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Conjugated linoleic acid inhibits glucose metabolism, leptin and adiponectin secretion in primary cultured rat adipocytes.

Abstract：

:Conjugated linoleic acid (CLA) supplementation has been reported to induce insulin resistance in animals and humans, however, the underlying mechanisms remain unclear. The aim of this study was to examine the direct effects of CLA on leptin and adiponectin secretion, two hormones with actions known to influence insulin sensitivity. Isolated rat adipocytes were incubated with CLA (1-200microM) in the absence and presence of insulin (1.6nM). CLA inhibited both basal and insulin-stimulated leptin gene expression and secretion (-30 to -40%, P<0.05-0.01). CLA also inhibited basal adiponectin production (-20 to -40%, P<0.05-0.01), but not in the presence of insulin. CLA (50-200muM) decreased basal glucose uptake (P<0.05-0.01) and significantly increased the proportion of glucose metabolized to lactate (P<0.01). Insulin treatment partially prevented the inhibitory effects of CLA on glucose uptake and induced a significant increase (P<0.05-0.01) in the percentage of glucose metabolized to lactate. A strong inverse relationship was observed between the increase in the anaerobic utilization of glucose and the decreases of both leptin and adiponectin secretion. In addition, lipolysis and the expression of the adipogenic transcription factor PPARgamma were decreased by CLA. These results indicate that CLA inhibits leptin and adiponectin secretion and suggest that increased anaerobic metabolism of glucose may be involved in these effects. The inhibition of PPARgamma could also mediate the inhibition of adiponectin induced by CLA. Furthermore, the inhibition of leptin and adiponectin production induced by CLA may contribute to insulin resistance observed in CLA-treated animals and humans.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Pérez-Matute P,Marti A,Martínez JA,Fernández-Otero MP,Stanhope KL,Havel PJ,Moreno-Aliaga MJ

doi

10.1016/j.mce.2007.01.013

subject

Has Abstract

pub_date

2007-03-30 00:00:00

pages

50-8

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(07)00033-0

journal_volume

268

pub_type

杂志文章

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