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Increased serum level and impaired response to glucose fluctuation of asprosin is associated with type 2 diabetes mellitus

Abstract

Aims/Introduction

Asprosin is a novel secreted adipokine that is induced by fasting and promotes hepatic glucose release. In healthy humans, circulating asprosin shows circadian oscillation with an acute drop coinciding with the onset of eating. The present study investigated whether this circadian oscillation still exists in patients with type 2 diabetes mellitus.

Materials and Methods

We recruited 60 patients with type 2 diabetes mellitus and 60 individuals with normal glucose tolerance (NGT). All participants completed a 75‐g oral glucose tolerance test. Fasting and 2‐h postprandial serum asprosin concentrations were measured by the enzyme‐linked immunosorbent assay method. Partial correlation coefficients were calculated to analyze the relationships between serum asprosin level and parameters of glucose metabolism. Multiple logistic regression analysis was used to determine the association of serum asprosin level with diabetes.

Results

Both fasting and postprandial asprosin levels were significantly higher in patients with type 2 diabetes mellitus. The postprandial asprosin level was apparently lower than fasting asprosin level in individuals with NGT. The fasting asprosin level closely correlated with type 2 diabetes mellitus after multiple adjustment (odds ratio 2.329, P = 0.023). Asprosin correlated negatively with change in blood glucose (r = −0.502, P < 0.001) and change in C‐peptide (r = −0.467, P < 0.001) in individuals with NGT, but not in type 2 diabetes mellitus patients.

Conclusions

Serum asprosin level decreased coinciding with the onset of the oral glucose tolerance test in individuals with NGT, whereas this circadian oscillation was disturbed in type 2 diabetes mellitus patients. The impaired response of asprosin to glucose fluctuation in type 2 diabetes mellitus patients might be one of the reasons for the onset of type 2 diabetes mellitus.

Cited products
Source:Journal of Diabetes Investigation     by Xy Zhang, H Jiang, Xj Ma, et al.
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