Establishing a novel chronic fatigue model and evaluate the possibility of appetite hormones using in chronic fatigue diagnosis.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K16586
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Applied health science
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: Hu Di 国立研究開発法人理化学研究所, 生命機能科学研究センター, 研究員 (60758580)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 慢性疲労 / ストレス / 内分泌異常 / レプチン / グレリン / コルチコステロン / ACTH

Outline of Final Research Achievements

The detailed pathogenic mechanism of chronic fatigue syndrome is not yet known, fundamental treatment methods have not been established.In this study, rats have applied for 14-day fatigue loading and succeeded in creating a chronic fatigue model. In addition to a prolonged recovery of spontaneous activity, this model showed dynamic changes in sleeping during fatigue loading short time rest, a weight-load forced swimming test’s time decreased, increased in oxidative stress, stress-related hormone elevation, and negative feedback regulation abnormality, etc. On the other hand, after 14-day fatigue loading the appetite-stimulating hormone ghrelin increased, and the anorexigenic hormone leptin significantly decreased. Furthermore, aMSH, which has a suppression of food intake effect, was elevated. The rise of both appetite-promoting ghrelin and food-depressing aMSH suggested dysfunction of the appetite-controlling center associated with the accumulation of fatigue.

Free Research Field

神経内分泌学

Academic Significance and Societal Importance of the Research Achievements

本研究は、疲労の回復が1週間に遅延するモデルを確立させた。このモデルはヒトの慢性疲労症候群に近い状態を示しており、疲労研究の新たなルーツとしてレプチンとグレリンの慢性疲労における意義を検討した。疲労負荷早期に両ホルモンが同時に上昇し、疲労負荷後期にグレリンの増加とレプチンの低下が見られ、さらに摂食抑制効果を持つaMSHが上昇すした。こうした変動は疲労の蓄積に伴う食欲制御中枢の機能異常を示唆し、両ホルモンの疲労深刻度を表す指標としての可能性を示した。本研究は食欲機能制御異常だけではなくストレス関連ホルモンのネガティブフィードバック制御異常にも突き止めており、慢性疲労の脳内発症機序解明につながる。