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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Abcc9tm1Cfb
targeted mutation 1, Charles F Burant
MGI:2155916
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Abcc9tm1Cfb/Abcc9tm1Cfb involves: CD-1 MGI:2653868
hm2
Abcc9tm1Cfb/Abcc9tm1Cfb Not Specified MGI:3622096


Genotype
MGI:2653868
hm1
Allelic
Composition
Abcc9tm1Cfb/Abcc9tm1Cfb
Genetic
Background
involves: CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcc9tm1Cfb mutation (0 available); any Abcc9 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased spontaneous death observed at 6 weeks of age in males and at 10 weeks of age in females

growth/size/body
• weight gain begins to lag relative to that of wild-type mice after 6 weeks of age

homeostasis/metabolism
• at 10-12 weeks of age, fasted homozygotes show a small but significant reduction of serum glucose levels relative to wild-type mice
• however, no significant differences are noted in fasted serum electrolytes at 6-8 weeks of age or in fed or fasting serum insulin levels and fed or fasting serum triglyceride levels at 10-12 weeks of age relative to wild-type mice
• in response to i.p. injection of glucose (2 g/kg), homozygotes display a significantly improved glucose tolerance curve, with peak serum glucose levels of ~250 mg/dl at 30 min post-injection relative to 420 mg/dl in wild-type mice
• during in vivo hyperinsulinemic euglycemic clamp studies, homozygotes require a higher glucose infusion rate to maintain target serum glucose levels than wild-type mice
• in response to 0.5 U/kg of insulin challenge, homozygotes exhibit a more rapid and sustained decrease in serum glucose than wild-type mice, with 50% of mutants either succumbing to hypoglycemia or requiring glucose injections to restore glucose levels
• increased insulin action is intrinsic to skeletal muscle, as shown by a 59% increase in in vitro insulin-stimulated glucose uptake into the soleus muscle

muscle
• following incubation with insulin, male homozygotes show a 1.5-fold increase in in vitro glucose uptake into skeletal (soleus) muscle relative to wild-type males
• however, in the absence of insulin, in vitro glucose uptake into mutant skeletal muscle is similar to that in wild-type, indicating normal basal glucose transport

cellular
• following incubation with insulin, male homozygotes show a 1.5-fold increase in in vitro glucose uptake into skeletal (soleus) muscle relative to wild-type males
• however, in the absence of insulin, in vitro glucose uptake into mutant skeletal muscle is similar to that in wild-type, indicating normal basal glucose transport




Genotype
MGI:3622096
hm2
Allelic
Composition
Abcc9tm1Cfb/Abcc9tm1Cfb
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcc9tm1Cfb mutation (0 available); any Abcc9 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 30 weeks of age, 65% of males and 35% of females die suddenly

cardiovascular system
• glibenclamide-sensitive KATP current is absent in aortic smooth muscle cells
• exhibit transient, repeated episodes of coronary artery vasospasm
• calcium channel antagonists reduce coronary artery vasospasms
• exhibit repeated episodes of spontaneous ST segment elevation that are often followed by slow heart rate, however show normal baseline resting heart rate, PR intervals and QRS
• ST segment depression is seen during the recovery phase of the transient ischemic events
• do not show a drop in blood pressure with pinacidil administration or any response to glyburide as in wild-type
• seen in conscious 12- to 18-week old mice
• seen in conscious 12- to 18-week old mice

muscle
• glibenclamide-sensitive KATP current is absent in aortic smooth muscle cells
• exhibit transient, repeated episodes of coronary artery vasospasm
• calcium channel antagonists reduce coronary artery vasospasms





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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last database update
07/16/2019
MGI 6.14
The Jackson Laboratory