Mouse Genome Informatics
tg
    Tg(Ckm-IGF1R*K1003R)1Dlr/0
FVB/N-Tg(Ckm-IGF1R*K1003R)1Dlr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
homeostasis/metabolism
• 2-fold at 3 to 4 weeks of age
• 2-fold at 3 to 4 weeks of age
• total body glucose disposal, glycolysis, and glycogen synthesis are reduced compared to in wild-type mice
• at 7 to 12 weeks
• glycogen synthesis is reduced compared to in wild-type mice
• following stimulation with IGF-I, muscle fails to exhibit an increase in glucose uptake unlike in similarly treated wild-type muscle

muscle
• insulin stimulated glucose uptake is 1.5-fold compared to 5-fold in wild-type mice
• following stimulation with IGF-I, muscle fails to exhibit an increase in glucose uptake unlike in similarly treated wild-type muscle

endocrine/exocrine glands

cellular
• insulin stimulated glucose uptake is 1.5-fold compared to 5-fold in wild-type mice
• following stimulation with IGF-I, muscle fails to exhibit an increase in glucose uptake unlike in similarly treated wild-type muscle
• glucose transport activity in skeletal muscle and brown adipose tissue is reduced 50% compared to in wild-type cells

growth/size
• 20% from birth to 4 weeks of age and 10% from 4 weeks of age through adulthood
• mice exhibit modest growth retardation from birth to 4 weeks of age and a smaller reduction in growth from 4 weeks of age through adulthood compared to in wild-type mice

liver/biliary system

Mouse Models of Human Disease
OMIM IDRef(s)
Diabetes Mellitus, Noninsulin-Dependent; NIDDM 125853 J:71205