Université Clermont-Auvergne, INRAE, UMR1019, Unité Nutrition Humaine, Clermont-Ferrand, France.
UMR1331 Toxalim, Université de Toulouse, INRAE, ENVT, INP-Purpan, UPS, Toulouse, France.
J Physiol Biochem. 2023 May;79(2):397-413. doi: 10.1007/s13105-022-00940-2. Epub 2022 Dec 27.
Obesity is a major contributor to the silent and progressive development of type 2 diabetes (T2D) whose prevention could be improved if individuals at risk were identified earlier. Our aim is to identify early phenotypes that precede T2D in diet-induced obese minipigs. We fed four groups of minipigs (n = 5-10) either normal-fat or high-fat high-sugar diet during 2, 4, or 6 months. Morphometric features were recorded, and metabolomics and clinical parameters were assessed on fasting plasma samples. Multivariate statistical analysis on 46 morphometrical and clinical parameters allowed to differentiate 4 distinct phenotypes: NFC (control group) and three others (HF2M, HF4M, HF6M) corresponding to the different stages of the obesity progression. Compared to NFC, we observed a rapid progression of body weight and fat mass (4-, 7-, and tenfold) in obese phenotypes. Insulin resistance (IR; 2.5-fold increase of HOMA-IR) and mild dyslipidemia (1.2- and twofold increase in total cholesterol and HDL) were already present in the HF2M and remained stable in HF4M and HF6M. Plasma metabolome revealed subtle changes of 23 metabolites among the obese groups, including a progressive switch in energy metabolism from amino acids to lipids, and a transient increase in de novo lipogenesis and TCA-related metabolites in HF2M. Low anti-oxidative capacities and anti-inflammatory response metabolites were found in the HF4M, and a perturbed hexose metabolism was observed in HF6M. Overall, we show that IR and progressively obese minipigs reveal phenotype-specific metabolomic signatures for which some of the identified metabolites could be considered as potential biomarkers of early progression to TD2.
肥胖是 2 型糖尿病(T2D)无声且渐进发展的主要原因,如果能更早地识别出处于危险中的个体,那么 T2D 的预防就可以得到改善。我们的目的是确定在饮食诱导肥胖小型猪中先于 T2D 出现的早期表型。我们用正常脂肪或高脂肪高糖饮食喂养四组小型猪(n=5-10),喂养时间为 2、4 或 6 个月。记录形态计量学特征,并在禁食血浆样本上评估代谢组学和临床参数。对 46 个体形态计量学和临床参数进行多元统计分析,可将其分为 4 种不同的表型:NFC(对照组)和其他 3 种(HF2M、HF4M 和 HF6M),对应肥胖进展的不同阶段。与 NFC 相比,我们观察到肥胖表型的体重和脂肪量快速增加(分别增加 4、7 和 10 倍)。胰岛素抵抗(IR;HOMA-IR 增加 2.5 倍)和轻度血脂异常(总胆固醇和 HDL 分别增加 1.2 和 2 倍)在 HF2M 中已经存在,并在 HF4M 和 HF6M 中保持稳定。血浆代谢组学揭示了肥胖组中 23 种代谢物的细微变化,包括从氨基酸到脂质的能量代谢逐渐转变,以及在 HF2M 中新生脂肪生成和 TCA 相关代谢物的短暂增加。在 HF4M 中发现低抗氧化能力和抗炎反应代谢物,在 HF6M 中观察到己糖代谢紊乱。总的来说,我们表明胰岛素抵抗和逐渐肥胖的小型猪表现出特定表型的代谢组学特征,其中一些鉴定出的代谢物可以被认为是早期进展为 TD2 的潜在生物标志物。