle
• however, at 12 weeks of age mice fasted for 4 h show similar metabolic activity (VO2, VCO2, and heat production) to controls under inactive conditions




Genotype
MGI:4820871
cn10
Allelic
Composition
Gt(ROSA)26Sortm1(Foxo1)Jnk/Gt(ROSA)26Sor+
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Foxo1)Jnk mutation (0 available); any Gt(ROSA)26Sor mutation (534 available)
Pdpk1tm1Maka mutation (0 available); any Pdpk1 mutation (127 available)
Tg(CAG-cat-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice a tend towards increased in body weight compared with Pdpk1tm1Maka/Pdpk1tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice




Genotype
MGI:4820873
cn11
Allelic
Composition
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdpk1tm1Maka mutation (0 available); any Pdpk1 mutation (127 available)
Tg(CAG-cat-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mice exhibit increased apoptosis in the pituitary compared with wild-type mice
• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice
• however, corticotroph development in the anterior pituitary at E18.5 is normal
• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice
• however, melanotrophs development in the intermediate pituitary at E18.5 is normal

nervous system
• mice exhibit increased apoptosis in the pituitary compared with wild-type mice
• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice
• however, corticotroph development in the anterior pituitary at E18.5 is normal
• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice
• however, melanotrophs development in the intermediate pituitary at E18.5 is normal
• Pomc1 neurons exhibit a blunted influx of calcium ions in response to leptin compared with similarly treated wild-type neurons

homeostasis/metabolism
• following intraperitoneal leptin injection, mice exhibit a lesser decrease in body weight and food intake compared with similarly treated wild-type mice
• at 16 weeks in fed and fasted states

adipose tissue
• especially visceral fat mass

behavior/neurological
• food intake is increased compared to in wild-type mice

endocrine/exocrine glands
• mice exhibit increased apoptosis in the pituitary compared with wild-type mice
• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice
• however, corticotroph development in the anterior pituitary at E18.5 is normal
• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice
• however, melanotrophs development in the intermediate pituitary at E18.5 is normal




Genotype
MGI:4820872
cn12
Allelic
Composition
Gt(ROSA)26Sortm2(Foxo1)Jnk/Gt(ROSA)26Sor+
Pdpk1tm1Maka/Pdpk1tm1Maka
Tg(CAG-cat-lacZ)11Miya/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Foxo1)Jnk mutation (0 available); any Gt(ROSA)26Sor mutation (534 available)
Pdpk1tm1Maka mutation (0 available); any Pdpk1 mutation (127 available)
Tg(CAG-cat-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• female mice exhibit a tended towards increased adiposity compared with wild-type mice

behavior/neurological
• mice exhibit increased food intake compared with wild-type mice and Pdpk1tm1Maka/Pdpk1tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice

growth/size/body
• at 16 weeks, mice are significantly heavier than Pdpk1tm1Maka/Pdpk1tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice




Genotype
MGI:5543677
cn13
Allelic
Composition
Rock1tm1.1Itl/Rock1tm1.1Itl
Tg(Npy-hrGFP)1Lowl/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rock1tm1.1Itl mutation (0 available); any Rock1 mutation (8 available)
Tg(Npy-hrGFP)1Lowl mutation (1 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• leptin fails to depolarize POMC+ neurons and increase firing rate unlike in control neurons




Genotype
MGI:5543676
cn14
Allelic
Composition
Rock1tm1.1Itl/Rock1tm1.1Itl
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rock1tm1.1Itl mutation (0 available); any Rock1 mutation (8 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue

homeostasis/metabolism
• modest defect in the ability of insulin to decrease blood glucose

behavior/neurological
• during the dark phase
• however, movement during the light phase is normal

growth/size/body

skeleton
N
• mice exhibit normal femur length, bone mineral density and bone mineral content




Genotype
MGI:5569627
cn15
Allelic
Composition
Htr2ctm2Jke/Y
Tg(Pomc1-cre)16Lowl/0
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze mutation (4 available); any Gt(ROSA)26Sor mutation (534 available)
Htr2ctm2Jke mutation (0 available); any Htr2c mutation (9 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• ability of the serotonin receptor 2C agonist mCPP to depolarized Pomc-expressing neurons is abolished in mutants




Genotype
MGI:5524040
cn16
Allelic
Composition
Nhlh2tm2Thbr/Nhlh2tm2Thbr
Tg(Pomc-EGFP)1Low/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nhlh2tm2Thbr mutation (0 available); any Nhlh2 mutation (4 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
Tg(Pomc-EGFP)1Low mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• mice exhibit normal uteri weight and fertility

nervous system
N
• mice exhibit normal numbers of Gnrh+ neurons

growth/size/body
N
• mice exhibit normal weight

adipose tissue
N
• mice exhibit normal visceral and subcutaneous fat depots




Genotype
MGI:5569624
cn17
Allelic
Composition
Htr2ctm2Jke/Htr2ctm2Jke
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2ctm2Jke mutation (0 available); any Htr2c mutation (9 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• animals are born at Mendelian frequency and show no increased mortality compared to controls

growth/size/body
N
• when fed a regular chow diet, body weights of mutants are similar to controls at weaning and between 8 and 20 weeks of age
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet; at 20 weeks on the HFHS-diet, mutants are 25% heavier than controls due to adiposity
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have increased body weights compared to controls
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet
• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

behavior/neurological
• daily food intake is elevated relative to controls when fed a regular chow diet; when diet is transitioned to a high fat, high sugar (HFHS) diet for 1 week, food intake is significantly increased relative to controls
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show a higher food intake compared to controls
• administration of d-flenfluaramine or the more specific serotonin 2C receptor agonist mCPP strongly suppresses food intake in control mice, but mutants are not affected
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show increased total physical activity compared to controls; this increase is restricted to the dark phase
• when animals are switched to a high fat high sugar diet for 1 week, physical activity does not increase relative to the chow diet
• total activity due to increased dark cycle activity is increased compared to controls when fed a regular chow diet

homeostasis/metabolism
N
• on a regular chow diet, mutants and controls have similar respiratory exchange ratios when fed a regular chow diet
• chow-fed or HFHS-fed (high fat, high sugar) animals have similar circulating leptin levels
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet
• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet
• at the beginning of the light phase (7 am), chow-fed mice show modestly higher glucose levels than controls; levels are significantly elevated in postabsorptive (4-5 hour morning-fasted animals) but not in overnight (12-24 h) fasted mice
• high fat, high sugar (HFHS) fed mutants also have elevated glucose levels in the postabsorptive period compared to HFHS-fed controls
• higher plasma glucagon levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting
• HFHS-fed (high fat, high sugar) animals do not show additionally increased plasma glucagon levels compared to chow-fed mutants
• higher plasma insulin levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting
• HFHS-fed (high fat, high sugar) animals have a greater increase in plasma insulin compared to chow-fed mutants
• increased energy intake and expenditure are observed when fed a regular chow diet
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have lower oxygen consumption relative to body weight compared to controls on the same diet while carbon dioxide production is similar to controls
• VO2 (and VCO2) are increased compared to controls when fed a regular chow diet
• when animals are switched to a high fat high sugar diet for 1 week, oxygen consumption/ C02 production does not increase relative to the chow diet
• on the high fat high sugar diet for 1 week, respiratory exchange ratio (RER) is slightly decreased in mutants and controls compared to animals on a regular chow diet, but over a 24 hour period, mutants show a modest increase relative to controls
• 20 week-old mutants which had been fed an HFHS (high fat, high sugar) diet for 12 weeks have a higher RER during the dark phase
• hyperinsulinemic-euglycemic clamp experiments in postabsorptive and overnight-fasted 8-9 week old mice show reduced insulin sensitivity




Genotype
MGI:5426233
cn18
Allelic
Composition
Leprtm1Jke/Leprtm1Jke
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Leprtm1Jke mutation (2 available); any Lepr mutation (83 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice exhibit normal circulating glucagon levels in the fed and carbohydrate-refed state
• compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice
• compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice
• mice exhibit normal basal glucose turnover compared with Leprtm1Jke homozygotes
• insulin-stimulated glucose disposal is impaired compared to in wild-type mice
• however, mice exhibit normal circulating glucose levels at 6, 8 and 12 weeks
• in the pancreas compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• at 8 and 12 weeks compared with Leprtm1Jke homozygotes
• compared with wild-type mice
• compared with Leprtm1Jke homozygotes
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice

growth/size/body
• in male mice after 12 weeks compared with Leprtm1Jke homozygotes
• in male mice between 4 and 12 weeks less severe after 12 weeks compared with wild-type mice
• in female mice

behavior/neurological
• compared with wild-type mice
• during the dark phase compared with wild-type mice

adipose tissue
• in male mice at 20 weeks compared with Leprtm1Jke homozygotes
• in male mice at 12 and 20 weeks compared with wild-type mice

endocrine/exocrine glands
• in the pancreas compared with wild-type mice

liver/biliary system
• compared with Leprtm1Jke homozygotes
• compared with wild-type mice




Genotype
MGI:5569623
cn19
Allelic
Composition
Htr2ctm2Jke/Y
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2ctm2Jke mutation (0 available); any Htr2c mutation (9 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• daily food intake is elevated relative to controls when fed a regular chow diet; when diet is transitioned to a high fat, high sugar (HFHS) diet for 1 week, food intake is significantly increased relative to controls
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show a higher food intake compared to controls
• administration of d-flenfluaramine or the more specific serotonin 2C receptor agonist mCPP strongly suppresses food intake in control mice, but mutants are not affected
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show increased total physical activity compared to controls; this increase is restricted to the dark phase
• when animals are switched to a high fat high sugar diet for 1 week, physical activity does not increase relative to the chow diet
• total activity due to increased dark cycle activity is increased compared to controls when fed a regular chow diet

growth/size/body
N
• when fed a regular chow diet, body weights of mutants are similar to controls at weaning and between 8 and 20 weeks of age
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet; at 20 weeks on the HFHS-diet, mutants are 25% heavier than controls due to adiposity
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have increased body weights compared to controls
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet
• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

homeostasis/metabolism
N
• on a regular chow diet, mutants and controls have similar respiratory exchange ratios when fed a regular chow diet
• chow-fed or HFHS-fed (high fat, high sugar) animals have similar circulating leptin levels
• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet
• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet
• at the beginning of the light phase (7 am), chow-fed mice show modestly higher glucose levels than controls; levels are significantly elevated in postabsorptive (4-5 hour morning-fasted animals) but not in overnight (12-24 h) fasted mice
• high fat, high sugar (HFHS) fed mutants also have elevated glucose levels in the postabsorptive period compared to HFHS-fed controls
• higher plasma glucagon levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting
• HFHS-fed (high fat, high sugar) animals do not show additionally increased plasma glucagon levels compared to chow-fed mutants
• higher plasma insulin levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting
• HFHS-fed (high fat, high sugar) animals have a greater increase in plasma insulin compared to chow-fed mutants
• increased energy intake and expenditure are observed when fed a regular chow diet
• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have lower oxygen consumption relative to body weight compared to controls on the same diet while carbon dioxide production is similar to controls
• VO2 (and VCO2) are increased compared to controls when fed a regular chow diet
• when animals are switched to a high fat high sugar diet for 1 week, oxygen consumption/ C02 production does not increase relative to the chow diet
• on the high fat high sugar diet for 1 week, respiratory exchange ratio (RER) is slightly decreased in mutants and controls compared to animals on a regular chow diet, but over a 24 hour period, mutants show a modest increase relative to controls
• 20 week-old mutants which had been fed an HFHS (high fat, high sugar) diet for 12 weeks have a higher RER during the dark phase
• hyperinsulinemic-euglycemic clamp experiments in postabsorptive and overnight-fasted 8-9 week old mice show reduced insulin sensitivity

mortality/aging
N
• animals are born at Mendelian frequency and show no increased mortality compared to controls




Genotype
MGI:3804312
cn20
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Foxo1*)Jcbr/Gt(ROSA)26Sor+
Pdpk1tm1Jcbr/Pdpk1tm1Jcbr
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Foxo1*)Jcbr mutation (0 available); any Gt(ROSA)26Sor mutation (534 available)
Pdpk1tm1Jcbr mutation (0 available); any Pdpk1 mutation (127 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• expression of the mutant foxo1 restores body weight, food consumption and blood glucose levels to normal
• mutants have reduced basal and stress-induced corticosterone levels, similar to double Pdk1tm1Jcbr Tg(Pomc1-cre)16Lowl mutants

endocrine/exocrine glands
• same reduction in corticotrophs as seen in double Pdk1tm1Jcbr Tg(Pomc1-cre)16Lowl mutants

nervous system
• same reduction in corticotrophs as seen in double Pdk1tm1Jcbr Tg(Pomc1-cre)16Lowl mutants




Genotype
MGI:3804310
cn21
Allelic
Composition
Pdpk1tm1Jcbr/Pdpk1tm1Jcbr
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdpk1tm1Jcbr mutation (0 available); any Pdpk1 mutation (127 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• males and females fed either a normal chow diet or a high-fat chow diet display slightly but significantly increased body weight, although over time, weight normalizes
• corticosterone replacement in mutants increases food intake and body weight

homeostasis/metabolism
• reduction in plasma corticosterone concentrations is seen as early as 3 weeks of age, with levels continuing to decrease over time
• mutants show an impairment in stress-induced corticosterone production
• injection of ACTH analog does not increase plasma corticosterone to the level of control mice, consistent with adrenal insufficiency
• corticosterone replacement in mutants increases food intake and body weight
• initially, mutants exhibit an elevation in serum leptin levels at 8 weeks of age, however by 18 weeks of age, they show lower serum leptin levels than controls but have an unchanged body weight
• glucose-stimulated insulin secretion is lower than in controls
• analysis of glucose-stimulated insulin secretion shows that although insulin secretion is lower, their blood glucose concentration is also lower than in controls
• initial elevation in serum glucose levels at 8 weeks of age
• old mutants perform better than controls during glucose tolerance tests
• old mutants show significantly increased insulin sensitivity during insulin tolerance tests than controls

endocrine/exocrine glands
• decrease in melanotroph numbers in the intermediate lobe of the pituitary, but do not see an obvious change in fur color or skin pigmentation
• glucose-stimulated insulin secretion is lower than in controls

adipose tissue
• at 18 weeks of age, mutants show reduced epigonadal fat-pad mass

behavior/neurological
• significant hyperphagia at 8 weeks of age but not at 10 weeks of age
• corticosterone replacement in mutants increases food intake and body weight

nervous system
• decrease in melanotroph numbers in the intermediate lobe of the pituitary, but do not see an obvious change in fur color or skin pigmentation




Genotype
MGI:5912228
cn22
Allelic
Composition
Tg(CAG-PPARG,-tdTomato)#Sig/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-PPARG,-tdTomato)#Sig mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• threefold larger increase in body weight than controls after intraperitoneal rosiglitazone injection on 45% HFD




Genotype
MGI:5912229
cn23
Allelic
Composition
Tg(CAG-PPARG*,-tdTomato)#Sig/0
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-PPARG*,-tdTomato)#Sig mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological

growth/size/body
N
• body water content
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)

adipose tissue
N
• gonadal fat pad morphology 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet
• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet

homeostasis/metabolism
N
• fasted circulating glucose level

integument
• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet




Genotype
MGI:3655815
tg24
Allelic
Composition
Tg(Pomc1-cre)16Lowl/0
Genetic
Background
involves: 129 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pomc1-cre)16Lowl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• transgenic mice have identical body weights to wild-type littermates





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
06/30/2020
MGI 6.15
The Jackson Laboratory