A novel role of C-type natriuretic peptide (CNP) in energy expenditure.

Research Project

Project/Area Number	15H06915
Research Category	Grant-in-Aid for Research Activity Start-up
Allocation Type	Single-year Grants
Research Field	Metabolomics
Research Institution	National Cardiovascular Center Research Institute
Principal Investigator	Bae Cho-Rong 国立研究開発法人国立循環器病研究センター, 研究所, 流動研究員 (80760793)
Project Period (FY)	2015-08-28 – 2017-03-31
Project Status	Completed (Fiscal Year 2016)
Budget Amount *help	¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000) Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	CNP / エネルギー代謝 / 肥満 / 炎症 / インスリン感受性 / 脂肪細胞 / ペプチド / 過剰発現マウス / 代謝学 / 内分泌学
Outline of Final Research Achievements	OBJECTIVE: C-type natriuretic peptide (CNP) is expressed in diverse tissues, including adipose, and exerts its effects by binding to and activating its receptor, guanylyl cyclase B (GCB). However, the function of CNP in adipose tissue during high-fat diet (HFD)-induced obesity is unclear. METHODS: To determine the role of CNP in obesity, we generated transgenic (Tg) mice that overexpressed CNP specifically in adipose tissue (CNP Tg). RESULTS: CNP Tg mice showed decreased fat weight due to changes in lipid metabolism, including increased lipolysis, and an increase in energy expenditure by beige adipocytes in WAT during HFD-induced obesity. This response led to reduced inflammation. In addition, Ad-CNP Tg mice showed improved glucose tolerance and insulin resistance. CONCLUSION: Our results suggest that CNP protects against inflammation and insulin resistance, and increases energy expenditure during HFD-induced obesity in mice.