Liu Wei, Zhou Xianghai, Li Yufeng, Zhang Simin, Cai Xiaoling, Zhang Rui, Gong Siqian, Han Xueyao, Ji Linong
Department of Endocrinology and Metabolism, Peking University People's Hospital.
Department of Endocrinology and Metabolism, Pinggu Hospital, Beijing, China.
Medicine (Baltimore). 2020 Feb;99(6):e19052. doi: 10.1097/MD.0000000000019052.
Disturbances in adipocytokine profiles can contribute to peripheral insulin resistance and impairment of insulin production, which are 2 primary pathophysiological mechanisms involved in type 2 diabetes mellitus (T2DM). Previous studies of disturbed adipocytokine profiles have resulted in ambiguous findings; therefore, we conducted the current study comparing leptin, resistin, and adiponectin concentrations in patients with newly diagnosed T2DM who had normal body mass index (BMI) and those who were obese.We studied a population-based cohort of healthy participants and those with newly diagnosed T2DM. A normal BMI group was randomly selected; age- and sex-matched obese participants were recruited. Circulating leptin, resistin, and adiponectin concentrations were measured and compared between groups using analysis of variance; binary logistic regression analysis was then performed to compare the normal BMI and obese groups.In total, 85 healthy participants and 38 patients with diabetes (19 with normal BMI and 17 who were obese) were enrolled. After adjustment for BMI and waist circumference, the median leptin concentration was higher in the obese group (6.77 (3.89-10.73) ng/mL) than in the normal BMI group (1.69 (0.80-3.89) ng/mL) (P = .007), whereas the median adiponectin concentration was lower in the obese group (1.03 (0.75-2.36) μg/mL vs 3.36 (0.59-7.63) μg/mL, P = .03). In addition, the adiponectin/leptin ratio was higher in the normal BMI group (145.6 (41.3-495.9) ng/mL) than in the obese group (20.55 (8.74-36.94) ng/mL, P = .002).Compared with the normal BMI T2DM group, the obese T2DM group exhibited a disturbed adipocytokine profile in the form of a significantly increased leptin concentration and reduced adiponectin level. Further studies are needed to determine the causal relationship for this difference and evaluate its importance for personalized diabetic treatment.
脂肪细胞因子谱的紊乱可导致外周胰岛素抵抗和胰岛素分泌受损,这是2型糖尿病(T2DM)涉及的两个主要病理生理机制。先前关于脂肪细胞因子谱紊乱的研究结果并不明确;因此,我们开展了本研究,比较体重指数(BMI)正常的新诊断T2DM患者与肥胖患者的瘦素、抵抗素和脂联素浓度。我们研究了一个基于人群的健康参与者队列以及新诊断的T2DM患者。随机选择一个BMI正常组;招募年龄和性别匹配的肥胖参与者。测量循环中的瘦素、抵抗素和脂联素浓度,并使用方差分析比较组间差异;然后进行二元逻辑回归分析以比较BMI正常组和肥胖组。总共纳入了85名健康参与者和38例糖尿病患者(19例BMI正常,17例肥胖)。在调整BMI和腰围后,肥胖组的瘦素浓度中位数(6.77(3.89 - 10.73)ng/mL)高于BMI正常组(1.69(0.80 - 3.89)ng/mL)(P = 0.007),而肥胖组的脂联素浓度中位数较低(1.03(0.75 - 2.36)μg/mL对3.36(0.59 - 7.63)μg/mL,P = 0.03)。此外,BMI正常组的脂联素/瘦素比值(145.6(41.3 - 495.9)ng/mL)高于肥胖组(20.55(8.74 - 36.94)ng/mL,P = 0.002)。与BMI正常的T2DM组相比,肥胖的T2DM组呈现出脂肪细胞因子谱紊乱,表现为瘦素浓度显著升高和脂联素水平降低。需要进一步研究以确定这种差异的因果关系,并评估其对个性化糖尿病治疗的重要性。