Phenotypes Associated with This Genotype

Genotype
MGI:4838529

• Allelic Composition: Akt2^tm1.1Mbb/Akt2^tm1.1Mbb; Pten^tm1Hwu/Pten^tm1Hwu; Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA

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

homeostasis/metabolism

hyperglycemia ( J:160759 )

• about 25-30% increase in fasting glucose levels at 1 month of age

impaired glucose tolerance ( J:160759 )

• glucose intolerance

liver/biliary system

liver/biliary system phenotype ( J:160759 )

N • the liver phenotype observed in single Pten mutants is significantly reduced, with liver weights, triglyceride levels in the liver and fatty liver almost similar to controls

abnormal liver morphology ( J:218587 )

♂ • progenitor cell accumulation in the periductal region of livers occurs later than in single conditional Pten homozygotes, when injury conditions are already present

decreased susceptibility to hepatic steatosis ( J:218587 )

♂ • mice do not show development of steatosis compared to single conditional Pten homozygotes

neoplasm

increased tumor latency ( J:218587 )

♂ • mice exhibit a 6-month delay in liver tumor onset compared to conditional Pten homozygotes

♂ • no mice develop liver tumors between 9 and 12 months of age and 25% of mice older than 12 months develop liver nodules

♂ • however, treatment of 3 month old mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) to induce liver injury leads to massive expansion of hepatic progenitors and development of premalignant lesions