Phenotypes associated with this allele

• Allele Symbol: Prkar2b^tm1Gsm
• Allele Name: targeted mutation 1, G Stanley McKnight
• Allele ID: MGI:2158642
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Prkar2b^tm1Gsm/Prkar2b^tm1Gsm	B6.129-Prkar2b^tm1Gsm	MGI:3041829
hm2	Prkar2b^tm1Gsm/Prkar2b^tm1Gsm	involves: 129X1/SvJ * C57BL/6	MGI:3041828
hm3	Prkar2b^tm1Gsm/Prkar2b^tm1Gsm	Not Specified	MGI:3041827

Genotype
MGI:3041829

hm1

• Allelic Composition: Prkar2b^tm1Gsm/Prkar2b^tm1Gsm
• Genetic Background: B6.129-Prkar2b^tm1Gsm

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

behavior/neurological

abnormal food intake ( J:72414 )

• while mice appeared to eat less than controls during diabetogenic study, when consumption was correlated with differences in body weight, mutant mice consumed more calories/g mouse/day

• leptin levels did not correlate with food consumption

growth/size/body

decreased body weight ( J:72414 )

• males weighed 20% less than controls between 16 and 20 weeks of age

• weighed less than controls on diabetogenic (high fat, high sucrose) diet over the course of 15 weeks, but change in percent body weight at the end of the diabetogenic diet was similar to controls

• increased weight correlated with leptin levels

decreased susceptibility to diet-induced obesity ( J:72414 )

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:72414 )

N • normal glucose levels

N • before study on diabetogenic diet, mice had comparable plasma glucose levels to controls

N • glucose levels increased during diabetogenic study, and these levels did not differ from those in controls

decreased susceptibility to diet-induced obesity ( J:72414 )

decreased circulating insulin level ( J:72414 )

• at all time points, before and during diabetogenic study, mice had lower plasma insulin levels than control mice

• insulin levels did increase over the course of the study, however, but never reached the levels seen in controls

decreased circulating leptin level ( J:72414 )

• by the end of the 15 week test period on the diabetogenic diet, leptin levels were comparable to controls

• in plasma, compared to controls, before start of diabetogenic diet

• delayed increase in plasma leptin levels, compared to controls, on diabetogenic diet

decreased circulating cholesterol level ( J:72414 )

• lower levels than wild-type mice fed the diabetogenic diet

• hepatic cholesterol concentration similar to controls after diabetogenic diet

• no differences in plasma triglyceride or free fatty acids

decreased circulating LDL cholesterol level ( J:72414 )

• lower levels than wild-type mice fed the diabetogenic diet

• no differences in plasma HDL

decreased circulating VLDL cholesterol level ( J:72414 )

• lower levels than wild-type mice fed the diabetogenic diet

• no differences in plasma HDL

improved glucose tolerance ( J:72414 )

• prevention of induction of diet-induced glucose intolerance, measured by glucose disposal after glucose injection

• diet-induced insulin resistance did not occur; glucose clearance after insulin injection remained the same before and after diabetogenic study

decreased liver triglyceride level ( J:72414 )

• in liver of males after diabetogenic diet

• no difference in plasma triglyceride, compared to controls, after diabetogenic diet

liver/biliary system

decreased liver triglyceride level ( J:72414 )

• in liver of males after diabetogenic diet

• no difference in plasma triglyceride, compared to controls, after diabetogenic diet

decreased susceptibility to diet-induced hepatic steatosis ( J:72414 )

• unlike wild-type controls on high fat diet, homozygous null mice do not develop liver steatosis

Genotype
MGI:3041828

hm2

• Allelic Composition: Prkar2b^tm1Gsm/Prkar2b^tm1Gsm
• Genetic Background: involves: 129X1/SvJ * C57BL/6

behavior/neurological

enhanced behavioral response to addictive substance ( J:47453 )

• typical acute behavioral response to dopaminergic agents (amphetamine or cocaine), but increased sensitization to chronic amphetamine exposure

• pharmacokinetics in brain similar to controls

impaired coordination ( J:47453 )

• on rotarod

• no obvious cerebellar or locomotor defects, however

Genotype
MGI:3041827

hm3

• Allelic Composition: Prkar2b^tm1Gsm/Prkar2b^tm1Gsm
• Genetic Background: Not Specified

adipose tissue

decreased white adipose tissue amount ( J:34751 )

• both males and females had fat pads from 3 locations (reproductive, inguinal, and retroperitoneal) weighing ~50% that of wild-type controls

behavior/neurological

polyphagia ( J:34751 )

• females showed significant increase in food intake

• males also had increased food intake, but this difference was not statistically significant

growth/size/body

decreased body weight ( J:34751 )

• females weighed significantly less than wild-type controls

• males weighed less, but this difference was not statistically significant

decreased susceptibility to diet-induced obesity ( J:34751 )

• after 4 months on high fat (58%) diet, mice failed to become obese, whereas wild-type controls did

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:34751 )

N • normal postprandial triglyceride blood levels, plasma cholesterol, serum free fatty acid, serum glycerol, insulin, glucose, and thyroid hormones levels

decreased circulating leptin level ( J:34751 )

• in plasma

increased body temperature ( J:34751 )

abnormal energy expenditure ( J:34751 )

• increased, assessed by oxygen consumption

decreased susceptibility to diet-induced obesity ( J:34751 )

• after 4 months on high fat (58%) diet, mice failed to become obese, whereas wild-type controls did

decreased triglyceride level ( J:34751 )

• concluded from normal cellularity of fat pads and reduced adipocyte size

liver/biliary system

decreased susceptibility to diet-induced hepatic steatosis ( J:34751 )

• unlike wild-type controls on high fat diet, homozygous null mice do not develop liver steatosis