Children's Nutrition Research Centre, Queensland Children's Medical Research Institute, The University of Queensland, Royal Children's Hospital, Herston, Queensland, Australia; Centre for Integrative Clinical and Molecular Medicine, School of Medicine, The University of Queensland, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia; School of Medicine, The University of Queensland, Adelaide, South Australia, Australia.
Nutr Res. 2013 Oct;33(10):781-8. doi: 10.1016/j.nutres.2013.07.019. Epub 2013 Aug 26.
Although obesity is a key predisposing risk factor in the development of insulin resistance (IR) and type 2 diabetes mellitus, not all obese individuals develop IR. This study aimed to identify key anthropometric and biochemical parameters that predict insulin sensitivity in overweight and obese adults. Based on previous literature, we hypothesized that markers of insulin sensitivity would be negatively correlated with plasma concentrations of free fatty acids and liver enzymes. Forty nondiabetic adult participants (body mass index ≥ 25.0 kg/m²) were recruited. Data collection included anthropometric measurements and fasting plasma samples for the quantification of liver enzymes (alanine transaminase, aspartate transaminase, γ-glutamyl transpeptidase), blood lipid profile, and markers of insulin sensitivity. Questionnaires relating to dietary intake, physical activity, and fatigue were also completed. Insulin and Homeostasis Model of Assessment (HOMA) scores were significantly correlated with indirect measures of central obesity (P < .05). Glycosylated hemoglobin, insulin, and HOMA scores for IR were all positively correlated with selected liver function markers (P < .05). Scores of HOMA-IR were significantly positively correlated with plasma phospholipid levels of n-3 fatty acids (P = .04) and ratio of n-3/n-6 fatty acids (P < .05) and negatively correlated with n-6 fatty acids (P = .03). No significant correlations were found between markers of insulin sensitivity and cholesterol levels, physical activity, or self-reported fatigue. These results have reinforced the integral role of liver function in the development of IR. Despite previous data linking elevations in free fatty acid to the development of IR, we found no relationship between these variables in this study.
尽管肥胖是导致胰岛素抵抗（IR）和 2 型糖尿病的主要危险因素，但并非所有肥胖者都会出现 IR。本研究旨在确定预测超重和肥胖成年人胰岛素敏感性的关键人体测量学和生化参数。根据先前的文献，我们假设胰岛素敏感性标志物与游离脂肪酸和肝酶的血浆浓度呈负相关。本研究共招募了 40 名非糖尿病成年参与者（BMI≥25.0 kg/m²）。数据收集包括人体测量学测量和空腹血浆样本，用于定量测定肝酶（丙氨酸转氨酶、天冬氨酸转氨酶、γ-谷氨酰转肽酶）、血脂谱和胰岛素敏感性标志物。还完成了与饮食摄入、体力活动和疲劳相关的问卷。胰岛素和稳态模型评估（HOMA）评分与中心性肥胖的间接测量指标显著相关（P<0.05）。糖化血红蛋白、胰岛素和 HOMA 评分均与某些肝功能标志物呈正相关（P<0.05）。HOMA-IR 评分与 n-3 脂肪酸的血浆磷脂水平呈显著正相关（P=0.04）和 n-3/n-6 脂肪酸的比值呈负相关（P<0.05）。胰岛素敏感性标志物与胆固醇水平、体力活动或自我报告的疲劳之间无显著相关性。这些结果进一步证实了肝功能在 IR 发展中的重要作用。尽管先前的数据表明游离脂肪酸升高与 IR 的发展有关，但在本研究中未发现这些变量之间存在关系。
