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Association between Serum Leptin and Adiponectin Levels with Risk of Insulin Resistance and Impaired Glucose Tolerance in Non-Diabetic Women

非糖尿病女性之脂肪細胞激素與胰島素阻抗之相關性研究

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摘要


肥胖是胰島素阻抗及第二型糖尿病的危險因子。最近發現,由脂肪細胞所分泌的一些蛋白質(瘦體素、酯聯素)與胰島素阻抗性有關。本篇研究目的在於探討非糖尿病女性其脂肪細胞酵素包括瘦體素、酯聯素與胰島素抗阻及葡萄糖不耐症之間的相關性。個案選自在2003年2月至2004年2月間小港醫院準備參加減重門診的婦女,排除已知有糖尿病的患者以及目前正在使用降血壓、降血脂及降血糖的藥物後,共有190位個案。以問卷收集個案的基本資料,生活習慣,過去疾病史及藥物史。所有個案在隔夜空腹後抽血分析血糖、總膽固醇、高密度膽固醇、三酸甘油酯、胰島素及瘦體素、酯聯素。所有個案在給予口服75克葡萄糖水試驗後2小時,抽血測量血糖值以判斷個案是否有葡萄糖不耐症。計算HOMA-IR作為胰島素抗阻程度的指標,並且測量血壓、腰圍及BMI。統計分析以皮爾斯相關分析BMI、胰島素、瘦體素及酯聯素間的相關性;以複迴歸分析控制相關因子後分析瘦體素、酯聯素與胰島素阻抗的相關性。多變數分析的結果顯示,在控制了包括BMI在內的相關變數後,瘦體素及酯聯素兩者分別與HOMA-IR或空腹胰島素濃度有顯著的統計相關,其中瘦體素與HOMA-IR及空腹胰島素濃度為正相關,而酯聯素與HOMA-IR及空腹胰島素濃度為負相關。而控制了包括BMI在內的可能干擾因子後,adiponectin與葡萄糖不耐症仍有顯著的統計相關,瘦體素則無統計上的顯著差異。在控制了肥胖的因素後,瘦體素和酯聯素分別與胰島素抗阻性及空腹胰島素濃度之間仍有顯著統計相關,推論分泌自脂肪細胞的瘦體素及酯聯素可能與肥胖者發生胰島素阻抗的機轉有關。而在控制了肥胖等相關因子後,酯聯素與葡萄糖不耐症仍有統計上顯著差異,推論較低的血清酯聯素濃度可能與發生血糖代謝異常或糖尿病有相關,而瘦體素則較無關。

並列摘要


Obesity is a well known risk factor for insulin resistance and type 2 diabetes. Recently discovered adipocyte-derived proteins (leptin and adiponectin) might contribute to the pathologic mechanism linking obesity and insulin resistance. Atotal of 190 non-diabetic women were recruited from the Obesity Clinic of Kaohsiung Municipal Hsiao-Kang Hospital, Taiwan, between February 2003 and February 2004. All participants completed a simple questionnaire. Blood pressure and body mass index were measured; blood samples for fasting glucose, total cholesterol, high-density lipoprotein cholesterol, triglyceride, leptin, adiponectin, and fasting insulin level were collected after an overnight fast. Two-hour glucose level after a 75-g glucose tolerance test was determined. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as the index of insulin resistance. Multivariate linear regression analyses were used to analyze the relationship between adipocytokines and insulin resistance after adjusting for possible confounding factors. Leptin and adiponectin were found to be independently associated with HOMA-IR and fasting insulin concentration, but in divergent directions, after adjusting for potential confounding factors. Adiponectin, but not leptin, was associated with impaired glucose tolerance after adjusting for potential confounding factors. The results suggest that leptin and adiponectin may be involved in the pathophysiologic link between obesity and insulin resistance independently. Low levels of adiponectin may increase the risks of developing impaired glucose metabolism and type 2 diabetes.

並列關鍵字

Adipocytokines adiponectin insulin resistance leptin obesity

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