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Phenotypes Associated with This Genotype
Genotype
MGI:3629188
Allelic
Composition
Akt2tm1.1Mbb/Akt2tm1.1Mbb
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Akt2tm1.1Mbb mutation (2 available); any Akt2 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• homozygotes develop into adulthood without apparent growth defects but exhibit a mild but significant fasting hyperglycemia, which is more pronounced during fed states
• homozygotes develop inadequate compensatory hyperinsulinemia
• in response to oral glucose load, 2-mo-old homozygotes display a mild glucose intolerance, with increased blood glucose levels at all time points measured
• in response to i.p. administration of insulin, homozygotes display significantly elevated blood glucose levels relative to wild-type mice at all time points measured (at 60 min; 70.8 7.9 mg/dl vs 22.3 1.1 mg/dl, respectively)
• in euglycemic-hyperinsulinemic clamp expts, homozygotes exhibit peripheral insulin resistance along with complete failure of insulin to suppress hepatic glucose output
• notably, circulating free fatty acid concentrations remain normal

muscle
• in euglycemic-hyperinsulinemic clamp studies, 2-5-mo-old homozygotes show a ~50% reduction in total body insulin-dependent glucose disposal relative to wild-type mice
• insulin-stimulated hexose uptake into the glycolytic extensor digitorum longus (EDL) muscle is severely blunted in the presence of 0.33 nM insulin; however, no impairment is noted upon exposure of the mutant EDL to a higher insulin concentration (13.3 nM)
• insulin-stimulated deoxyglucose uptake into the oxidative soleus muscle is not significantly impaired at either an intermediate or maximal concentration of insulin

endocrine/exocrine glands
• pancreata from 2- to 3-month-old male homozygotes respond to insulin resistance with an increase in islet mass (~4-fold) and number (~2-fold) relative to wild-type mice

adipose tissue
• in euglycemic-hyperinsulinemic clamp studies, insulin-stimulated hexose uptake is mildly impaired in mutant adipocytes

cellular
• in euglycemic-hyperinsulinemic clamp studies, 2-5-mo-old homozygotes show a ~50% reduction in total body insulin-dependent glucose disposal relative to wild-type mice
• insulin-stimulated hexose uptake into the glycolytic extensor digitorum longus (EDL) muscle is severely blunted in the presence of 0.33 nM insulin; however, no impairment is noted upon exposure of the mutant EDL to a higher insulin concentration (13.3 nM)
• insulin-stimulated deoxyglucose uptake into the oxidative soleus muscle is not significantly impaired at either an intermediate or maximal concentration of insulin

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Noninsulin-Dependent; NIDDM 125853 J:71491


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
08/23/2016
MGI 6.05
The Jackson Laboratory