Bitoin suppresses an appetite of mice by modifications of gene expression by enhancement of histon biotinylation in hypothalamus

2014 Fiscal Year Final Research Report

• Project/Area Number: 24614009
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Integrated Nutrition Science
• Research Institution: University of Niigata Prefecture
• Principal Investigator: SONE Hideyuki 新潟県立大学, 人間生活学部, 准教授 (90398511)
• Co-Investigator(Renkei-kenkyūsha): KAMIYAMA Shin 新潟県立大学, 人間生活学部, 講師 (70525401)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ビオチン / 摂食抑制 / 視床下部 / アセチルCoAカルボキシラーゼ-2

Outline of Final Research Achievements

In this study, we investigated whether biotin suppresses the food intake of mouse by measuring nutrient and hormonal regulators in the periphery and gene expressions related to feeding regulation in hypothalamus. Food intake of biotin group was significantly less than that of control group. But, blood glucose, ghrelin, insulin, adiponectin, CCK and GLP-1 in plasma of biotin group were almost same as those of control group. The level of mRNA expression of leptin did not show a significant difference between both groups. In the hypothalamus, the ACC2 mRNA expression was augmented by 150% in biotin group compared with that in control group, though ACC1, MCD, NPY and POMC were not changed between both groups. Additionally, biotin increased the biotinylation of histons coiling DNA of coding region for ACC2. These data strongly suggest that biotin potentiate to suppress an appetite by upregulation of ACC2 mRNA by the enhancement of the histon biotinylation in hypothalamus.

Free Research Field

栄養生理学