Circulating Levels of Betatrophin and Irisin Are Not Associated with Pancreatic β-Cell Function in Previously Diagnosed Type 2 Diabetes Mellitus Patients.

Lingshu Wang,Peng Lin,Tianyi He,Ruxing Zhao,Wenjuan Li,Kai Liang,Jun Song,Fuqiang Liu,Yu Sun,Li Chen,Xinguo Hou,Chuan Wang,Jun Qin,Jinbo Liu,Yiran Lu

doi:10.1155/2016/2616539

Lingshu Wang, Peng Lin + Show 13 more

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https://doi.org/10.1155/2016/2616539

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Abstract

Betatrophin and irisin are two recently identified hormones which may participate in regulating pancreatic β-cell function. However, the associations of these two hormones with β-cell function remain unclear. The present study aims to demonstrate the associations of circulating betatrophin and irisin levels with β-cell function, assessed by the area under the curve (AUC) of C-peptide, and the possible correlation between these two hormones in previously diagnosed type 2 diabetes mellitus (T2DM) patients. In total, 20 age-, sex-, and body mass index- (BMI-) matched normal glucose tolerance (NGT) subjects and 120 previously diagnosed T2DM patients were included in this study. Partial correlation analysis was used to evaluate the relationships between these two hormones and indexes of β-cell function and insulin resistance. Our results showed that betatrophin levels were significantly elevated, while irisin levels were significantly decreased, in patients with T2DM compared with NGT subjects. However, partial correlation analysis showed that betatrophin levels did not correlate with β-cell function-related variables or insulin resistance-related variables before or after controlling multiple covariates, while irisin correlated positively with insulin sensitivity but is not associated with β-cell function-related variables. Besides, no correlation was observed between betatrophin and irisin levels. Hence we concluded that betatrophin and irisin were not associated with β-cell function in previously diagnosed T2DM patients.

Highlights

It has been suggested that the best treatment, and a potential cure, for both type 1 mellitus (T1DM) and type 2 diabetes mellitus (T2DM), is to replace or regenerate the pancreatic βcell mass [1]
For lacking direct evidence of the role of betatrophin in islet β-cell replication in the human model and the fact that there were relatively few clinical studies focusing on the above issue, we first measured the circulating betatrophin levels in age, sex- and body mass index- (BMI-)matched healthy normal glucose tolerance (NGT) and T2DM subjects
Contradictory to the results of Zhang et al [10], we found betatrophin and irisin levels lacked a significant correlation in T2DM subjects, which might remind us to be very careful when applying the results from animal models to humans

Summary

Introduction

It has been suggested that the best treatment, and a potential cure, for both type 1 mellitus (T1DM) and type 2 diabetes mellitus (T2DM), is to replace or regenerate the pancreatic βcell mass [1]. Two recently identified hormones, betatrophin and irisin, might be involved in this process [2], their specific physiological effects on pancreatic βcell have not been confirmed. Overexpression of betatrophin in mice livers was reported to induce a striking increase of β-cell proliferation rate 17-fold higher than the controls. These inspiring discoveries were later challenged by either genetic ablation of betatrophin or its overexpression, which showed no significant effect on β-cell mass in mice [6, 7]. The relevance of betatrophin with β-cell function needs to be further warranted, especially in human subjects

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