Asprosin, a novel glucogenic adipokine, is encoded by two exons (exon 65 and exon 66) of the gene Fibrillin 1 (FBN1) and mainly synthesized and released by white adipose tissue during fasting. Asprosin plays a complex role in the central nervous system (CNS), peripheral tissues, and organs. It is involved in appetite, glucose metabolism, insulin resistance (IR), cell apoptosis, etc. In this review, we will summarize the newly discovered roles of asprosin in metabolic diseases including diabetes, obesity, polycystic ovarian syndrome (PCOS), and cardiovascular disease (CVD), which may contribute to future clinical diagnosis and treatment.
WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT
• Rosiglitazone is able to increase serum adiponectin levels significantly in Type 2 diabetic patients.
• The role of genetic factors that determine the marked interindividual variability in glucose‐lowering efficacy of rosiglitazone in Chinese patients is not known.
• The current study was designed to evaluate the impact of the adiponectin common allele 45T/G and −11377C/G polymorphisms on the response to rosiglitazone monotherapy in Chinese patients with Type 2 diabetes (T2D).
WHAT THIS STUDY ADDS
• The genetic polymorphisms of adiponectin alleles 45T/G and −11377C/G as well as their common diplotypes are significantly associated with an attenuated fasting plasma glucose, postprandial plasma glucose and homeostasis model assessment for insulin resistance as well as an enhanced adiponectin concentration in Chinese patients with T2D after rosiglitazone treatment.
AIMS The aim of the present study was to evaluate the impact of adiponectin allele T45G and C‐11377G genetic polymorphisms on efficacy of rosiglitazone in Chinese patients with type 2 diabetes (T2D).
METHODS Patients with T2D (n = 255) and 120 healthy volunteers were enrolled to identify 45T/G and –11377C/G genotypes by polymerase chain reaction‐restriction fragment length polymorphism assay. Forty‐two T2D patients with different 45T/G or –11377C/G genotypes received orally rosiglitazone as a single‐dose therapy (4 mg day‐1 p.o.) for 12 weeks. Serum triglyceride, fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycated hemoglobin, fasting serum insulin, postprandial serum insulin, total cholesterol, homeostasis model assessment for insulin resistance (HOMA‐IR), low‐density lipoprotein‐cholesterol, high‐density lipoprotein‐cholesterol (HDL‐c) and adiponectin concentration were determined before and after rosiglitazone treatment.
RESULTS We showed an attenuated rosiglitazone effect in patients with –11377CG+GG heterozygote genotype on FPG, PPG, HOMA‐IR compared with –11377CC homozygote genotype. However, we found an enhanced rosiglitazone effect on serum adiponectin concentration in patients with –11377CC homozygote genotype compared with –11377CG+GG heterozygote genotype (P = 0.000) and in patients with 45TG + GG heterozygote genotype compared with 45TT homozygote genotype (P = 0.018). Finally, our results showed that there was an enhanced effect in patients with –11377/45 CGTT diplotype compared with other discovered diplotypes on FPG (P = 0.001) and PPG (P = 0.003) after rosiglitazone treatment.
CONCLUSIONS These data suggest that the adiponectin allele 45T/G and –11377C/G polymorphisms are significantly associated with the therapeutic efficacy of multiple‐dose rosiglitazone in Chinese patients with T2D.
Obesity and diabetes are associated with inflammation, endothelial dysfunction and insulin resistance in the muscle microvasculature. Inflammation-induced microvascular insulin resistance is an early event and plays a causative role in the development of metabolic insulin resistance in diet-induced obesity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.