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目的了解初诊断2型糖尿病患者血清内脂素、瘦素水平变化,探讨内脂素与各项代谢指标之间的相关性。方法选取新诊断或患病时间短的2型糖尿病者(n=57)与健康人群(n=61例)进行对比,根据BMI分为超重亚组和正常体重亚组,检测内脂素和瘦素水平,并检测胰岛素、血糖、糖化血红蛋白等相关生化指标,测量人体腰臀比、体重指数等参数,分析内脂素与上述指标的关系。结果糖尿病组FPGHbA1CHOMA-IRTCTGWHR较健康对照组升高,两者差异有统计学意义(P﹤0.01),FinsLDL-CHDL-CBMI两组差异无统计学意义(P﹥0.05);糖尿病组检测的内脂素、瘦素较NGT稍高,但差异无统计学意义(P﹥0.05);每组中超重亚组瘦素较体重正常亚组间升高,差异有统计学意义(P﹤0.01);而内脂素虽升高但差异无统计学意义(P﹥0.05);内脂素与瘦素以及其他临床指标相关分析提示糖尿病组内脂素与WHRHbA1C呈负相关(r=-0.34,和r=-0.26),与瘦素及其他参数包括BMI、HOMA-IR无明显相关。结论內脂素的升高与脂肪组织分布特点(如女性下半身肥胖)的关系更密切;并推测內脂素可能是糖尿病病理生理中的一种代偿机制。瘦素仅与体重状态有关,非糖尿病发病独立因素。
Objective To understand the changes of serum visfatin and leptin in newly diagnosed type 2 diabetic patients and to explore the correlation between visfatin and various metabolic parameters. Methods Patients with type 2 diabetes mellitus newly diagnosed or with short duration of illness (n = 57) were compared with healthy people (n = 61). According to BMI, they were divided into overweight and normal weight subgroups. Insulin, blood glucose, glycosylated hemoglobin and other related biochemical indicators, measuring body waist-hip ratio, body mass index and other parameters, the analysis of visfatin and the above indicators. Results The levels of FPGHbA1CHOMA-IRTCTGWHR in diabetic group were significantly higher than those in healthy control group (P <0.01), while there was no significant difference in FinsLDL-CHDL-CBMI between the two groups (P> 0.05) (P> 0.05). The levels of leptin in overweight subgroups in each group were significantly higher than those in normal weight groups (P <0.01), while the differences were statistically significant Visfatin and leptin and other clinical indicators showed that there was a negative correlation between visfatin and WHRHbA1C in diabetic patients (r = -0.34, r = -0.26), no significant correlation with leptin and other parameters including BMI and HOMA-IR. Conclusions The relationship between the increase of visfatin and the distribution of adipose tissue (such as lower body fat of female) is more close. It is speculated that visfatin may be a compensatory mechanism in the pathophysiology of diabetes. Leptin is only related to weight status, independent of non-diabetic pathogenesis.