Department of Pediatrics, Ruth Children's Hospital, Rambam Medical Center, Haifa 3109601, Israel.
Department of Women and Child Health, University of Padova, Via Giustiniani, 3, 35128 Padova, Italy.
J Clin Endocrinol Metab. 2023 Apr 13;108(5):1053-1060. doi: 10.1210/clinem/dgac700.
The "carbohydrate-insulin model" claims that adipose tissue insulin sensitivity explains development of obesity via adipocyte energy storage and/or low postprandial metabolic fuel levels.
We tested whether adipose tissue insulin sensitivity predicts changes in the degree of obesity over time.
This secondary analysis of an observational study of youth with obesity included 213 youths at a pediatric weight management clinic. Adipose tissue insulin sensitivity/resistance and whole-body insulin sensitivity were evaluated using oral glucose tolerance test (OGTT)-derived surrogates in the face of changes in the degree of obesity over time. The main outcome measure was change in body mass index (BMI) z score.
Mean BMI z change was 0.05 ± 0.28 (range, -1.15 to 1.19), representing a broad distribution of changes in the degree of obesity over a follow-up period of 1.88 ± 1.27 years. Adipose tissue insulin resistance was not associated with changes in the degree of obesity in univariate or multivariate analyses (adjusted for baseline age, BMI z score, sex, ethnicity, and time of follow-up). Low postprandial free fatty acid concentrations or their suppression during the OGTT were not associated with changes in the degree of obesity in univariate or multivariate analyses. Whole-body insulin sensitivity was not associated with changes in the degree of obesity in univariate or multivariate analyses.
In this secondary analysis, in youth with obesity, adipose tissue insulin resistance is not protective from increases of the degree of obesity and skeletal muscle insulin resistance is not associated with increases of the degree of obesity.The analysis was performed using data derived from NCT00000112 and NCT00536250.
“碳水化合物-胰岛素模型”声称，脂肪组织胰岛素敏感性通过脂肪细胞能量储存和/或餐后代谢燃料水平低来解释肥胖的发展。
我们测试了脂肪组织胰岛素敏感性是否可以预测肥胖程度随时间的变化。
这项对肥胖青少年进行的观察性研究的二次分析包括了 213 名在儿科体重管理诊所的肥胖青少年。在随时间肥胖程度变化的情况下，使用口服葡萄糖耐量试验（OGTT）衍生的替代物评估脂肪组织胰岛素敏感性/抵抗和全身胰岛素敏感性。主要观察指标是体重指数（BMI）z 评分的变化。
平均 BMI z 变化为 0.05±0.28（范围，-1.15 至 1.19），代表肥胖程度随 1.88±1.27 年随访期的广泛变化。在单变量或多变量分析中，脂肪组织胰岛素抵抗与肥胖程度的变化无关（调整基线年龄、BMI z 评分、性别、种族和随访时间）。OGTT 期间餐后游离脂肪酸浓度低或其抑制与肥胖程度的变化无关。单变量或多变量分析中，全身胰岛素敏感性与肥胖程度的变化无关。
在这项二次分析中，在肥胖青少年中，脂肪组织胰岛素抵抗不能预防肥胖程度的增加，而骨骼肌胰岛素抵抗与肥胖程度的增加无关。该分析使用了源自 NCT00000112 和 NCT00536250 的数据。
