Novel mechanism for energy metabolism regulated by a Ca2+-sensor protein

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08200
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: Nishitani Tomoe 国立研究開発法人国立循環器病研究センター, 研究所, 室長 (50393244)
• Co-Investigator(Kenkyū-buntansha): 中川 修 国立研究開発法人国立循環器病研究センター, 研究所, 部長 (40283593)
• Co-Investigator(Renkei-kenkyūsha): WAKABAYASHI Shigeo 大阪医科大学, 生命科学講座薬理学, 非常勤講師 (70158583) ; NAKAO Shu 立命館大学, 生命科学部生命医科学科, 助教 (30646956)
• Research Collaborator: KAWAKAMI Haruka 国立研究開発法人国立循環器病研究センター, 研究所, 研究補助員
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: カルシウム / 代謝異常 / ミトコンドリア

Outline of Final Research Achievements

Obesity is a leading cause of life-threatening diseases, thus clarifying its molecular mechanism is important. We have previously reported that mice lacking a Ca2+ sensor protein NCS-1(NCS1-/-) exhibited significant obesity. Using metabolic cages, we found that food intake and locomotor activity were similar between the two groups. However, energy metabolism (i.e. O2 consumption/CO2 emission) were significantly lower in NCS1-/- mice. In the cellular level, indicators for mitochondrial function and number (respiratory rate, and the levels of UCP1, PGC-1α) were also decreased. Metabolome analyses demonstrated that the metabolites involved in energy consumption were decreased whereas those in energy storage were increased, leading to massive obesity. Taken together, these results suggest that NCS-1 is a novel regulator of energy metabolism in adipocytes, and hence can be an important target for treatment of metabolic syndrome.

Free Research Field

細胞生理学