Li Xiaoxia, Zhao Yi, Jin Yanan, Zhang Tianjing, Chang Xiaoyu, Liao Sha, Xu Hongxia, Liu Xiuying, Yang Jianjun, Zhang Jianjun, Zhang Yuhong
Department of Epidemiology, School of Public Health and Management, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, People's Republic of China.
Ningxia Center for Disease Control and Prevention, Yinchuan, Ningxia Hui Autonomous Region, People's Republic of China.
PLoS One. 2017 Aug 7;12(8):e0182273. doi: 10.1371/journal.pone.0182273. eCollection 2017.
Although experimental studies have shown that adiponectin and leptin modulate glucose tolerance and insulin resistance, it remains unclear whether these adipocytokines exert similar effects in general human populations. We evaluated the associations of serum adiponectin and leptin with β-cell function and insulin resistance in a population with low obesity prevalence. A cross-sectional study of 783 rural residents, aged 25-74 years, recruited in Ningxia, China was conducted during 2008-2012. β-cell function and insulin resistance were estimated using the Homeostasis Model Assessment. Serum adiponectin and leptin were measured with ELISA. Serum adiponectin concentrations (mean ± SD) were highest in subjects with normal glucose tolerance (36.65 ± 61.13 μg/ml), intermediate in those with impaired fasting glucose (25.92 ± 34.48 μg/ml), and lowest in those with diabetes (15.08 ± 12.14 μg/ml) (p = 0.001). A similar pattern of differences was found for β-cell function, whereas opposite results were observed for insulin resistance and blood glucose. After adjustment for confounders including metabolic syndrome components, serum adiponectin (μg/ml) was inversely associated with β-cell function (%β) [β (95% CI): -7.57 (-12.33, -2.81)] and insulin resistance (100/%S) [β (95% CI): -0.21 (-0.33, -0.09)]. A significant inverse association also existed between serum leptin and β-cell function, but serum leptin was not significantly associated with insulin resistance. The present study suggests that adiponectin and leptin play a role in the development of insulin resistance and diabetes independent of metabolic syndrome.
尽管实验研究表明脂联素和瘦素可调节葡萄糖耐量和胰岛素抵抗，但这些脂肪细胞因子在一般人群中是否发挥类似作用仍不清楚。我们在肥胖患病率较低的人群中评估了血清脂联素和瘦素与β细胞功能及胰岛素抵抗之间的关联。2008年至2012年期间，对中国宁夏招募的783名年龄在25至74岁的农村居民进行了一项横断面研究。使用稳态模型评估法估算β细胞功能和胰岛素抵抗。采用酶联免疫吸附测定法测量血清脂联素和瘦素。血清脂联素浓度（均值±标准差）在糖耐量正常的受试者中最高（36.65±61.13μg/ml），在空腹血糖受损者中居中（25.92±34.48μg/ml），在糖尿病患者中最低（15.08±12.14μg/ml）（p = 0.001）。β细胞功能也发现了类似的差异模式，而胰岛素抵抗和血糖则观察到相反的结果。在对包括代谢综合征组分在内的混杂因素进行调整后，血清脂联素（μg/ml）与β细胞功能（%β）呈负相关[β（95%可信区间）：-7.57（-12.33，-2.81）]以及与胰岛素抵抗（100/%S）呈负相关[β（95%可信区间）：-0.21（-0.33，-0.09）]。血清瘦素与β细胞功能之间也存在显著的负相关，但血清瘦素与胰岛素抵抗无显著关联。本研究表明，脂联素和瘦素在胰岛素抵抗和糖尿病的发生发展中发挥作用，独立于代谢综合征。
