Ma Chifa, Liu Yiwen, He Shuli, Zeng Jingbo, Li Pingping, Ma Chunxiao, Ping Fan, Zhang Huabing, Xu Lingling, Li Wei, Li Yuxiu
Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Department of Nutrition, Peking Union Medical College Hospital, Beijing, China.
Ann Transl Med. 2021 Feb;9(4):327. doi: 10.21037/atm-20-6119.
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 β-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.
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-α (TNF-α) and interleukin-6 (IL-6), and oxidative stress markers superoxide dismutase (SOD), and 8-oxo-2'-deoxyguanosine (8-oxo-dG) were measured. Islet β-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.
Individuals in the middle and highest tertile of GF had reduced β-cell function, and increased plasma SOD and TNF-α 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-α, 8-oxo-dG and SOD levels, but negatively associated with β-cell function, whereas IL-6, TNF-α, 8-oxo-dG and SOD levels were negatively associated with β-cell function (P<0.05).
GF may increase inflammation and oxidative stress markers in individuals with NGT, which could contribute to reduced β-cell function. Thus, maintaining glucose stability after a meal may have beneficial effects on delaying β-cell dysfunction, suggesting that diet and exercise strategies to decrease diet related GF are warranted.
血糖波动(GF)可能对糖尿病患者产生有害影响;然而,基于糖耐量正常(NGT)人群,关于短期血糖波动、炎症/氧化应激标志物与胰岛β细胞功能之间关联的临床数据并不充分。因此,我们旨在通过横断面分析,在中国209例糖耐量正常的人群中探究这些关联。
根据2小时口服葡萄糖耐量试验(OGTT)期间四个时间点(0、30、60、120分钟)的最大-最小血糖水平计算血糖波动三分位数,将个体进行分类。检测血浆炎症标志物肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6),以及氧化应激标志物超氧化物歧化酶(SOD)和8-氧代-2'-脱氧鸟苷(8-氧代-dG)。根据OGTT早期(30分钟)和总阶段(120分钟)的处置指数(DI)评估胰岛β细胞功能,并根据胰岛素敏感性进行调整。
与血糖波动最低三分位数的个体相比,血糖波动处于中间和最高三分位数的个体β细胞功能降低,血浆SOD和TNF-α水平升高(P<0.05)。多元线性回归分析表明,血糖波动与TNF-α、8-氧代-dG和SOD水平呈正相关,但与β细胞功能呈负相关,而IL-6、TNF-α、8-氧代-dG和SOD水平与β细胞功能呈负相关(P<0.05)。
血糖波动可能会增加糖耐量正常个体的炎症和氧化应激标志物水平,这可能导致β细胞功能降低。因此,餐后维持血糖稳定可能对延缓β细胞功能障碍具有有益作用,这表明有必要采取饮食和运动策略来减少与饮食相关的血糖波动。