阿迪波金内脏脂肪素在糖尿病及相关代谢紊乱发病机制中的作用

Title:Adipokine Visfatin’s Role in Pathogenesis of Diabesity and Related Metabolic Derangements

Volume: 18 Issue: 2

关键词: 内脏脂肪素，代谢紊乱，炎症，高脂血症，糖尿病，脂肪因子，糖尿病。

摘要: Visfatin is one of the prominent adipokines secreted by adipose tissue. The level of visfatin increases significantly in persons with obesity owing to increased body mass index (BMI). During obesity, the adipocytes, which populate adipose tissue, undergo hypertrophy and hyperplasia and secrete a number of adipocytokines including visfatin. Visfatin, which also acts as an enzyme nicotinamide phosphoribosyl transferase, is one of the prominent adipokines that influence metabolic homeostasis in the body. Visfatin exists in two forms, extracellular and intracellular, and enacts a multitude of actions. The direct and indirect evidence gathered from in-vitro, in-vivo and clinical studies indicate that visfatin modulates obesity and metabolic syndrome-related pathophysiological activities including enhanced inflammation, angiogenesis, synthesis of NAD mononucleotide, and upregulation of antiapoptotic proteins in a number of cell types. It has been implicated in a number of obesity-related alterations and metabolic derangement such as diabetes, cardiovascular complications and some forms of cancers. In this review, the novel hypothesis about the role of visfatin in diabesity has been proposed which implies recent advances in studies about the pathophysiological roles of visfatin during obesity and chronic high glucose in the circulation. Visfatin at high concentration attracts immune cells and produces chronic inflammation in adipocytes. Additionally, it induces insulin resistance in many tissues and causes pancreatic beta cells dysfunction at later stages. Further, its potential as an important target to develop molecular medicine in diabesity and related metabolic syndrome has been highlighted.

Cite this article as:

Adipokine Visfatin’s Role in Pathogenesis of Diabesity and Related Metabolic Derangements, Current Molecular Medicine 2018; 18 (2) . https://dx.doi.org/10.2174/1566524018666180705114131