Abstract
Conjugated linoleic acid (CLA) causes insulin resistance and hepatic steatosis in conjunction with depletion of adipokines in some rodent models. Our objective was to determine whether the maintenance of adipokines, mainly leptin and adiponectin, by either removing CLA from diets or using an adiponectin enhancer, rosiglitazone (ROSI), could attenuate CLA-induced insulin resistance. Male C57BL/6 mice were consecutively fed two experimental diets containing 1.5% CLA mixed isomer for 4 weeks followed by a diet without CLA for 4 weeks. CLA significantly depleted adiponectin but not leptin and was accompanied by hepatic steatosis and insulin resistance. These effects were attenuated after switching mice to the diet without CLA along with restoration of adiponectin. To further elucidate the role of adiponectin in CLA-mediated insulin resistance, ROSI was used in a subsequent study in male ob/ob mice fed either control (CON) or CLA diet. ROSI maintained significantly higher adiponectin levels in CON- and CLA-fed mice and prevented the depletion of epididymal adipose tissue and the development of insulin resistance. In conclusion, we show that insulin resistance induced by CLA may be related more to adiponectin depletion than to leptin and that maintaining adiponectin levels alone either by removing CLA or using ROSI can attenuate these effects.
Highlights
Conjugated linoleic acid (CLA) causes insulin resistance and hepatic steatosis in conjunction with depletion of adipokines in some rodent models
Significant differences were observed at day 6, and adiponectin levels continued to decrease over time (Fig. 2B)
Leptin levels were less responsive to dietary CLA and were not significantly different compared with baseline (Fig. 2A)
Summary
Conjugated linoleic acid (CLA) causes insulin resistance and hepatic steatosis in conjunction with depletion of adipokines in some rodent models. Feeding CLA to mice is associated with lipodystrophy and worsening of insulin sensitivity [16, 21,22,23,24] These effects have been attributed to a rapid and significant reduction of adipose tissue and a sharp decline in insulinsensitizing adipokines such as adiponectin and leptin [23]. We further investigated the role of adiponectin in insulin resistance mediated by CLA in leptin-deficient ob/ob mice To this end, we used the peroxisome proliferator-activated receptor g (PPARg) agonist rosiglitazone (ROSI) in conjunction with CLA and Abbreviations: AOX, acetyl-coenzyme A oxidase; CLA, conjugated linoleic acid; c 9t11, cis 9,trans; CON, control; FBG, fasting blood glucose; IL-6, interleukin-6; PPARg, peroxisome proliferator-activated receptor g; ROSI, rosiglitazone; TG, triglyceride; TNF-a, tumor necrosis factor-a
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