期刊
ANNALS OF TRANSLATIONAL MEDICINE
卷 9, 期 4, 页码 -出版社
AME PUBL CO
DOI: 10.21037/atm-20-6119
关键词
beta-cell function; glucose fluctuation; inflammation; oxidative stress
资金
- CAMS Innovation Fund for Medical Sciences (CIFMS) [CIFMS2016-I2M-4-001]
- Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences [2017PT32020, 2018PT32001, 2019PT320007]
Research on individuals with normal glucose tolerance has shown that glucose fluctuation may increase inflammation and oxidative stress markers, leading to a decrease in islet beta-cell function.
Backgrounds: Glucose fluctuation (GF) may have detrimental effects in individuals with diabetes; however, clinical data on the association between short-term GF, inflammation/oxidative stress markers, and islet beta-cell function based on a population with normal glucose tolerance (NGT) are insufficient. Therefore, we aimed to explore these associations in a Chinese population of 209 individuals with NGT in a cross-sectional analysis. Methods: Individuals were categorized based on GF tertiles, calculated as the maximum-minimum glucose levels among four time points (0, 30, 60, 120 min) during 2-hour oral glucose tolerance test (OGTT). Plasma inflammation markers tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and oxidative stress markers superoxide dismutase (SOD), and 8-oxo-2'-deoxyguanosine (8-oxo-dG) were measured. Islet beta-cell function was estimated according to the disposition index (DI) at the early (30 min) and total (120 min) phase of the OGTT, adjusted for insulin sensitivity. Results: Individuals in the middle and highest tertile of GF had reduced beta-cell function, and increased plasma SOD and TNF-alpha levels compared with those in the lowest tertile of GF (P<0.05). Multiple linear regression analysis indicated that GF was positively associated with TNF-alpha, 8-oxo-dG and SOD levels, but negatively associated with beta-cell function, whereas IL-6, TNF-alpha, 8-oxo-dG and SOD levels were negatively associated with beta-cell function (P<0.05). Conclusions: GF may increase inflammation and oxidative stress markers in individuals with NGT, which could contribute to reduced beta-cell function. Thus, maintaining glucose stability after a meal may have beneficial effects on delaying beta-cell dysfunction, suggesting that diet and exercise strategies to decrease diet related GF are warranted.
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