Impairment of adipsin expression is secondary to the onset of obesity in db/db mice.
The nature of the primary biochemical lesions in genetically obese mice, which might prove to be useful models for human obesity, remains totally obscure. The recent finding that the expression of adipsin was virtually suppressed in both db/db and ob/ob adult mice has opened new perspectives, suggesting a potential role for this defect in the pathogenesis of obesity. To be of etiological significance, adipsin deficiency must be present very early in life when excess fat storage starts to develop. We show here that at 10 days of age db/db pups exhibit significantly overdeveloped adipose tissue as compared with lean (+/db) pups but similar levels of both adipose tissue adipsin mRNA and serum adipsin. Adipsin expression was still normal in obese mice 15 days old but frankly deficient at 30 days of age when hyperinsulinemia has developed. Thus the defect in adipsin expression in db/db mice is a secondary feature which cannot be ascribed a role in the onset of obesity.
Unité de Recherches sur la Physiopathologie de la Nutrition Inserm U177, Paris, France.
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I
Dugail
A
A
Quignard-Boulangé
X
X
Le Liepvre
M
M
Lavau
D000273:Adipose Tissue / Q000201:enzymology / Q000254:growth & development*; D000375:Aging; D000818:Animals; D015153:Blotting, Western; D001835:Body Weight; D011416:Complement Factor D; D007328:Insulin / Q000097:blood; D051379:Mice; D008817:Mice, Mutant Strains; D009765:Obesity / Q000235:genetics* / Q000378:metabolism; D009929:Organ Size; D012333:RNA, Messenger / Q000235:genetics; D012016:Reference Values; D012697:Serine Endopeptidases / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D013489:Suppression, Genetic; D014158:Transcription, Genetic
D007328:Insulin; D012333:RNA, Messenger; D012697:Serine Endopeptidases; C493488:CFD protein, human; D011416:Complement Factor D; C493491:complement factor D, mouse