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Original Article

Circulating preptin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects

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Pages 52-56 | Received 06 Jan 2008, Published online: 08 Jul 2009
 

Abstract

Background. Preptin is a novel hormone that is co-secreted with insulin and amylin from the pancreatic β-cells. Preptin increases glucose-mediated insulin secretion, while the binding of endogenous preptin by antipreptin antibodies decreases glucose-mediated insulin secretion. Thus, it appears to act as a physiological amplifier of glucose-mediated insulin secretion.

Aim. In this study, we investigate whether plasma preptin levels are different in non-diabetic subjects and patients with impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM).

Method. Fifty patients with T2DM, 56 subjects with IGT, and 54 sex- and age-matched normal controls participated in the study. Plasma preptin levels were measured with a radioimmunoassay. The relationships between plasma preptin levels and anthropometric and metabolic parameters were also assessed.

Results. Plasma preptin levels were higher in patients with T2DM compared to patients with IGT and controls (456±14 versus 416±13 and 398±13 ng/L, P<0.05 and P<0.01, respectively). Plasma preptin levels were lower in males than females (403±10 versus 432±10 ng/L, P<0.05). Fasting plasma preptin levels correlated positively with diastolic blood pressure (DBP) (r=0.20, P<0.01), triglyceride (TG) (r=0.24, P<0.01), total cholesterol (TC) (r=0.24, P<0.01), high-density lipoprotein cholesterol (HDL-C) (r=0.18, P<0.05), free fatty acids (FFA) (r=0.21, P<0.01), 2-h blood glucose after glucose overload (2hOGTT) (r=0.18, P<0.05), glycosylated haemoglobin (HbA1c) (r=0.19, P<0.01), and homeostasis model assessment-insulin resistance index (HOMAIR) (r=0.13, P<0.05) in simple regression analysis of pooled data, while in multiple stepwise regression analysis, only DBP, TG, HDL-C, and FFA were independently related with plasma preptin levels.

Conclusion. The present work suggests a potential role of preptin in the pathogenesis of T2DM.

Acknowledgements

This work was supported by research grants from the National Natural Science Foundation of China (30771037), Chongqing Municipal Education Commission (KJ 050304), and the National Institutes of Health (R01-DK 58895 to G.B.).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. GangYi Yang and Ling Li contributed equally to this project.

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