Dietary conjugated linoleic acid increases PPAR gamma gene expression in adipose tissue of obese rat, and improves insulin resistance.
Conjugated linoleic acid (CLA) is a class of positional, geometric, conjugated dienoic isomers of linoleic acid. Dietary CLA supplementation has resulted in a dramatic decrease in body fat mass in mice. However, some but not all studies in mice and humans have found that CLA promoted insulin resistance, and there were conflicting reports on the effects of CLA on peroxisomal proliferator-activated receptor-gamma (PPAR gamma) activation and expression. The objective of present study was to investigate the effect of CLA on insulin resistance and its molecular mechanisms. Fifty male Wistar rats were randomly designed to the control, high-fat and high-fat with CLA (0.75, 1.50, and 3.00 g in per 100 g diet) groups. The effect of CLA on insulin sensitivity and the mechanism of resisting diabetes by CLA were investigated by RT-PCR assay. The results showed that supplementation with CLA significantly reduced body weight gain and white fat pad weight in the rats, the levels of plasma free fatty acids (FFA), triglycerides (TGs), cholesterin (TC), leptin, insulin and blood glucose concentration in the obese rats of CLA group were also decreased compared to the rats in the high-fat group. Dietary CLA increased the mRNA expression of PPAR gamma, fatty acid binding proteins (aP2), fatty acid transporter protein (FATP), acyl-CoA synthetase (ACS) and adiponectin in the adipose tissues of obese rats. The results suggest that CLA may ameliorate insulin resistance by activating PPAR gamma, and increasing the expression of PPAR gamma target genes such as ap2, FATP, FAT, and adiponectin in the white adipose tissue.
Zhou
Xiao-Rong
XR
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China.
Sun
Chang-Hao
CH
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China.
Liu
Jia-Ren
JR
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China; Department of Food Science, Cornell University, Stocking Hall, Ithaca, NY 14853-7201, USA.
Zhao
Dan
D
Department of Nutrition and Food Hygiene, Public Health College of Harbin Medical University, 157 BaoJian Road, NanGang District, Harbin 150081, PR China.
D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects*; D007333:Insulin Resistance / Q000235:genetics*; D044243:Linoleic Acids, Conjugated / Q000008:administration & dosage* / Q000494:pharmacology; D008297:Male; D009765:Obesity / Q000235:genetics / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D052242:Adiponectin; D050556:Fatty Acid-Binding Proteins; D044243:Linoleic Acids, Conjugated; D047495:PPAR gamma; D012333:RNA, Messenger; C493570:Slc27a1 protein, rat