Circulating preptin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects
Circulating preptin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects
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DOI:
10.1080/07853890802244142
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发表时间:
2009-01-01
影响因子:
4.4
通讯作者:
Li, Ke
中科院分区:
文献类型:
--
作者:
Yang, Gangyi;Li, Ling;Li, Ke
Background. Preptin is a novel hormone that is co-secreted with insulin and amylin from the pancreatic -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 (45614 versus 41613 and 39813 ng/L, P0.05 and P0.01, respectively). Plasma preptin levels were lower in males than females (40310 versus 43210 ng/L, P0.05). Fasting plasma preptin levels correlated positively with diastolic blood pressure (DBP) (r=0.20, P0.01), triglyceride (TG) (r=0.24, P0.01), total cholesterol (TC) (r=0.24, P0.01), high-density lipoprotein cholesterol (HDL-C) (r=0.18, P0.05), free fatty acids (FFA) (r=0.21, P0.01), 2-h blood glucose after glucose overload (2hOGTT) (r=0.18, P0.05), glycosylated haemoglobin (HbA1c) (r=0.19, P0.01), and homeostasis model assessment-insulin resistance index (HOMAIR) (r=0.13, P0.05) 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.