About   Help   FAQ
Phenotypes Associated with This Genotype
Genotype
MGI:3618231
Allelic
Composition
Gcktm1Hrt/Gck+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gcktm1Hrt mutation (0 available); any Gck mutation (24 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 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
• 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
• 60 week old mice exhibit longer PR intervals
• treatment with insulin or rosiglitazone shortens the PR interval
• 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
• 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)
• fasting glucose levels are increased
• treatment with rosiglitazone does not change fasting glucose levels
• 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)
• homeostasis model assessment of insulin resistance (HOMA-IR) levels are increased
• treatment with rosiglitazone results in a decrease in HOMA-IR levels

cellular
• cristae density of the mitochondria is decreased in the myocardium
• mitochondrial volume density and number are increased in the myocardium
• treatment with insulin or rosiglitazone restores these properties to normal levels

endocrine/exocrine glands
• 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


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
10/08/2019
MGI 6.14
The Jackson Laboratory