mortality/aging
N |
• unlike homozygous null mice, mice with loss of expression in the liver after birth are viable
|
liver/biliary system
• at 6 - 8 weeks of age, but not at P17, the number of proliferating cells is increased
|
• by P28 livers are hypertrophic
|
• ratio of liver weight to body weight is increased to about 25 - 30% compared to about 5% in heterozygous mice
|
• dramatic depletion of glycogen in hepatocytes
|
• up to a 17-fold increase in triglyceride levels in the liver at P17
|
• cells with abnormal cytoplasm are apparent at P17
|
• accumulation of lipid droplets
• elevated triglyceride levels at P17
• treating mice with rapamycin reduces neutral lipid accumulation but does not alter the increase in liver size
|
pale liver
(
J:134288
)
• by P28
|
homeostasis/metabolism
• increases with age
|
• by P17
|
hypoglycemia
(
J:134288
)
• present by 6 weeks of age but not at P17
• at 10 weeks of age fasting glucose level is almost 2-fold lower than in control littermates
• however, glucose tolerance is not significantly different from controls
|
• slightly lower at P17
|
• dramatic decrease by P28 which persists as mice age
|
• dramatic depletion of glycogen in hepatocytes
|
• increases with age
|
• increases with age
|
• increases with age
|
• up to a 17-fold increase in triglyceride levels in the liver at P17
|
growth/size/body
• by 4 - 6 weeks of age
|
• by P28 livers are hypertrophic
|
• ratio of liver weight to body weight is increased to about 25 - 30% compared to about 5% in heterozygous mice
|
adipose tissue
• visibly leaner with a substantial reduction in visceral adipose tissue by 6 - 8 weeks of age
|
cellular
• at 6 - 8 weeks of age, but not at P17, the number of proliferating cells is increased
|