Department of Internal Medicine, Maastricht University Medical Center, Maastricht, the Netherlands; School for Cardiovascular Diseases (CARIM), Maastricht, the Netherlands; Top Institute of Food and Nutrition (TIFN), Wageningen, the Netherlands.
Department of Internal Medicine, Maastricht University Medical Center, Maastricht, the Netherlands; School for Cardiovascular Diseases (CARIM), Maastricht, the Netherlands.
Clin Nutr. 2021 May;40(5):2654-2662. doi: 10.1016/j.clnu.2021.03.042. Epub 2021 Apr 15.
Dicarbonyl compounds contribute to the formation of advanced glycation endproducts (AGEs) and the development of insulin resistance and vascular complications. Dicarbonyl stress may already be detrimental in obesity. We evaluated whether diet-induced weight loss can effectively reverse dicarbonyl stress in abdominally obese men.
Plasma samples were collected from lean (n = 25) and abdominally obese men (n = 52) in the fasting state, and during a mixed meal test (MMT). Abdominally obese men were randomized to 8 weeks of dietary weight loss or habitual diet, followed by a second MMT. The α-dicarbonyls methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG) and AGEs were measured by UPLC-MS/MS. Skin autofluorescence (SAF) was measured using the AGE reader. T-tests were used for the cross-sectional analysis and ANCOVA to assess the treatment effect.
Postprandial glucose, MGO and 3-DG concentrations were higher in obese men as compared to lean men (p < 0.05 for all). Fasting dicarbonyls, AGEs, and SAF were not different between lean and obese men. After the weight loss intervention, fasting MGO levels tended to decrease by 25 nmol/L (95%-CI: -51-0.5; p = 0.054). Postprandial dicarbonyls were decreased after weight loss as compared to the control group: iAUC of MGO decreased by 57% (5280 nmol/L∙min; 95%-CI: 33-10526; p = 0.049), of GO by 66% (11,329 nmol/L∙min; 95%-CI: 495-22162; p = 0.041), and of 3-DG by 45% (20,175 nmol/L∙min; 95%-CI: 5351-35000; p = 0.009). AGEs and SAF did not change significantly after weight loss.
Abdominal obesity is characterized by increased postprandial dicarbonyl stress, which can be reduced by a weight loss intervention. Registered under ClinicalTrials.gov Identifier no. NCT01675401.
二羰基化合物有助于形成晚期糖基化终末产物（AGEs）和胰岛素抵抗以及血管并发症的发展。二羰基应激在肥胖中可能已经有害。我们评估了饮食诱导的体重减轻是否可以有效逆转腹部肥胖男性的二羰基应激。
空腹时从瘦（n=25）和腹部肥胖男性（n=52）中采集血浆样本，并在混合餐测试（MMT）期间进行采集。腹部肥胖男性随机分为 8 周饮食减肥或习惯性饮食，然后进行第二次 MMT。通过 UPLC-MS/MS 测量α-二羰基物甲基乙二醛（MGO）、乙二醛（GO）和 3-脱氧葡萄糖（3-DG）和 AGEs。使用 AGE 读取器测量皮肤自发荧光（SAF）。使用 t 检验进行横截面分析，使用 ANCOVA 评估治疗效果。
与瘦男性相比，肥胖男性的餐后血糖、MGO 和 3-DG 浓度更高（所有 p<0.05）。空腹二羰基物、AGEs 和 SAF 在瘦男性和肥胖男性之间没有差异。减肥干预后，空腹 MGO 水平下降了 25nmol/L（95%CI：-51-0.5；p=0.054）。与对照组相比，减肥后餐后二羰基物减少：MGO 的 iAUC 降低了 57%（5280nmol/L·min；95%CI：33-10526；p=0.049），GO 降低了 66%（11329nmol/L·min；95%CI：495-22162；p=0.041），3-DG 降低了 45%（20175nmol/L·min；95%CI：5351-35000；p=0.009）。减肥后 AGEs 和 SAF 没有明显变化。
腹部肥胖的特点是餐后二羰基应激增加，体重减轻干预可以降低二羰基应激。在 ClinicalTrials.gov 标识符下注册 NCT01675401。
