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Green tea (‐)‐epigallocatechin‐3‐gallate counteracts daytime overeating induced by high‐fat diet in mice
Author(s) -
Li Hongyu,
Kek Huiling Calvina,
Lim Joy,
Gelling Richard Wayne,
Han Weiping
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600162
Subject(s) - overeating , medicine , endocrinology , epigallocatechin gallate , appetite , meal , circadian rhythm , obesity , diet induced obese , energy homeostasis , hypothalamus , ampk , biology , chemistry , insulin resistance , biochemistry , polyphenol , antioxidant , protein kinase a , enzyme
Scope High‐fat diet (HFD) induces overeating and obesity. Green tea (‐)‐epigallocatechin‐3‐gallate (EGCG) reduces HFD‐induced body weight and body fat gain mainly through increased lipid metabolism and fat oxidation. However, little is known about its effect on HFD‐induced alterations in feeding behavior. Methods and results Three diet groups of wildtype C57B/6j male mice at 5 months old were fed on normal chow diet, 1 week of HFD (60% of energy) and 3 months of HFD (diet‐induced obesity (DIO)) prior to EGCG supplement in respective diet. EGCG had no effect on feeding behavior in normal chow diet group. Increased daytime feeding induced by HFD was selectively corrected by EGCG treatment in HFD groups, including reversed food intake, feeding frequency and meal size in HFD + EGCG group, and reduced food intake and feeding frequency in DIO + EGCG group. Moreover, EGCG treatment altered diurnally oscillating expression pattern of key appetite‐regulating genes, including AGRP, POMC, and CART, and key circadian genes Clock and Bmal1 in hypothalamus of DIO mice, indicating its central effect on feeding regulation. Conclusion Our study demonstrates that EGCG supplement specifically counteracts daytime overeating induced by HFD in mice, suggesting its central role in regulating feeding behavior and energy homeostasis.