Bhadel P, Shrestha S, Sapkota B, Li J Y, Tao H
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, Hengyang, Hunan Province, China.
Department of Pharmacy, Nepal Cancer Hospital and Research Center, Harisiddhi, Lalitpur, Nepal.
J Biol Regul Homeost Agents. 2020 Feb 21;34(1). doi: 10.23812/19-244-E.
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.
糖尿病是一组代谢紊乱疾病，其特征为高血糖，会增加心血管、微血管和大血管并发症的风险。关于糖尿病控制和管理的创新性治疗试验一直在进行。本综述旨在探讨导致2型糖尿病（T2DM）发病机制的潜在影响和机制及其与脂肪因子的关系。脂肪因子是一种新发现的激素，由原纤蛋白1（FBN1基因）编码，在禁食条件下由白色脂肪以5-10 nM的水平分泌，通过细胞膜受体作用于肝脏并激活G蛋白cAMP-PKA途径。禁食期间，作为低血糖的代偿机制，脂肪因子的分泌会增加。与健康受试者相比，T2DM患者和糖调节受损患者的脂肪因子浓度更高。脂肪因子的基因缺陷可能会导致人类食欲不振和极度消瘦的问题。减弱脂肪因子活性或消耗脂肪因子可能成为治疗T2DM和肥胖症的一种新型治疗创新方法。因此，脂肪因子可能成为未来糖尿病管理治疗靶点的一个指引。
