Abstract | BACKGROUND:
Miglitol is an oral anti-diabetic drug that acts by inhibiting carbohydrate absorption in the small intestine. Recent studies have shown that miglitol reduces obesity in humans and rodents. However, its mechanisms have remained unclear. The purpose of this study was to determine whether miglitol generates heat by activating uncoupling protein 1 (UCP1), an enzyme involved in thermogenesis, in brown adipose tissue (BAT) in mice. METHODS: RESULTS: At 8 weeks, body weight, epididymal and subcutaneous white adipose tissue and the HOMA-R value of the HFM mice were significantly less than those of the HF mice. Food intake was not different between the HF and HFM mice. VO2 and BAT temperature were significantly higher in the HFM mice. Miglitol significantly enhanced the gene and protein expressions of UCP1 and the expressions of proteins related to β3-adrenergic signaling. CONCLUSIONS:
Miglitol's anti- obesity effect was attributed to increased energy expenditure by upregulating UCP1 in BAT (i.e., by thermogenesis) and to enhancement of β3-adrenergic signaling in BAT.
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Authors | Satoru Sugimoto, Hisakazu Nakajima, Kazuki Kodo, Jun Mori, Kensuke Matsuo, Kitaro Kosaka, Wataru Aoi, Kanji Yoshimoto, Hiroshi Ikegaya, Hajime Hosoi |
Journal | Nutrition & metabolism
(Nutr Metab (Lond))
Vol. 11
Issue 1
Pg. 14
(Mar 26 2014)
ISSN: 1743-7075 [Print] England |
PMID | 24669882
(Publication Type: Journal Article)
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