TY - JOUR
T1 - Conjugated linoleic acid inhibits glucose metabolism, leptin and adiponectin secretion in primary cultured rat adipocytes
AU - Pérez-Matute, P.
AU - Marti, A.
AU - Martínez, J. A.
AU - Fernández-Otero, M. P.
AU - Stanhope, Kimber
AU - Havel, Peter J
AU - Moreno-Aliaga, M. J.
PY - 2007/3/30
Y1 - 2007/3/30
N2 - 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 (1-200 μM) in the absence and presence of insulin (1.6 nM). 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 (50-200 μM) 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 PPARγ 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 PPARγ 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.
AB - 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 (1-200 μM) in the absence and presence of insulin (1.6 nM). 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 (50-200 μM) 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 PPARγ 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 PPARγ 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.
KW - Adiponectin
KW - Conjugated linoleic acid
KW - Cultured rat adipocytes
KW - Insulin resistance
KW - Leptin
KW - Peroxisome proliferator-activated receptor γ
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U2 - 10.1016/j.mce.2007.01.013
DO - 10.1016/j.mce.2007.01.013
M3 - Article
C2 - 17321040
AN - SCOPUS:33947253411
VL - 268
SP - 50
EP - 58
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
SN - 0303-7207
IS - 1-2
ER -