Division of Medicine, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
PLoS One. 2013 Aug 30;8(8):e74215. doi: 10.1371/journal.pone.0074215. eCollection 2013.
Adiponectin is an adipose tissue derived hormone which strengthens insulin sensitivity. However, there is little data available regarding the influence of a positive energy challenge (PEC) on circulating adiponectin and the role of obesity status on this response.
The purpose of this study was to investigate how circulating adiponectin will respond to a short-term PEC and whether or not this response will differ among normal-weight(NW), overweight(OW) and obese(OB).
We examined adiponectin among 64 young men (19-29 yr) before and after a 7-day overfeeding (70% above normal energy requirements). The relationship between adiponectin and obesity related phenotypes including; weight, percent body fat (%BF), percent trunk fat (%TF), percent android fat (%AF), body mass index (BMI), total cholesterol, HDLc, LDLc, glucose, insulin, homeostatic model assessment insulin resistance (HOMA-IR) and β-cell function (HOMA-β) were analyzed before and after overfeeding.
Analysis of variance (ANOVA) and partial correlations were used to compute the effect of overfeeding on adiponectin and its association with adiposity measurements, respectively. Circulating Adiponectin levels significantly increased after the 7-day overfeeding in all three adiposity groups. Moreover, adiponectin at baseline was not significantly different among NW, OW and OB subjects defined by either %BF or BMI. Baseline adiponectin was negatively correlated with weight and BMI for the entire cohort and %TF, glucose, insulin and HOMA-IR in OB. However, after controlling for insulin resistance the correlation of adiponectin with weight, BMI and %TF were nullified.
Our study provides evidence that the protective response of adiponectin is preserved during a PEC regardless of adiposity. Baseline adiponectin level is not directly associated with obesity status and weight gain in response to short-term overfeeding. However, the significant increase of adiponectin in response to overfeeding indicates the physiological potential for adiponectin to attenuate insulin resistance during the development of obesity.
脂联素是一种源自脂肪组织的激素，可增强胰岛素敏感性。然而，关于正能挑战（PEC）对循环脂联素的影响，以及肥胖状态对此反应的作用，数据很少。
本研究旨在探讨短期 PEC 对循环脂联素的影响，以及正常体重（NW）、超重（OW）和肥胖（OB）人群对此反应是否存在差异。
我们在 64 名年轻男性（19-29 岁）进行了为期 7 天的过度喂养（高于正常能量需求的 70%）前后检查了脂联素。在过度喂养前后，分析了脂联素与肥胖相关表型之间的关系，包括体重、体脂肪百分比（%BF）、躯干脂肪百分比（%TF）、躯干脂肪百分比（%AF）、体重指数（BMI）、总胆固醇、高密度脂蛋白胆固醇（HDLc）、低密度脂蛋白胆固醇（LDLc）、血糖、胰岛素、稳态模型评估胰岛素抵抗（HOMA-IR）和β细胞功能（HOMA-β）。
方差分析（ANOVA）和偏相关分析分别用于计算过度喂养对脂联素的影响及其与肥胖测量指标的相关性。在所有三个肥胖组中，经过 7 天的过度喂养后，循环脂联素水平显著升高。此外，根据%BF 或 BMI 定义的 NW、OW 和 OB 三组之间，基线脂联素水平无显著差异。整个队列中，基线脂联素与体重和 BMI 呈负相关，与 OB 中的%TF、葡萄糖、胰岛素和 HOMA-IR 呈负相关。然而，在控制胰岛素抵抗后，脂联素与体重、BMI 和%TF 的相关性被消除。
我们的研究提供了证据，表明在 PEC 期间，脂联素的保护反应不受肥胖的影响。基线脂联素水平与肥胖状态和短期过度喂养后的体重增加没有直接关系。然而，脂联素在过度喂养后的显著增加表明，脂联素在肥胖发展过程中具有减轻胰岛素抵抗的生理潜力。
