Abstract
The aim of this study was to investigate the interacting effects of dietary fat concentration and trans‐10, cis‐12 conjugated linoleic acid (t10, c12 CLA) on the development of lipodystrophy and mechanisms involved. Male ICR mice received low fat (5 g/100 g, LF) or high fat (30 g/100 g, HF) diets, with or without 0.5 g/100 g t10, c12 CLA (>98% pure) for 27 d. CLA suppressed energy intake (EI) in LF but not HF mice. CLA elevated hepatic cholesterol (CHL) concentration as early as d 13 (P < 0.01) and by d 27 there was a modest increase in triglyceride (P = 0.085). LF/CLA and HF/CLA mice had gradual lost in visceral fat and liver enlargement. The lipodystrophic state occurred in the absence of hyperinsulinemia but was accompanied by reduced leptin, adiponectin and visfatin mRNA in visceral fat; and increased SREBP protein expression, but not FAS expression in liver. Compared to respective control, LF/CLA mice had higher liver CHL concentration than HF/CLA mice. Mice in experiment 2 received the LF diet, LF/CLA diet or were pair‐fed LF diet to the EI of the CLA group (LF/PF). On d 27, LF/CLA mice had ablation of visceral fat and hepatomegaly. The LF/PF mice had significantly higher visceral fat mass and adipokine mRNA but no hepatomegaly. Thus, t10, c12 CLA‐induced lipodystrophy was dietary fat concentration dependent and involved the adipokines. Liver CHL accumulation may reflect an early abnormality in the development of lipodystrophy.
Published Version
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