Dysfunctional atrial natriuretic peptide physiology in subcutaneous adipocytes of adults with obesity: etiology, relation with cardiometabolic risk, and impact of exercise intervention. (R-7523)

An obesity epidemic is emerging. However, within obese individuals significant differences in magnitude of cardiometabolic risk may be present, leading to metabolic healthy (minority) vs. metabolic unhealthy (majority) obese individuals. In the obese state adipose tissue dysfunction plays a prominent role in the development of such metabolically unhealthy phenotype: fat mass reduction depends highly on fat mobilization (lipolysis) capacity, a process stimulated upon exercise and under tight control of endocrine hormones. Here, a role for atrial natriuretic peptide (ANP) in lipolysis was discovered. We have recently found novel significant abnormalities in fat cell ANP physiology, specifically in the subcutaneous depot, in obese men. Therefore, it can be hypothesized that fat mass gain, and development of a metabolically unhealthy phenotype, can be due to abnormalities in ANP physiology. The origin of this 'natriuretic handicap' deserves deeper study to contribute to novel therapy for obesity (first project aim). To lower adipose tissue mass and prevent the development of a metabolically unhealthy phenotype, exercise intervention is often implemented. This is however not always sufficient in fat mass reduction, which may be due to disturbances in ANP physiology. The use of exercise training in the treatment of the 'natriuretic handicap' in obese individuals remains a major field of research to prevent or treat cardiometabolic diseases in the obese (second project aim).

Keywords:atriaal natriuretic peptide ANP, obese, unhealthy metabolic phenotype

Disciplines:Morphological sciences