Charlesworth John A, Kriketos Adamandia D, Jones Jane E, Erlich Jonathan H, Campbell Lesley V, Peake Philip W
Department of Nephrology, Prince of Wales Hospital and the University of New South Wales, Randwick, New South Wales 2031, Australia.
Metabolism. 2005 Jun;54(6):821-8. doi: 10.1016/j.metabol.2005.01.028.
Renal failure is associated with a range of metabolic abnormalities including insulin resistance and dyslipidemia. We examined the role of creatinine clearance (CrCl) and body composition in the development of insulin resistance in patients with primary renal disease and a variable degree of renal failure. We also determined the effect of a high-fat meal on postprandial triglyceride levels in a subgroup of these patients.
Forty-four patients with primary renal disease (men, 25; women, 19; age, 21-75 years) were compared to 44 controls matched for age, sex, and body composition. Renal biochemistry, plasma glucose, insulin, lipids, and nonesterified fatty acids were measured in the fasting state. Insulin sensitivity was calculated using the Homeostasis Model Assessment for Insulin Resistance (HOMA-R), and pancreatic beta-cell secretory capacity by HOMA- beta . Fourteen normotriglyceridemic subjects from each group consumed an 80-g fat meal to examine their postprandial metabolic response.
Although there was no significant difference between HOMA-R for the controls and the entire patient group ( P = .06), HOMA-R was significantly higher in patients with CrCl less than 60 mL/min than those with CrCl greater than 60 mL/min or control subjects ( P < .01 for each pair). Exponential analysis of the relationship between CrCl and HOMA-R and - beta showed a line of best fit that was superior to that obtained by linear regression analysis ( P < .01 and P < .005, respectively). HOMA-R in renal patients was correlated with several parameters of body composition, including central fat (kilogram) ( P < .005). There was no difference in body fat parameters or HOMA-R for the patient and control subgroups undergoing a fat meal challenge. However, the patient subgroup showed a greater postprandial incremental rise in plasma triglycerides compared to controls ( P < .02).
Patients with renal disease exhibit metabolic features typically associated with the metabolic syndrome. Insulin resistance increased with decline in renal function and was significantly higher in patients with CrCl less than 60 mL/min compared to subjects with CrCl greater than 60 mL/min or carefully matched controls. Renal patients also showed significant postprandial hypertriglyceridemia.
肾衰竭与一系列代谢异常相关,包括胰岛素抵抗和血脂异常。我们研究了肌酐清除率(CrCl)和身体组成在原发性肾病及不同程度肾衰竭患者胰岛素抵抗发生中的作用。我们还确定了高脂餐对这些患者亚组餐后甘油三酯水平的影响。
将44例原发性肾病患者(男性25例,女性19例;年龄21 - 75岁)与44例年龄、性别和身体组成相匹配的对照者进行比较。在空腹状态下测量肾脏生化指标、血浆葡萄糖、胰岛素、血脂和非酯化脂肪酸。使用胰岛素抵抗稳态模型评估(HOMA - R)计算胰岛素敏感性,使用HOMA - β计算胰腺β细胞分泌能力。每组14例正常甘油三酯血症受试者食用80克脂肪餐,以检查其餐后代谢反应。
虽然对照组和整个患者组的HOMA - R之间无显著差异(P = 0.06),但CrCl低于60 mL/min的患者的HOMA - R显著高于CrCl高于60 mL/min的患者或对照者(每对比较P < 0.01)。对CrCl与HOMA - R和 - β之间关系的指数分析显示,最佳拟合线优于线性回归分析得到的线(分别为P < 0.01和P < 0.005)。肾病患者的HOMA - R与身体组成的几个参数相关,包括中心脂肪(千克)(P < 0.005)。接受脂肪餐挑战的患者亚组和对照亚组的体脂参数或HOMA - R无差异。然而,患者亚组与对照组相比,餐后血浆甘油三酯的增量上升更大(P < 0.02)。
肾病患者表现出通常与代谢综合征相关的代谢特征。胰岛素抵抗随肾功能下降而增加,CrCl低于60 mL/min的患者的胰岛素抵抗显著高于CrCl高于60 mL/min的受试者或精心匹配的对照者。肾病患者还表现出显著的餐后高甘油三酯血症。