The aim was to investigate the amounts of saliva and serum asprosin in order to determine whether it is related to obesity and whether salivary glands synthesize asprosin or not.
As Olfr734 deficiency dramatically attenuates both fasting and high-fat-diet-induced glucose production, our results demonstrate a critical role of OLFR734 as a receptor of Asprosin to maintain glucose homeostasis during fasting and in obesity.
Asprosin levels are elevated in adult obese men as well as in mice, and reductions in asprosin protect against the hyperinsulinism associated with metabolic syndrome in mice with diet-induced obesity, which indicates a potential therapeutic role of asprosin in obesity and type 2 diabetes.
Reduction and fragmentation of elastic fibers in the skin of obese mice is associated with altered mRNA expression levels of fibrillin-1 and neprilysin.
Thus, in addition to performing a glucogenic function, asprosin is a centrally acting orexigenic hormone that is a potential therapeutic target in the treatment of both obesity and diabetes.