| Literature DB >> 35998626 |
Shuangyuan Wang1, Mian Li1, Hong Lin1, Guixia Wang2, Yu Xu1, Xinjie Zhao3, Chunyan Hu1, Yi Zhang1, Ruizhi Zheng1, Ruying Hu4, Lixin Shi5, Rui Du1, Qing Su6, Jiqiu Wang1, Yuhong Chen1, Xuefeng Yu7, Li Yan8, Tiange Wang1, Zhiyun Zhao1, Ruixin Liu1, Xiaolin Wang3, Qi Li3, Guijun Qin9, Qin Wan10, Gang Chen11, Min Xu1, Meng Dai1, Di Zhang1, Xulei Tang12, Zhengnan Gao13, Feixia Shen14, Zuojie Luo15, Yingfen Qin15, Li Chen16, Yanan Huo17, Qiang Li18, Zhen Ye4, Yinfei Zhang19, Chao Liu20, Youmin Wang21, Shengli Wu22, Tao Yang23, Huacong Deng24, Jiajun Zhao25, Shenghan Lai26, Yiming Mu27, Lulu Chen28, Donghui Li29, Guowang Xu3, Guang Ning30, Weiqing Wang31, Yufang Bi32, Jieli Lu33.
Abstract
Although previous studies suggest that amino acids (AAs) and microbiota-related metabolites (MRMs) are associated with type 2 diabetes mellitus (T2DM), the results remain unclear among normoglycemic populations. We test 28 serum AAs and 22 MRMs in 3,414 subjects with incident diabetes and matched normoglycemic controls from the China Cardiometabolic Disease and Cancer Cohort (4C) Study. In fully adjusted logistic regression models, per SD increment of branched-chain AAs, aromatic AAs, asparagine, alanine, glutamic acid, homoserine, 2-aminoadipic acid, histidine, methionine, and proline are positively associated with incident T2DM. In the MRM panel, serum carnitines, N-acetyltryptophan, and uric acid are positively associated with incident T2DM. Causal mediation analyses indicate 34 significant causal mediation linkages, with 88.2% through obesity and lipids. Variances explained in the serum metabolites are modestly limited in the comprehensive catalog of risk factor-metabolite-diabetes associations. These findings reveal that systematic AAs and MRMs change profile before T2DM onset and support a potential role of metabolic alterations in the pathogenesis of diabetes.Entities:
Keywords: amino acid; diabetes; mediation; microbiota-related metabolites; risk factor
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Year: 2022 PMID: 35998626 PMCID: PMC9512668 DOI: 10.1016/j.xcrm.2022.100727
Source DB: PubMed Journal: Cell Rep Med ISSN: 2666-3791