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| 正常人、糖耐量异常者和糖尿病患者的循环preptin水平 |
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| Circulating preptin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects |
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| Yang G., Li L., Chen W., Liu H., Boden G., Li K. 2009/5/29 18:39:20 |
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Annals of Medicine, 2009, Volume 41, Issue 1
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| 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. © 2009 Informa UK Ltd. |
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| Correspondence Address: Yang, G.; Department of Endocrinology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China; email: gangyiyang@yahoo.com.cn |
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 疾病资源中心
王燕燕 王曙
上海交通大学附属瑞金医院内分泌科
患者，女，69岁。2009年1月无明显诱因下出现乏力，当时程度较轻，未予以重视。2009年3月患者乏力症状加重，尿色逐渐加深，大便习惯改变，颜色变淡。4月18日入我院感染科治疗，诉轻度头晕、心慌，体重减轻10kg。无肝区疼痛，无发热，无腹痛、腹泻、腹胀、里急后重，无恶性、呕吐等。入院半月前于外院就诊，查肝功能：ALT 601IU/L，AST 785IU/L，TBIL 97.7umol/L，白蛋白 41g/L，甲状腺功能：游离T3 30.6pmol/L，游离T4 51.9pmol/L，心电图示快速房颤。
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