预测复杂生活方式干预代谢无应答的因素——一项对随机对照试验的复制分析。
Predicting Factors for Metabolic Non-Response to a Complex Lifestyle Intervention-A Replication Analysis to a Randomized-Controlled Trial.
机构信息
Department of Endocrinology and Metabolic Medicine, Campus Benjamin Franklin, Charité University Medicine, Hindenburgdamm 30, 12203 Berlin, Germany.
Deutsches Zentrum für Diabetesforschung e.V., Geschäftsstelle am Helmholtz-Zentrum München, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
出版信息
Nutrients. 2022 Nov 9;14(22):4721. doi: 10.3390/nu14224721.
BACKGROUND
T2DM heterogeneity affects responsiveness to lifestyle treatment. Beta-cell failure and nonalcoholic fatty liver disease (NAFLD) independently predict T2DM, but NAFLD inconsistently predicts metabolic response to lifestyle intervention.
AIM
We attempt to replicate a prediction model deducted from the Tübinger Lifestyle Intervention Program by assessing similar metabolic factors to predict conversion to normal glucose regulation (NGR) in a comparable lifestyle intervention trial.
METHODS
In the Optimal Fiber Trial (OptiFiT), 131 Caucasian participants with prediabetes completed a one-year lifestyle intervention program and received a fiber or placebo supplement. We compared baseline parameters for responders and non-responders, assessed correlations of major metabolic changes and conducted a logistic regression analysis for predictors of remission to NGR.
RESULTS
NGR was achieved by 33 participants, respectively. At baseline, for the placebo group only, 1 h and 2 h glucose levels, glucose AUC and Cederholm index predicted conversion to NGR. HOMA-beta, HOMA-IR or liver fat indices did not differ between responders and non-responders of the placebo or the fiber group. Changes in waist circumference or fatty liver index correlated with changes in glycemia and insulin resistance, but not with changes in insulin secretion. Insulin-resistant NAFLD did not predict non-response. Differences in compliance did not explain the results.
CONCLUSIONS
Higher post-challenge glucose levels strongly predicted the metabolic non-response to complex lifestyle intervention in our cohort. Depending on the specific intervention and the investigated cohort, fasting glucose levels and insulin sensitivity might contribute to the risk pattern. Beta-cell function did not improve in accordance with other metabolic improvements, qualifying as a potential risk factor for non-response. We could not replicate previous data suggesting that an insulin-resistant fatty liver is a specific risk factor for treatment failure. Replication studies are required.
背景
2 型糖尿病（T2DM）异质性影响生活方式治疗的反应性。β细胞衰竭和非酒精性脂肪性肝病（NAFLD）独立预测 T2DM，但 NAFLD 对生活方式干预的代谢反应预测不一致。
目的
我们尝试通过评估类似的代谢因素来复制从图宾根生活方式干预计划中推导出来的预测模型，以预测类似的生活方式干预试验中向正常血糖调节（NGR）的转变。
方法
在 Optimal Fiber Trial（OptiFiT）中，131 名白种人前驱糖尿病患者完成了为期一年的生活方式干预计划，并接受了纤维或安慰剂补充剂。我们比较了应答者和无应答者的基线参数，评估了主要代谢变化的相关性，并进行了逻辑回归分析，以预测向 NGR 的缓解。
结果
分别有 33 名参与者达到了 NGR。在基线时，仅对于安慰剂组，1 小时和 2 小时血糖、血糖 AUC 和 Cederholm 指数预测了向 NGR 的转变。对于安慰剂或纤维组的应答者和无应答者，HOMA-β、HOMA-IR 或肝脂肪指数没有差异。腰围或脂肪肝指数的变化与血糖和胰岛素抵抗的变化相关，但与胰岛素分泌的变化无关。胰岛素抵抗性 NAFLD 不能预测无反应。依从性的差异不能解释结果。
结论
在我们的队列中，更高的餐后血糖水平强烈预测了对复杂生活方式干预的代谢无反应。根据具体的干预措施和研究队列，空腹血糖水平和胰岛素敏感性可能有助于风险模式。β细胞功能没有随着其他代谢改善而改善，这是无反应的潜在危险因素。我们无法复制先前的数据，表明胰岛素抵抗性脂肪肝是治疗失败的特定危险因素。需要进行复制研究。
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