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Appetite suppressing effect of t10, c12 conjugated linoleic acid on mice is dependent on dietary fat level and the temporal pattern of energy intake is associated with changes in hypothalamic expression of genes involved in appetite control.
Author(s) -
So Martin H. H.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a461
Subject(s) - conjugated linoleic acid , appetite , endocrinology , medicine , linoleic acid , chemistry , neuropeptide y receptor , hypothalamus , fatty acid , biology , neuropeptide , biochemistry , receptor
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).

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