Establishment of sarcopenia obesity-model animal and elucidation of its pathophysiology

2021 Fiscal Year Final Research Report

• Project/Area Number: 18K19743
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
• Research Institution: Hiroshima University
• Principal Investigator: Ukena Kazuyoshi 広島大学, 統合生命科学研究科(総), 教授 (10304370)
• Co-Investigator(Kenkyū-buntansha): 岩越 栄子 広島大学, 統合生命科学研究科(総), 研究員 (50311296) ; 長谷川 博 広島大学, 人間社会科学研究科(総), 教授 (70314713)
• Project Period (FY): 2018-06-29 – 2022-03-31
• Keywords: 視床下部 / 小タンパク質 / 脂肪蓄積 / 筋肉

Outline of Final Research Achievements

We have discovered a novel secretory small protein, NPGL, in the hypothalamus. It has been found that NPGL stimulates feeding behavior and induces fat accumulation in the white adipose tissue, although the weight gain is not remarkable, and the cause is a decrease in bone length and the mass of skeletal muscle. Recently, attention has been focused on sarcopenia obesity, which increases fat and decreases muscle. Therefore, in this research, we considered that it is possible to produce model animals exhibiting sarcopenia obesity-like state by effectively utilizing the physiological function of NPGL. As a result of various NPGL gene overexpression and NPGL administration using mice and rats, it was found that rats overexpressed using an adeno-associated virus vector are suitable as sarcopenia-like model animals.

Free Research Field

神経内分泌学

Academic Significance and Societal Importance of the Research Achievements

近年、筋肉量の減少（サルコペニア）と肥満が組み合わさった状態であるサルコペニア肥満の増加が問題となっている。我々が独自に見出した因子であるNPGLの作用を亢進した動物は、短期間でサルコペニア肥満を模倣している可能性あり、これまで未解明であったサルコペニア肥満の病態解明を行う上で貴重なモデル動物に成り得ると考えている。そのため、リハビリテーション科学、スポーツ科学、体育、栄養学、健康科学の幅広い分野において重要な科学的知見を加える可能性を示すことができたことから、学術的及び社会的意義は極めて大きい。