Cholesterol feeding prevents adiposity in the obese female aromatase knockout (ArKO) mouse.

[aromatase deficiency]

The aromatase (ArKO ) knockout mouse develops obesity marked by increased gonadal fat depots . This obesity is characterized by pronounced hypertrophy and hyperplasia in adipocytes with corresponding increases in transcripts involved in fat development . Aromatase deficiency in mice and humans with natural mutations of the aromatase gene also leads to metabolic syndrome , particularly hepatic steatosis . In ArKO mice , this hepatic steatosis , the increased body weight and serum triglycerides are surprisingly prevented by cholesterol feeding . We sought to investigate whether the reduction in body weight upon cholesterol feeding is reflected in gonadal fat depots , which account for a large percentage of body weight in the ArKO mouse . Indeed , gonadal fat depots in female ArKO mice were significantly reduced after cholesterol feeding . Concomitantly , adipocyte hyperplasia and hypertrophy were dramatically reduced upon cholesterol feeding in ArKO mice . Real-time PCR analysis revealed concurrent changes with adipocyte volume in the levels of lipoprotein lipase , caveolin-1 and CD 59 transcripts . Little change was observed in levels of transcripts involved in de novo fatty acid synthesis , beta -oxidation , lipolysis , differentiation and cholesterol metabolism , suggesting that cholesterol feeding prevents hyperplasia and hypertrophy of ArKO adipocytes , possibly as a consequence of changes in transcript levels of lipoprotein lipase and therefore fatty acid uptake .

Diseases
Validation

Diseases presenting "hepatic steatosis" symptom

adrenal incidentaloma

aromatase deficiency

cushing syndrome

werner syndrome

x-linked adrenoleukodystrophy

zellweger syndrome

This symptom has already been validated