All Phenotypes Gck<+> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Gck⁺
wild type
MGI:2176806

Summary

33 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Gck^tm2Mgn/Gck⁺	129S6/SvEvTac-Gck^tm2Mgn	MGI:3713294
ht2	Gck^tm3Mgn/Gck⁺	129S6/SvEvTac-Gck^tm3Mgn	MGI:3713300
ht3	Gck^tm2Mgn/Gck⁺	B6.129S6-Gck^tm2Mgn	MGI:3713296
ht4	Gck^tm3Mgn/Gck⁺	B6.129S6-Gck^tm3Mgn	MGI:3713297
ht5	Gck^Gls006/Gck⁺	C3HeB/FeJ-Gck^Gls006	MGI:5446493
ht6	Gck^M1Btlr/Gck⁺	C57BL/6J-Gck^M1Btlr	MGI:5641256
ht7	Gck^Sgrd/Gck⁺	C57BL/6J-Gck^Sgrd	MGI:5490554
ht8	Gck^Sgrd-2Nwu/Gck⁺	C57BL/6J-Gck^Sgrd-2Nwu	MGI:5490557
ht9	Gck^em1(IMPC)H/Gck⁺	C57BL/6NTac-Gck^em1(IMPC)H/H	MGI:6262505
ht10	Gck^tm1Ts/Gck⁺	either: (involves: 129S7/SvEvBrd * C57BL/6J) or (involves: 129S7/SvEvBrd * DBA/2J)	MGI:2176950
ht11	Gck^tm1Efr/Gck⁺	involves: 129P2/OlaHsd * C57BL/6	MGI:2176960
ht12	Gck^tm1.2Mgn/Gck⁺	involves: 129S6/SvEvTac * C57BL/6	MGI:3590686
ht13	Gck^tm1Tka/Gck⁺	involves: 129X1/SvJ * ICR	MGI:3583686
ht14	Gck^Gena348/Gck⁺	involves: BALB/c * C3H/He	MGI:3044560
ht15	Gck^m1Rge/Gck⁺	involves: C3HeB/FeJ	MGI:4820839
ht16	Gck^Rgsc702/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038221
ht17	Gck^Rgsc475/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038220
ht18	Gck^Rgsc236/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3590138
ht19	Gck^Rgsc553/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3590139
ht20	Gck^Rgsc735/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3590140
ht21	Gck^Rgsc552/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3590141
ht22	Gck^Rgsc149/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3590142
ht23	Gck^Rgsc392/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038218
ht24	Gck^Rgsc341/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038216
ht25	Gck^Rgsc272/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038214
ht26	Gck^Rgsc210/Gck⁺	involves: C57BL/6J * DBA/2J	MGI:3038212
ht27	Gck^Rgsc149/Gck⁺	involves: C57BL/6JJcl * DBA/2JJcl	MGI:3798893
ht28	Gck^Rgsc960/Gck⁺	involves: C57BL/6JJcl * DBA/2JJcl	MGI:3811738
cn29	Gck^tm1.1Mgn/Gck⁺ Tg(Ins2-cre)25Mgn/0	involves: 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:3603012
cn30	Gck^tm1Ydor/Gck⁺ Tg(Ins1-cre/ERT)1Lphi/0	involves: C57BL/6 * C57BL/6J * CD-1	MGI:6690684
cn31	Gck^tm1Ydor/Gck⁺ Tg(Ins2-cre)25Mgn/0	involves: C57BL/6 * C57BL/6J * DBA	MGI:6690664
cn32	Gck^tm1Hrt/Gck⁺ Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺	involves: C57BL/6 * DBA	MGI:3618231
cx33	Gck^tm1Tka/Gck⁺ Irs1^tm1Tka/Irs1^tm1Tka	involves: 129X1/SvJ * C57BL/6 * CBA * ICR	MGI:3583687

Allelic Composition	Gck^tm2Mgn/Gck⁺
Genetic Background	129S6/SvEvTac-Gck^tm2Mgn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm2Mgn mutation (2 available); any Gck mutation (64 available)

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

homeostasis/metabolism

abnormal glucose homeostasis ( J:121910 )

• ratio between plasma insulin and blood glucose level is significantly higher throughout the 120-minute period after glucose challenge

abnormal insulin secretion ( J:121910 )

• mice are less sensitive to glucose and islets secret insulin in response to 8.0mM glucose

hyperglycemia ( J:121910 )

• fasted 4-week old mice display mild hyperglycemia

impaired glucose tolerance ( J:121910 )

• glucose regulation is impaired in mice

decreased glucokinase activity ( J:121910 )

• glucokinase activity is reduced ~43% compared to wild-type mice

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:121910 )

N	• islets have similar morphology and total insulin content to wild-type islets when mice are fed a normal diet

abnormal insulin secretion ( J:121910 )

• mice are less sensitive to glucose and islets secret insulin in response to 8.0mM glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:121910

Allelic Composition	Gck^tm3Mgn/Gck⁺
Genetic Background	129S6/SvEvTac-Gck^tm3Mgn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm3Mgn mutation (2 available); any Gck mutation (64 available)

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

homeostasis/metabolism

abnormal glucose homeostasis ( J:121910 )

• ratio between plasma insulin and blood glucose level is significantly lower throughout the 120-minute period after glucose challenge

• insulin/glucose ratio in fasted, adults is significantly greater than in wild-type

abnormal insulin secretion ( J:121910 )

• mice are more sensitive to glucose and islets secret insulin in response to 2.5 mM glucose

hypoglycemia ( J:121910 )

• fasted 4-week old mice display mild hypoglycemia

decreased glucokinase activity ( J:121910 )

• glucokinase activity is reduced by 38% relative to wild-type

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:121910 )

N	• islets have similar morphology and total insulin content to wild-type islets when mice are fed a normal diet

abnormal insulin secretion ( J:121910 )

• mice are more sensitive to glucose and islets secret insulin in response to 2.5 mM glucose

Allelic Composition	Gck^tm2Mgn/Gck⁺
Genetic Background	B6.129S6-Gck^tm2Mgn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm2Mgn mutation (2 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:121910 )

Allelic Composition	Gck^tm3Mgn/Gck⁺
Genetic Background	B6.129S6-Gck^tm3Mgn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm3Mgn mutation (2 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hypoglycemia ( J:121910 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
hyperinsulinemic hypoglycemia		DOID:13317	OMIM:PS256450	J:121910

Allelic Composition	Gck^Gls006/Gck⁺
Genetic Background	C3HeB/FeJ-Gck^Gls006

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Gls006 mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:189544 )

N	• mice exhibit normal insulin sensitivity

decreased insulin secretion ( J:189544 )

• in fasted mice at P30

increased circulating glucose level ( J:189544 )

• 1.3-fold at birth

• in fasted and ad libitum fed mice

• after glucose stimulation

hyperglycemia ( J:189544 )

• mild

decreased circulating insulin level ( J:189544 )

• in fasted mice at P30

impaired glucose tolerance ( J:189544 )

decreased glucokinase activity ( J:189544 )

• intermediate

endocrine/exocrine glands

decreased pancreatic beta cell mass ( J:189544 )

• slightly

small pancreatic islets ( J:189544 )

decreased insulin secretion ( J:189544 )

• in fasted mice at P30

Allelic Composition	Gck^M1Btlr/Gck⁺
Genetic Background	C57BL/6J-Gck^M1Btlr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^M1Btlr mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

impaired glucose tolerance ( J:221479 )

• 30 minutes after glucose administration

Allelic Composition	Gck^Sgrd/Gck⁺
Genetic Background	C57BL/6J-Gck^Sgrd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Sgrd mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:196563 )

decreased circulating insulin level ( J:196563 )

Allelic Composition	Gck^Sgrd-2Nwu/Gck⁺
Genetic Background	C57BL/6J-Gck^Sgrd-2Nwu

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Sgrd-2Nwu mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:196563 )

Allelic Composition	Gck^em1(IMPC)H/Gck⁺
Genetic Background	C57BL/6NTac-Gck^em1(IMPC)H/H

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^em1(IMPC)H mutation (3 available); any Gck mutation (64 available)

Data Sources

IMPC Data for Gck

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

homeostasis/metabolism

increased circulating fructosamine level ( J:211773 )

IMPC - HAR

increased circulating glucose level ( J:211773 )

IMPC - HAR

increased fasting circulating glucose level ( J:211773 )

IMPC - HAR

increased circulating alkaline phosphatase level ( J:211773 )

IMPC - HAR

impaired glucose tolerance ( J:211773 )

IMPC - HAR

Allelic Composition	Gck^tm1Ts/Gck⁺
Genetic Background	either: (involves: 129S7/SvEvBrd * C57BL/6J) or (involves: 129S7/SvEvBrd * DBA/2J)

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Ts mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:29255 )

• hyperglycemia in fed and fasted states; normal insulin levels observed

impaired glucose tolerance ( J:29255 )

• decreased glucose tolerance shown in glucose tolerance tests

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:29255

Allelic Composition	Gck^tm1Efr/Gck⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Efr mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

abnormal glucose homeostasis ( J:28756 )

• heterozygotes exhibit abnormal hepatic glucose metabolism: hyperglycemia and hyperinsulinemia reduce hepatic glucose production by only 47% vs 72% in wild-type mice

• also, the fraction of hepatic UDPG pool derived from plasma glucose via the "direct" pathway is significantly reduced relative to wild-type

hyperglycemia ( J:28756 )

• at 5-6 months, heterozygous males show normoglycemia in the fed state

• however, heterozygotes show a mild (25%) increase in overnight fasting glucose levels relative to wild-type mice

• in contrast, plasma insulin levels remain unchanged relative to wild-type in both the fed and fasted state

impaired glucose tolerance ( J:28756 )

• heterozygotes display reduced tolerance to glucose relative to wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:28756

Allelic Composition	Gck^tm1.2Mgn/Gck⁺
Genetic Background	involves: 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1.2Mgn mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

decreased insulin secretion ( J:51826 )

• insulin secretion in response to the hyperglycemic clamp is decreased by 60%

hyperglycemia ( J:51826 )

• plasma glucose concentration increases over time (117 mg/dl vs. 73 mg/dl in wild-type at 2 days and 304 mg/dl vs. 175 mg/dl in wild-type at 6-10 weeks of age)

impaired glucose tolerance ( J:51826 )

• 70% reduction in glucose infusion rate in hyperglycemic clamp studies

decreased liver glycogen level ( J:51826 )

• intermediate levels of hepatic glycogen under normal conditions

• hepatic glycogen synthesis is decreased by more than 90% in response to the hyperglycemic clamp

liver/biliary system

decreased liver glycogen level ( J:51826 )

• intermediate levels of hepatic glycogen under normal conditions

• hepatic glycogen synthesis is decreased by more than 90% in response to the hyperglycemic clamp

hepatic steatosis ( J:51826 )

• intermediate amount of steatosis

endocrine/exocrine glands

decreased insulin secretion ( J:51826 )

• insulin secretion in response to the hyperglycemic clamp is decreased by 60%

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:51826

Allelic Composition	Gck^tm1Tka/Gck⁺
Genetic Background	involves: 129X1/SvJ * ICR

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Tka mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

decreased insulin secretion ( J:30334 )

• heterozygous islets show normal insulin secretion in response to 0.1 mM or 3 mM glucose but not in response to 10 mM glucose; a less pronounced defect is noted in response to 20 mM glucose

• in contrast, heterozygous islets display a relatively normal insulin secretion in response to glibenclamide or arginine

hyperglycemia ( J:30334 )

• at 10 weeks, heterozygotes display significantly higher blood glucose levels both before and after a glucose load relative to wild-type mice

• however, heterozygotes have normal blood glucose levels at birth

impaired glucose tolerance ( J:30334 )

• heterozygotes exhibit mild glucose intolerance due to an impaired insulin response to glucose

increased urine glucose level ( J:30334 )

• ~50% of heterozygotes display mild glycosuria within a day, suggesting the development of early-onset mild diabetes mellitus

endocrine/exocrine glands

decreased insulin secretion ( J:30334 )

• heterozygous islets show normal insulin secretion in response to 0.1 mM or 3 mM glucose but not in response to 10 mM glucose; a less pronounced defect is noted in response to 20 mM glucose

• in contrast, heterozygous islets display a relatively normal insulin secretion in response to glibenclamide or arginine

renal/urinary system

increased urine glucose level ( J:30334 )

• ~50% of heterozygotes display mild glycosuria within a day, suggesting the development of early-onset mild diabetes mellitus

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:30334

Allelic Composition	Gck^Gena348/Gck⁺
Genetic Background	involves: BALB/c * C3H/He

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Gena348 mutation (3 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:79719 , J:82809 , J:90389 )

impaired glucose tolerance ( J:90389 )

• blood glucose levels are elevated in heterozygous mice throughout an intraperitoneal glucose tolerance test

growth/size/body

increased body weight ( J:82809 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:90389

Allelic Composition	Gck^m1Rge/Gck⁺
Genetic Background	involves: C3HeB/FeJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^m1Rge mutation (0 available); any Gck mutation (64 available)

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

homeostasis/metabolism

decreased insulin secretion ( J:162903 )

• marginally in beta cells of male mice

hyperglycemia ( J:162903 )

• slightly in fed mice from the first days of life

• significantly at 30 days of age

• at 30 days during a glucose tolerance test

increased circulating insulin level ( J:162903 )

• in fasted male mice and after oral glucose administration at 90 and 180 days

impaired glucose tolerance ( J:162903 )

insulin resistance ( J:162903 )

• slightly in male mice

endocrine/exocrine glands

decreased pancreatic beta cell mass ( J:162903 )

• in male, but not female, mice

small pancreatic islets ( J:162903 )

• in male, but not female, mice

decreased insulin secretion ( J:162903 )

• marginally in beta cells of male mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:162903

Allelic Composition	Gck^Rgsc702/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc702 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

decreased circulating insulin level ( J:88919 )

• mutants have impaired glucose responsive insulin secretion

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc475/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc475 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

decreased circulating insulin level ( J:88919 )

• mutants have impaired glucose responsive insulin secretion

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc236/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc236 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc553/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc553 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc735/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc735 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc552/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc552 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc149/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc149 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc392/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc392 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

decreased circulating insulin level ( J:88919 )

• mutants have impaired glucose responsive insulin secretion

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc341/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

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Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc341 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc272/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

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Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc272 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

decreased circulating insulin level ( J:88919 )

• mutants have impaired glucose responsive insulin secretion

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc210/Gck⁺
Genetic Background	involves: C57BL/6J * DBA/2J

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Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc210 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

hyperglycemia ( J:88919 )

• mutants have a free fed serum glucose level of 200 mg/dl or more, this was the basis for selection in the ENU screen

impaired glucose tolerance ( J:88919 )

• during an oral glucose tolerance test blood glucose levels are significantly higher

hematopoietic system

increased glycosylated hemoglobin level ( J:88919 )

• increased glycosylated hemoglobin indicating a prolonged increase in serum glucose

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:88919

Allelic Composition	Gck^Rgsc149/Gck⁺
Genetic Background	involves: C57BL/6JJcl * DBA/2JJcl

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc149 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:133634 )

• blood glucose of 11 week-old mice heterozygous for this mutation is elevated (289 mg/dL vs. a control range of 73.1-182.7 mg/dL)

Allelic Composition	Gck^Rgsc960/Gck⁺
Genetic Background	involves: C57BL/6JJcl * DBA/2JJcl

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^Rgsc960 mutation (1 available); any Gck mutation (64 available)

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

homeostasis/metabolism

hyperglycemia ( J:133634 )

• blood glucose at 11 wk = 254 mg/dL

Allelic Composition	Gck^tm1.1Mgn/Gck⁺ Tg(Ins2-cre)25Mgn/0
Genetic Background	involves: 129S6/SvEvTac * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1.1Mgn mutation (1 available); any Gck mutation (64 available)
Tg(Ins2-cre)25Mgn mutation (3 available)

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

homeostasis/metabolism

decreased insulin secretion ( J:51826 )

• 70% decrease in insulin secretion during hyperglycemic clamp studies

hyperglycemia ( J:51826 )

• blood glucose concentration is increased by about 50% compared to heterozygous Gck^tm1.1Mgn mice

• under fasting conditions, have a 25% increase in blood glucose concentration, without differences in basal insulin concentration

impaired glucose tolerance ( J:51826 )

• glucose turnover and glucose infusion rates during hyperglycemic clamp are reduced by about 60 and 70%, respectively

decreased glycogen level ( J:51826 )

• net glycogen synthesis in liver is reduced by about 50% during hyperglycemic clamp studies

endocrine/exocrine glands

decreased insulin secretion ( J:51826 )

• 70% decrease in insulin secretion during hyperglycemic clamp studies

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:51826

Allelic Composition	Gck^tm1Ydor/Gck⁺ Tg(Ins1-cre/ERT)1Lphi/0
Genetic Background	involves: C57BL/6 * C57BL/6J * CD-1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Ydor mutation (0 available); any Gck mutation (64 available)
Tg(Ins1-cre/ERT)1Lphi mutation (1 available)

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

homeostasis/metabolism

hypoglycemia ( J:302600 )

• mice treated with tamoxifen exhibit long-term, persistent hypoglycemia

impaired glucose tolerance ( J:302600 )

• 9-month-old tamoxifen-treated mice, but not 1.5-month-old tamoxifen-treated mice, exhibit abnormal glucose tolerance

endocrine/exocrine glands

increased pancreatic beta cell mass ( J:302600 )

• tamoxifen-treated mice exhibit an increase in beta cell mass at 1.5 months of age, but this increase is no longer seen at 9 months of age

Allelic Composition	Gck^tm1Ydor/Gck⁺ Tg(Ins2-cre)25Mgn/0
Genetic Background	involves: C57BL/6 * C57BL/6J * DBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Ydor mutation (0 available); any Gck mutation (64 available)
Tg(Ins2-cre)25Mgn mutation (3 available)

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

homeostasis/metabolism

increased insulin secretion ( J:302600 )

• islets secrete more insulin per beta cell following glucose stimulation at 1.5 months and 8 months of age

• however, 8-month-old mice treated with diazoxide, an opener of the beta cell K-ATP channels and suppressor of endogenous insulin secretion, and subsequently administered insulin show a similar decrease in blood glucose levels as controls indicating no insulin resistance

decreased fasting circulating glucose level ( J:302600 )

• overnight fasted glucose levels are lower

• fasting glucose levels are lower in mice fed a high-fat/high-sugar diet

hypoglycemia ( J:302600 )

• mice exhibit reduced random blood glucose levels, which persists for at least 15 months

• mice fed a high-fat/high-sugar diet for 37 weeks exhibit consistently lower random glucose levels, however body weight gain is similar to controls

increased circulating insulin level ( J:302600 )

• plasma insulin levels are increased

• insulin levels are higher in mice fed a high-fat/high-sugar diet

impaired glucose tolerance ( J:302600 )

• mice exhibit impaired glucose tolerance at 8 months of age, while maintaining fed and fasting hypoglycemia

• however, no difference in glucose tolerance tests are seen at 1.5 months of age

• mice fed a high-fat/high-sugar diet for 37 weeks show more severely impaired glucose tolerance than controls

• after 37 weeks of a high-fat/high-sugar diet, peak insulin levels 15 minutes following glucose injection are slightly, but significantly, reduced despite identical blood glucose levels, indicating a subtle defect in first-phase insulin response

endocrine/exocrine glands

decreased pancreatic beta cell mass ( J:302600 )

• the increase in beta cell mass seen in high-fat/high-sugar diet-fed mice is attenuated in mutants

increased pancreatic beta cell mass ( J:302600 )

• 62% increase in beta cell mass at 1.5 months of age

• the 62% increase in beta cell mass seen at 1.5 months of age is completely reversed by 8 months of age; the proportion of cre+ beta cells is decreased from 71% in young mice to 48% in older mice

• however, individual beta cell volume is unchanged

abnormal endocrine pancreas physiology ( J:302600 )

• islets exhibit an increased membrane potential response at 2.8 mmol/l glucose

abnormal pancreatic beta cell physiology ( J:302600 )

• beta cells exhibit approximately a 2-fold increase in cell cycle entry accompanied by a 62% increase in beta cell mass at 1.5 months of age

• marker analysis indicates that with age beta cells show cellular stress, DNA damage and cell death over time

increased pancreatic beta cell proliferation ( J:302600 )

increased insulin secretion ( J:302600 )

• islets secrete more insulin per beta cell following glucose stimulation at 1.5 months and 8 months of age

cellular

increased pancreatic beta cell proliferation ( J:302600 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial hyperinsulinemic hypoglycemia 3		DOID:0070216	OMIM:602485	J:302600

Allelic Composition	Gck^tm1Hrt/Gck⁺ Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
Genetic Background	involves: C57BL/6 * DBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Hrt mutation (0 available); any Gck mutation (64 available)
Speer6-ps1^{Tg(Alb-cre)21Mgn} mutation (6 available); any Speer6-ps1 mutation (4 available)

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

cardiovascular system

cardiac fibrosis ( J:250069 )

• mice exhibit cardiac fibrosis, showing increased levels of myocardial collagen which is broken and arranged in a disordered collagen fiber network around the myocardial cells

• treatment with insulin or rosiglitazone decreases collagen and glycoprotein content in the heart

abnormal heart echocardiography feature ( J:250069 )

• echocardiography indicates decreased left ventricle internal dimension during diastole and systole and increased left ventricle posterior wall thickness during diastole and systole in 60 week old mice

• left ventricle internal dimension during diastole is increased after treatment with insulin or rosiglitazone

prolonged PR interval ( J:250069 )

• 60 week old mice exhibit longer PR intervals

• treatment with insulin or rosiglitazone shortens the PR interval

prolonged QRS complex duration ( J:250069 )

• 60 week old mice exhibit longer QRS intervals

• treatment with insulin or rosiglitazone shortens the QRS interval

• however, changes in heart rates, P duration, QT intervals, and corrected QT intervals are not different from wild-type mice

homeostasis/metabolism

increased circulating glucose level ( J:105247 )

• from 2 weeks of age, mice showed increasing blood glucose levels in an age-dependent manner (from 3.8 mmol/L at 2 weeks to 8.9 mmol/L at 6 weeks); level at 6 weeks is significantly higher than control level (5.3 mmol/L)

increased fasting circulating glucose level ( J:250069 )

• fasting glucose levels are increased

• treatment with rosiglitazone does not change fasting glucose levels

impaired glucose tolerance ( J:105247 , J:250069 )

• mice display glucose intolerance (J:105247)

• glucose levels at 0, 30, 60, and 120 minutes after glucose injection are higher (J:250069)

• treatment with rosiglitazone decreases the impairment in the glucose tolerance response at the 60 and 120 minute time points (J:250069)

insulin resistance ( J:250069 )

• homeostasis model assessment of insulin resistance (HOMA-IR) levels are increased

• treatment with rosiglitazone results in a decrease in HOMA-IR levels

cellular

abnormal mitochondrial crista morphology ( J:250069 )

• cristae density of the mitochondria is decreased in the myocardium

increased mitochondrial number ( J:250069 )

• mitochondrial volume density and number are increased in the myocardium

• treatment with insulin or rosiglitazone restores these properties to normal levels

endocrine/exocrine glands

abnormal pancreatic beta cell physiology ( J:250069 )

• the homeostasis model assessment of beta-cell function (HOMA-Beta-cell) levels are decreased

• treatment with rosiglitazone does not change HOMA-Beta-cell levels

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
maturity-onset diabetes of the young type 2		DOID:0111100	OMIM:125851	J:105247 , J:250069

Allelic Composition	Gck^tm1Tka/Gck⁺ Irs1^tm1Tka/Irs1^tm1Tka
Genetic Background	involves: 129X1/SvJ * C57BL/6 * CBA * ICR

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gck^tm1Tka mutation (0 available); any Gck mutation (64 available)
Irs1^tm1Tka mutation (0 available); any Irs1 mutation (52 available)

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

growth/size/body

decreased body weight ( J:38899 )

• these mice exhibit a body weight that is ~70% of that of wild-type mice throughout life

postnatal growth retardation ( J:38899 )

• these mutants display a similar degree of growth retardation as Irs1^tm1Tka homozygous mutant mice

homeostasis/metabolism

increased circulating insulin level ( J:38899 )

• these mutants exhibit higher, although not statistically significant, fasting insulin levels (148% of wild-type levels)

impaired glucose tolerance ( J:38899 )

• at 15 weeks of age, these mutants display a similar degree of glucose intolerance to Gck^tm1Tka heterozygotes

• however, at 30-40 weeks, these mutants exhibit a "diabetic" glucose tolerance i.e. an exacerbated glucose intolerance relative to Gck^tm1Tka heterozygotes of the same genetic background

insulin resistance ( J:38899 )

• these mutants exhibit insulin resistance relative to Gck^tm1Tka heterozygotes of the same genetic background

endocrine/exocrine glands

increased pancreatic beta cell mass ( J:38899 )

• in these mutants, beta-cell mass per pancreas is 216% of wild-type in terms of area

• in contrast, the non-beta (i.e. alpha and delta) cell mass remains unchanged relative to wild-type

pancreatic islet hyperplasia ( J:38899 )

• a portion of pancreatic islets from these mutant mice appear enlarged due to beta-cell hyperplasia

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
type 2 diabetes mellitus		DOID:9352	OMIM:125853 OMIM:601283 OMIM:601407 OMIM:603694 OMIM:608036	J:38899

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)
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