脂肪细胞因子瘦素、脂联素及趋化素与胰岛素抵抗及妊娠期糖尿病的关联研究

Study on the relationship of adipose cytokines leptin,adiponectin,chemerin and insulin resistance in gestational diabetes mellitus

目的探讨血清脂肪细胞因子瘦素、脂联素及趋化素与体质量指数、各生化指标及胰岛素抵抗的关系及妊娠期糖尿病(GDM)发病中所起的作用。方法随机选取妊娠期糖尿病孕妇100例作为GDM组,正常孕妇100例作为对照组,对受试者进行相关生化指标如空腹血糖(FBG)、空腹胰岛素(FINS)、血脂等检测,根据公式计算胰岛素抵抗指数(HOMAIR)及胰岛β细胞功能指数(HOMA-β),并采用酶联免疫吸附法(ELISA法)测定血清瘦素、脂联素及趋化素水平,分析三者与临床生化指标及胰岛素抵抗的关系。结果 GDM孕妇血清瘦素水平明显增高(P<0.05),脂联素水平明显降低(P<0.05);趋化素在2组外周血中均有表达,差异无统计学意义(P>0.05)。GDM孕妇血清瘦素水平与产前BMI呈正相关(P<0.05),与FBG、FINS、HOMA-IR呈显著正相关(P均<0.01);正常孕妇血清瘦素水平与FBG、FINS、HOMA-IR均呈正相关(P均<0.05),与产前BMI无明显相关性(P>0.05)。2组孕妇血清瘦素水平与FINS、HOMA-IR相关系数差异有统计学意义P<0.05)。GDM孕妇血清脂联素水平与产前BMI、HOMA-IR呈明显负相关(P<0.05),而与FBG、FINS无明显相关性(P>0.05);正常孕妇血清脂联素水平与产前BMI、HOMA-IR、FINS呈负相关(P均<0.05),而与FBG无明显相关性(P均>0.05)。对所有受试者进行分析发现血清脂联素水平与产前BMI、HOMA-IR、FBG、FINS呈负相关(P均<0.05),其中与产前BMI独立相关(P<0.05)。血清趋化素水平与FBG、FINS、HOMA-IR呈明显正相关(P均<0.05),而与产前BMI无明显相关性(P>0.05)。结论 GDM孕妇存在较高的血清瘦素水平,且与血糖代谢、胰岛素抵抗密切相关。瘦素通过多种途径参与胰岛素与血糖之间的调节,导致胰岛素抵抗,并参与了GDM的发病。GDM孕妇较正常孕妇脂联素水平降低,血清脂联素水平与体内脂肪含量有关,脂联素参与了孕期糖代谢的调节,不仅是妊娠期胰岛素抵抗发生的机制之一,而且参与了GDM的发病。趋化素与了妊娠期糖代谢及胰岛素抵抗,但可能与GDM的发病无关。

Objective It is to analyze the relationship among adipose cytokines and various biochemical indexes and insu- lin resistance in gestational diabetes mellitus （GDM） and normal pregnant women, and to further explore the role of adipose eytokines in the pathogenesis of GDM. Methods By ease-control method, 100 GDM patients （GDM group） and 100 normal pregnant women （normal control group）were screened as research subjects. We detected various biochemical indexes, such as blood glucose, fasting insulin and blood lipids, then calculated HOMA - IR and HOMA -β. By using enzyme-linked immunosorbent assay （ELISA）, we determine adipose cytokines leptin, adiponectin and chemerin levels, analyze the relationship among adipose cytokines and biochemical indexes and insulin resistance. Results GDM patients compared with normal pregnant women, serum leptin levels were significantly higher, adiponectin levels were significantly lower （P 〈 0.05 ） , chemerin levels was not significantly different in both groups （ P 〉 0. 05 ）. In GDM patients, serum leptin levels was positively correlated with prenatal BMI （P 〈 0.05）, and was significant positively correlated with FBG, FINS, HOMA -IR （P 〈 0. 01 ）. In normal pregnant women, serum leptin levels was positively correlated with FBG, FINS, HOMA - IR （ P 〈 0.05 ）, was not significantly correlated with prenatal BMI （P 〉 0.05）. In both group, serum leptin and FINS, HOMA - IR correlation coefficients were statistically significant differences （P 〈 0.05）. In GDM patients, serum adiponeetin levels was negatively correlated with prenatal BMI, HOMA - IR （P 〈 0.05 ）, and was not significant correlated witb FBG, FINS （P 〉 0.05 ）. In normal pregnant women, adiponectin levels was negatively correlated with prenatal BMI, HOMA - IR, FINS （P 〈 0.05 ） , and was not signifi- cantly correlated with FBG （ P 〉 0.05 ）. In all subjects, serum adiponectin level was negatively correlated with prenatal BMI, HOMA - IR, FBG, FINS （ P 〈 0.05） , and was independently associated with prenatal BMI （P 〈 0.05 ）. In all subjects, ser- um chemerin levels was significantly correlated with FBG, FINS, HOMA -IR （P 〈0.05）, but was not significant correlated with prenatal BMI. Conclusion GDM patients has a higher level of serum leptin, which is closely related to glucose metabo- lism and insulin resistance. Leptin participate a variety of pathways that regulate insulin and blood glucose, lead to insulin re- sistance, and involved in the pathogenesis of GDM. GDM patients has a higher level of serum adiponectin compared to normal pregnant women,serum adiponectin level is associated with body fat content, adiponectin is involved in the regulation of glu- cose metabolism during pregnancy, not only is one of the mechanism of insulin resistance occurs during pregnancy, and hut al- so to be involved in the pathogenesis of GDM. Chemerin is involved in the glucose metabolism and insulin resistance during pregnancy, but may be not associated with the pathogenesis of GDM.