Department of Kinesiology, Faculty of Medicine, Laval University, Québec, QC, G1V 0A6, Canada.
Québec Heart and Lung University Research Centre, Québec, QC, Canada.
J Physiol Biochem. 2018 Nov;74(4):591-601. doi: 10.1007/s13105-018-0630-4. Epub 2018 Apr 26.
The contribution of adiposopathy to glucose-insulin homeostasis remains unclear. This longitudinal study examined the potential relationship between the adiponectin/leptin ratio (A/L, a marker of adiposopathy) and insulin resistance (IR: homeostasis model assessment (HOMA)), insulin sensitivity (IS: Matsuda), and insulin response to an oral glucose tolerance test before and after a 16-week walking program, in 29 physically inactive pre- and postmenopausal women with obesity (BMI, 29-35 kg/m; age, 47-54 years). Anthropometry, body composition, VOmax, and fasting lipid-lipoprotein and inflammatory profiles were assessed. A/L was unchanged after training (p = 0.15), despite decreased leptin levels (p < 0.05). While the Matsuda index tended to increase (p = 0.07), HOMA decreased (p < 0.05) and fasting insulin was reduced (p < 0.01) but insulin area under the curve (AUC) remained unchanged (p = 0.18) after training. Body fatness and VOmax were improved (p < 0.05) while triacylglycerols increased and HDL-CHOL levels decreased after training (p < 0.05). At baseline, A/L was positively associated with VOmax, HDL-CHOL levels, and Matsuda (0.37 < ρ < 0.56; p < 0.05) but negatively with body fatness, HOMA, insulin AUC, IL-6, and hs-CRP levels (- 0.41 < ρ < - 0.66; p < 0.05). After training, associations with fitness, HOMA, and inflammation were lost. Multiple regression analysis revealed A/L as an independent predictor of IR and IS, before training (partial R = 0.10 and 0.22), although A/L did not predict the insulin AUC pre- or post-intervention. A significant correlation was found between training-induced changes to A/L and IS (r = 0.38; p < 0.05) but not with IR or insulin AUC. Although changes in the A/L ratio could not explain improvements to glucose-insulin homeostasis indices following training, a relationship with insulin sensitivity was revealed in healthy women with obesity.
脂联素/瘦素比值与葡萄糖-胰岛素稳态的关系尚不清楚。本纵向研究旨在探讨脂联素/瘦素比值(A/L,脂病标志物)与胰岛素抵抗(稳态模型评估法(HOMA))、胰岛素敏感性(Matsuda 指数)以及口服葡萄糖耐量试验后胰岛素反应之间的潜在关系,在 29 名身体活动不足的绝经前和绝经后肥胖女性(BMI,29-35kg/m;年龄,47-54 岁)中,这些女性进行了 16 周的步行训练。评估了人体测量学、身体成分、最大摄氧量以及空腹血脂脂蛋白和炎症指标。尽管瘦素水平降低(p<0.05),但训练后 A/L 没有变化(p=0.15)。虽然 Matsuda 指数有升高趋势(p=0.07),但 HOMA 降低(p<0.05),空腹胰岛素降低(p<0.01),但胰岛素曲线下面积(AUC)不变(p=0.18)。训练后体脂和最大摄氧量增加(p<0.05),三酰甘油增加,高密度脂蛋白胆固醇水平降低(p<0.05)。在基线时,A/L 与最大摄氧量、高密度脂蛋白胆固醇水平和 Matsuda 呈正相关(0.37<p<0.56;p<0.05),与体脂、HOMA、胰岛素 AUC、白细胞介素-6 和超敏 C 反应蛋白水平呈负相关(-0.41<p<0.66;p<0.05)。训练后,与健康相关的因素、HOMA 和炎症的相关性消失。多元回归分析显示,A/L 是胰岛素抵抗和胰岛素敏感性的独立预测因子,在训练前(部分 R=0.10 和 0.22),尽管 A/L 不能预测干预前后的胰岛素 AUC。训练引起的 A/L 变化与胰岛素敏感性呈显著相关(r=0.38;p<0.05),但与胰岛素抵抗或胰岛素 AUC 无关。尽管脂联素/瘦素比值的变化不能解释训练后葡萄糖-胰岛素稳态指数的改善,但在肥胖的健康女性中发现了与胰岛素敏感性的关系。