Asprosin and type 2 diabetes mellitus: a novel potential therapeutic implication

Diabetes is a group of metabolic disorders that is characterized by hyperglycemia which increases the risks of cardiovascular, microvascular, and macrovascular complications. Innovative therapeutic trials regarding diabetes control and management are continually being undertaken. The present review was aimed to explore the potential effects and mechanisms that lead to the pathogenesis of type 2 diabetes mellitus (T2DM) and its relation with asprosin. Asprosin is a newly discovered hormone that is encoded by protein fibrillin 1 (FBN1 gene), secreted by white adipose during fasting conditions at 5-10 nM levels, which acts on the liver through cell membrane receptors and activates the G protein cAMP- PKA pathway. Asprosin secretion is increased during fasting as the compensatory mechanism in hypoglycemia. Asprosin concentration is higher in patients with T2DM and impaired glucose regulation compared to healthy subjects. Genetic deficiency of asprosin may cause problems of poor appetite and extreme leanness in humans. Attenuating asprosin activity or depleting asprosin may serve as a novel therapeutic innovation for the treatment of T2DM and obesity. Hence, asprosin may serve as a beacon for the target of a future therapy in diabetes management.