Leptin treatment markedly increased plasma adiponectin but barely decreased plasma resistin of ob/ob mice

Abstract

Delporte, Marie-Laure, Samira Ait El Mkadem, Muriel Quisquater, and Sonia M. Brichard. Leptin treatment markedly increased plasma adiponectin but barely decreased plasma resistin of ob/ob mice. Am J Physiol Endocrinol Metab 287: E446 -E453, 2004. First published May 4, 2004 10.1152/ajpendo.00488.2003 and leptin are two adipocytokines that control fuel homeostasis, body weight, and insulin sensitivity. Their interplay is still poorly studied. These hormones are either undetectable or decreased in obese, diabetic ob/ob mice. We examined the effects of leptin treatment on ApN gene expression, protein production, secretion, and circulating levels of ob/ob mice. We also briefly tackled the influence of this treatment on resistin, another adipocytokine involved in obesity-related insulin resistance. Leptin-treated (T) obese mice (continuous sc infusion for 6 days) were compared with untreated lean (L), untreated obese (O), and untreated pair-fed obese (PF) mice. Blood was collected throughout the study. At day 3 or day 6, fat pads were either directly analyzed (mRNA, ApN content) or cultured for up to 24 h (ApN secretion). The direct effect of leptin was also studied in 3T3-F442A adipocytes. Compared with L mice, ApN content of visceral or subcutaneous fat and ApN secretion by adipose explants were blunted in obese mice. Accordingly, plasma ApN levels of O mice were decreased by 50%. Leptin treatment of ob/ob mice increased ApN mRNAs, ApN content, and secretion from the visceral depot by 50 -80%. Leptin also directly stimulated ApN mRNAs and secretion from 3T3-F442A adipocytes. After 6 days of treatment, plasma ApN of ob/ob mice increased 2.5-fold, a rise that did not occur in PF mice. Plasma resistin of T mice was barely decreased. Leptin treatment, but not mere calorie restriction, corrects plasma ApN in obese mice by restoring adipose tissue ApN concentrations and secretion, at least in part, via a direct stimulation of ApN gene expression. Such a treatment only minimally affects circulating resistin. ApN restoration could, in concert with leptin, contribute to the metabolic effects classically observed during leptin administration.

Transplantation of wild-type white adipose tissue normalizes metabolic, immune and inflammatory alterations in leptin-deficient ob/ob mice

“…Serum adiponectin and resistin levels were slightly but significantly higher in both sham and transplanted ob/ob compared to WT mice, in agreement with some [18][19][20] though not other [21,22] previously published data. The reasons for the above-mentioned discrepancies in circulating adiponectin and resistin levels in ob/ob mice are currently unclear and may be secondary to experimental differences such as age, gender and genetic background of the mice studied by different investigators.…”

Conjugated linoleic acid fails to worsen insulin resistance but induces hepatic steatosis in the presence of leptin in ob/ob mice

“…However, the effect of leptin infusion on adiponectin concentrations was not reported, nor was it compared with a control-fed group. Leptin treatment has been shown to increase plasma adiponectin (24); therefore, although speculative, insulin concentrations and hepatic steatosis may have been attenuated by a leptin-induced increase in adiponectin. In the present study, induction of hyperinsulinemia and insulin resistance in ob/ob mice by CLA paralleled the depletion of adiponectin.…”

Impaired Expression of Cardiac Adiponectin in Leptin-Deficient Mice With Viral Myocarditis

“…Delporte and colleagues 24) have recently suggested a causal relationship exists between leptin and adiponectin in OB mice. The adiponectin content of visceral fat and adiponectin secretion by adipose tissue were blunted in OB mice.…”