한빛사논문
- 조회798
서울대학교병원
Hyunsuk Lee 1,2,3, Jaewon Choi 4,5, Jong-Il Kim 3,5, Richard M Watanabe 6,7, Nam H Cho 8, Kyong Soo Park 1,9,10, Soo Heon Kwak 1,9
1Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
2Department of Translational Medicine, Seoul National University College of Medicine, Seoul, Korea.
3Genomic Medicine Institute, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea.
4Division of Data Science Research, Innovative Biomedical Technology Research Institute, Seoul National University Hospital, Seoul, Korea.
5Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
6Departments of Population and Public Health Sciences and Physiology and Neuroscience, Keck School of Medicine of USC, Los Angeles, CA.
7USC Diabetes and Obesity Research Institute, Keck School of Medicine of USC, Los Angeles, CA.
8Department of Preventive Medicine, Ajou University School of Medicine, Suwon, Korea.
9Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
10Department of Genomic Medicine, Seoul National University Hospital, Seoul, Korea.
Corresponding author: Soo Heon Kwak
Abstract
Objective: While most genetic variants of type 2 diabetes (T2D) are suggested to be associated with β-cell dysfunction cross sectionally, their association with the longitudinal change of β-cell function remains largely unknown.
Research design and methods: We analyzed data from 6,311 participants without T2D at baseline (mean [SD] age 51.6 [8.7] years) from a community-based prospective cohort in Korea. Participants underwent biennial 2-h 75-g oral glucose tolerance tests (OGTTs) during 14 years of follow-up, and the OGTT-derived disposition index (DI) was used as a marker for β-cell function. Genetic risk was quantified using the genome-wide polygenic risk score (PRS) and was stratified into low (1st quintile), intermediate (2nd-4th quintiles), and high (5th quintile) genetic risk. Lifestyle was assessed according to Life's Essential 8.
Results: During a mean follow-up of 10.9 years, 374 (29.6%), 851 (22.5%), and 188 (14.9%) participants developed T2D in the high, intermediate, and low genetic risk groups, respectively. Compared with the low genetic risk group, participants in the high genetic risk group had a 25% lower DI at baseline. Furthermore, in longitudinal analysis, we observed a 1.83-fold faster decline in log2-transformed DI per year (-0.034 vs. -0.019, P = 2.1 × 10-3; per 1-SD increase in T2D PRS, P = 1.2 × 10-4). Healthy lifestyle attenuated the rate of decline in DI across all genetic risk groups.
Conclusions: Individuals with a higher genetic risk for T2D exhibited not only a lower OGTT-derived β-cell function at baseline but also a notably more rapid decline during follow-up. This information could be used to enable a focused precision prevention with lifestyle intervention.
논문정보
- Research article
- 2024년 06월 (BRIC 등록일 2024-06-04)
- 국내(교신)+국외 연구진
- 의약학 > 유전 및 유전체의학
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