한빛사논문
- 조회384
Kangjin Kim 1, Sanghun Lee 2, Sang-Chul Park 3, Nam-Eun Kim 1, Chol Shin 4 5, Seung Ku Lee 5, Youngae Jung 6, Dankyu Yoon 7, Hyeonjeong Kim 8, Sanghyun Kim 8, Geum-Sook Hwang 9, Sungho Won 10 11 12
1Department of Public Health Science, Graduate School of Public Health, Seoul National University, Seoul, South Korea.
2Department of Medical Consilience, Graduate School, Dankook University, Seoul, South Korea.
3Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
4Division of Pulmonary Sleep and Critical Care Medicine, Department of Internal Medicine, Korea University Ansan Hospital, Ansan, South Korea.
5Institute of Human Genomic Study, College of Medicine, Korea University Ansan Hospital, Ansan, South Korea.
6Integrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, South Korea.
7Division of Allergy and Chronic Respiratory Diseases, Center for Biomedical Sciences, National Institute of Health, Korea Center for Diseases Control and Prevention, Osong, Cheongju, South Korea.
8Korea Medical Institute, Seoul, South Korea.
9Integrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, South Korea.
10Department of Public Health Science, Graduate School of Public Health, Seoul National University, Seoul, South Korea.
11Interdisciplinary Program for Bioinformatics, College of Natural Science, Seoul National University, Seoul, South Korea.
12Institute of Health and Environment, Seoul National University, Seoul, South Korea.
Corresponding authors
Correspondence to Geum-Sook Hwang or Sungho Won.
Abstract
Recent investigations have revealed that the human microbiome plays an essential role in the occurrence of type 2 diabetes (T2D). However, despite the importance of understanding the involvement of the microbiota throughout the body in T2D, most studies have focused specifically on the intestinal microbiota. Extracellular vesicles (EVs) have been recently found to provide important evidence regarding the mechanisms of T2D pathogenesis, as they act as key messengers between intestinal microorganisms and the host. Herein, we explored microorganisms potentially associated with T2D by tracking changes in microbiota-derived EVs from patient urine samples collected three times over four years. Mendelian randomization analysis was conducted to evaluate the causal relationships among microbial organisms, metabolites, and clinical measurements to provide a comprehensive view of how microbiota can influence T2D. We also analyzed EV-derived metagenomic (N = 393), clinical (N = 5032), genomic (N = 8842), and metabolite (N = 574) data from a prospective longitudinal Korean community-based cohort. Our data revealed that GU174097_g, an unclassified Lachnospiraceae, was associated with T2D (β = −189.13; p = 0.00006), and it was associated with the ketone bodies acetoacetate and 3-hydroxybutyrate (r = −0.0938 and −0.0829, respectively; p = 0.0022 and 0.0069, respectively). Furthermore, a causal relationship was identified between acetoacetate and HbA1c levels (β = 0.0002; p = 0.0154). GU174097_g reduced ketone body levels, thus decreasing HbA1c levels and the risk of T2D. Taken together, our findings indicate that GU174097_g may lower the risk of T2D by reducing ketone body levels.
논문정보
- Research article
- 2022년 08월 (BRIC 등록일 2022-10-18)
- 국내(교신)+국외 연구진
- 의약학 > 유전 및 유전체의학
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