USDA Agricultural Research Service, Nutrition and Genomics Laboratory, JM-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
Department of Biomedical and Nutritional Sciences, University of Massachusetts Lowell, Lowell, MA, USA.
Metabolomics. 2021 Sep 22;17(10):88. doi: 10.1007/s11306-021-01835-x.
Obesity is a precursor of type 2 diabetes (T2D).
Our aim was to identify metabolic signatures of T2D and dietary factors unique to obesity.
We examined a subsample of the Boston Puerto Rican Health Study (BPRHS) population with a high prevalence of obesity and T2D at baseline (n = 806) and participants (without T2D at baseline) at 5-year follow-up (n = 412). We determined differences in metabolite profiles between T2D and non-T2D participants of the whole sample and according to abdominal obesity status. Enrichment analysis was performed to identify metabolic pathways that were over-represented by metabolites that differed between T2D and non-T2D participants. T2D-associated metabolites unique to obesity were examined for correlation with dietary food groups to understand metabolic links between dietary intake and T2D risk. False Discovery Rate method was used to correct for multiple testing.
Of 526 targeted metabolites, 179 differed between T2D and non-T2D in the whole sample, 64 in non-obese participants and 120 unique to participants with abdominal obesity. Twenty-four of 120 metabolites were replicated and were associated with T2D incidence at 5-year follow-up. Enrichment analysis pointed to three metabolic pathways that were overrepresented in obesity-associated T2D: phosphatidylethanolamine (PE), long-chain fatty acids, and glutamate metabolism. Elevated intakes of three food groups, energy-dense takeout food, dairy intake and sugar-sweetened beverages, associated with 13 metabolites represented by the three pathways.
Metabolic signatures of lipid and glutamate metabolism link obesity to T2D, in parallel with increased intake of dairy and sugar-sweetened beverages, thereby providing insight into the relationship between dietary habits and T2D risk.
肥胖是 2 型糖尿病(T2D)的前兆。
我们的目的是确定 T2D 的代谢特征和肥胖特有的饮食因素。
我们检查了基线时肥胖和 T2D 患病率较高的波士顿波多黎各健康研究(BPRHS)人群的亚样本(n=806)和 5 年随访时的参与者(基线时无 T2D,n=412)。我们根据整个样本和腹部肥胖状况,确定了 T2D 患者和非 T2D 患者之间代谢谱的差异。进行了富集分析,以确定代谢物之间存在差异的代谢途径。检查了肥胖特有的与 T2D 相关的代谢物与饮食食物组之间的相关性,以了解饮食摄入与 T2D 风险之间的代谢联系。使用错误发现率方法对多重检验进行了校正。
在 526 种靶向代谢物中,179 种在整个样本中 T2D 患者和非 T2D 患者之间存在差异,64 种在非肥胖患者中存在差异,120 种在腹部肥胖患者中存在差异。24 种代谢物中的 120 种被复制,并与 5 年随访时的 T2D 发病率相关。富集分析指出,三个代谢途径在肥胖相关的 T2D 中被过度代表:磷脂酰乙醇胺(PE)、长链脂肪酸和谷氨酸代谢。三种途径所代表的三种食物组的摄入量增加,包括能量密集型外卖食品、乳制品摄入和含糖饮料,与 13 种代谢物相关。
脂质和谷氨酸代谢的代谢特征将肥胖与 T2D 联系起来,同时增加了乳制品和含糖饮料的摄入,从而深入了解饮食习惯与 T2D 风险之间的关系。