This study tested the hypothesis that the effect of trans-10, cis-12 conjugated linoleic acid (t10, c12 CLA) on energy intake (EI) and body weight (BW)/composition is confounded by dietary fat concentration and involves hypothalamic appetite-controlling mechanisms. ICR mice received low-fat (LF; 5 g/100 g) or high-fat (HF; 30 g/100 g) diets, with or without 0.5 g/100 g t10, c12 CLA (>98% pure) for 27 d. By d 13, BW and cumulative EI of the mice fed CLA supplemented LF diet (LF/CLA) were 6.6 and 23.6% lower, respectively, than the LF mice. In the subsequent 14 d, their EI rebounded and did not differ from the LF group. BW and EI did not differ between the HF and CLA supplemented HF (HF/CLA) groups. Hypothalamic pro-opiomelanocortin (POMC) mRNA expression was elevated (P = 0.031) on d 13 but suppressed (P < 0.001) on d 27 due to CLA treatment. CLA also suppressed AMP-activated protein kinase alpha2 expression. Mice in Expt. 2 received the LF diet, the LF/CLA, or were pair-fed the LF diet to the EI of the CLA group (LF/PF). LF/CLA and LF/PF mice did not differ in the hypothalamic POMC:neuropeptide Y expression ratio on d 13, but it was significantly lower in the LF/PF group on d 27. We conclude that the habitual dietary fat concentration influences the magnitude of weight loss induced by dietary t10, c12 CLA. The effect is in part independent of EI. Hypothalamic neuropeptides and nutrient sensing mechanisms may play a role.
In literature, administration of conjugated linoleic acid (CLA) to rodents caused either no change or suppression in food intake. Objectives of the present study were to monitor the temporal change in energy intake (EI) and body weight (BW) of ICR mice habitually fed on low fat (5%, LF) or high fat (30%, HF) diet then given trans10, cis12‐CLA (0.5%, purity: 98%+) supplementation. mRNA expressions of hypothalamic appetite control markers were traced. Initial appetite suppression was noticed that gradually waned. Compared to unsupplemented control, CLA supplementation caused a 22.5% decrease in EI of the LF mice in the first two weeks (P < 0.05). However, CLA only caused a 4.8% drop (P = 0.306, ns) in EI of the HF mice. Accordingly, BW reduction of the LF+CLA and HF+CLA mice was 2.4 g and 0.5 g, respectively. Hypothalamic expression of pro‐opiomelanocortin (POMC) was increased by CLA supplementation (P< 0.05, 2‐way ANOVA). In the next two weeks, CLA had no effect on EI and BW gain, indicating a rebound in appetite of the LF+CLA mice. Hypothalamic expression of POMC was reduced whereas that of neuropeptide Y (NPY) was increased. The data indicated that CLA caused transient appetite suppression in LF mice but HF mice were relatively resistant to this effect. The temporal change in EI coincides with the shifts in the hypothalamic expressions of POMC and NPY.
(Supported by HKU‐CRCG).
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.
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