mortality/aging
• mortality after transverse aortic constriction is significantly higher in homozygotes than wild-type due to acute or subacute heart failure
|
homeostasis/metabolism
N |
• mice exhibit normal insulin tolerance and ceramide content in bones
|
• severe neointimal thickening and proliferation of vascular smooth muscle cells in response to mechanical injury to femoral artery
|
• on an atherogenic diet (high-fat/high-sucrose/high-salt) diet for 4 weeks, body weight is higher than in controls
|
• in the dark and light cycle at 36 weeks
|
• seen in homozygotes that die after transverse aortic constriction
|
• in the dark and light cycle at 36 weeks
|
• in the dark and light cycle at 36 weeks
|
• glucose-stimulated at 12 weeks
|
• fasting glucose levels increase by 40% at 3 weeks after transverse aortic constriction compared to 20% in wild-type
|
• after two weeks on a high fat/high sucrose diet
(J:77479)
• plasma glucose levels are higher than in wild-type after 4 weeks on a high-fat/high-sucrose/high-salt diet
(J:103106)
|
• at 12 weeks
|
• after two weeks on a high fat/high sucrose diet
|
• after two weeks on a high fat/high sucrose diet
|
• increased noradrenaline level in the brain at 36 weeks
|
• mice receiving adiponectin peripherally exhibit accumulation in the hypothalamus, brainstem, cortex, cerebellum and serum unlike in wild-type mice
|
• mice receiving adiponectin peripherally exhibit accumulation in the serum unlike in wild-type mice
|
• disturbed free fatty acid clearance from plasma in basal state, taking longer than wild-type controls
|
• after two weeks on a high fat/high sucrose diet
|
• increased in the urine at 6, 12 and 36 weeks
|
• increased adrenaline level in the urine at 6, 12 and 36 weeks
|
skeleton
N |
• mice exhibit normal bone resorption
|
• increased osteoclast surface to bone surface at 36 weeks
|
• at 36 weeks
|
• at 6 weeks
|
• at 36 weeks
|
• at 6 and 12 weeks
|
• at 6 weeks
|
• at 36 weeks
|
• 2-fold at 6 weeks
• however, this increase has largely vanished by 3 months
|
• at 36 weeks
|
• at 9 months
|
• affecting the axial and appendicular skeleton and the trabecular and cortical bones at 6 and, to a lesser extent, 12 weeks
|
• mice exhibit increased proliferation of osteoblast progenitors in young mice, decreased osteoblast proliferation in older mice, decreased apoptosis in osteoblast and decreased oxidative stress in osteoblasts compared with wild-type mice
• however, treatment with adiponectin reduces proliferation and increases apoptosis
|
• decreased bone formation rate at 36 weeks
|
• increased bone formation rate at 6 and 12 weeks
|
• better biomechanical properties (increased peak load) than wild-type mice
|
cardiovascular system
• 3 weeks after transverse aortic constriction, homozygotes exhibit greater pulmonary congestion than wild-type
|
• evident after mechanical injury to femoral artery
|
• 3 weeks after transverse aortic constriction, homozygotes show a 110% increase in heart-to-body weight compared to 53% increase in wild-type and significantly larger cross-sectional surface area of cardiac myocytes indicating much more extensive hypertrophy than in wild-type
|
• 3 weeks after transverse aortic constriction, homozygotes show greater left ventricle chamber dilation than wild-type
|
hemorrhage
(
J:106599
)
• seen in homozygotes that die after transverse aortic constriction
|
• 3 weeks after transverse aortic constriction, homozygotes show a larger decrease in left ventricular fractional shortening and left ventricular ejection fraction than wild-type
|
• increased compared to wild-type on a high-fat/high-sucrose/high-salt diet
|
• endothelium-dependent vasodilation in response to acetylcholine is significantly reduced compared to wild-type, however see no differences in endothelium-independent vasodilation in response to sodium nitroprusside
|
• severe neointimal thickening and proliferation of vascular smooth muscle cells in response to mechanical injury to femoral artery
|
• 3 weeks after transverse aortic constriction, homozygotes show exacerbated heart failure compared to wild-type controls
|
muscle
N |
• myoblasts exhibit normal proliferation and apoptosis
|
• 3 weeks after transverse aortic constriction, homozygotes show a larger decrease in left ventricular fractional shortening and left ventricular ejection fraction than wild-type
|
• endothelium-dependent vasodilation in response to acetylcholine is significantly reduced compared to wild-type, however see no differences in endothelium-independent vasodilation in response to sodium nitroprusside
|
respiratory system
• 3 weeks after transverse aortic constriction, homozygotes exhibit greater pulmonary congestion than wild-type
|
• seen in homozygotes that die after transverse aortic constriction
|
growth/size/body
• 3 weeks after transverse aortic constriction, homozygotes show a 110% increase in heart-to-body weight compared to 53% increase in wild-type and significantly larger cross-sectional surface area of cardiac myocytes indicating much more extensive hypertrophy than in wild-type
|
• at 9, but not 3, months
|
• on an atherogenic diet (high-fat/high-sucrose/high-salt) diet for 4 weeks, body weight is higher than in controls
|
adipose tissue
• fat pad weight fails to increase over time as in wild-type mice
|
• at 12 and 36 weeks
|
• white adipose tissue exhibits increased expression of brown adipose tissue markers compared with wild-type tissue
|
behavior/neurological
• slightly in older mice
|
cellular
• mice exhibit increased proliferation of osteoblast progenitors in young mice, decreased osteoblast proliferation in older mice, decreased apoptosis in osteoblast and decreased oxidative stress in osteoblasts compared with wild-type mice
• however, treatment with adiponectin reduces proliferation and increases apoptosis
|
• in osteoblasts
|
endocrine/exocrine glands
• glucose-stimulated at 12 weeks
|
hematopoietic system
• increased osteoclast surface to bone surface at 36 weeks
|
immune system
• increased osteoclast surface to bone surface at 36 weeks
|
liver/biliary system
N |
• hepatocytes exhibit normal proliferation and apoptosis
|
renal/urinary system
• increased in the urine at 6, 12 and 36 weeks
|
• increased adrenaline level in the urine at 6, 12 and 36 weeks
|