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作 者:高珊[1] 黎明[2] 陆菊明[3] 张秀娟[1] 任昶[1] 李海晖[1] 张荣洲[1]
机构地区:[1]首都医科大学附属北京朝阳医院京西院区内分泌科,100043 [2]中国医学科学院北京协和医院内分泌科 [3]解放军总医院内分泌科
出 处:《中国糖尿病杂志》2007年第3期149-152,共4页Chinese Journal of Diabetes
基 金:首都医学发展基金资助项目(2002-3034);北京市科技新星计划资助项目(2004A27)
摘 要:目的研究血清瘦素、脂联素与2型糖尿病(T2DM)一级亲属胰岛素抵抗(IR)相关性,探讨二者在T2DM发病中作用。方法收集既往无糖耐量异常史的T2DM一级亲属,分为糖耐量正常(NGT)组174例、空腹血糖受损(IFG)或糖耐量低减(IGT)组55例,及新发T2DM组71例;以其无糖尿病家族史的配偶或亲友中OGTT正常者114例作为正常对照组(NC)。酶联免疫法测定上述人群的血清真胰岛素(TI)、瘦素和脂联素水平。用HOMA-IR评价胰岛素抵抗(IR)状态。结果从NC至NGT、IGT/IFG到DM组,IR进行性加重(HOMA-IR分别为1.3±0.7、1.7±1.5、2.2±1.4和3.2±2.8,P<0.01);血清瘦素水平进行性增高(P<0.01),瘦素水平与HOMA-IR正相关(r=0.35,P<0.01);血清脂联素水平进行性降低(分别为20±12、17±11、13±8和10±6mg/L,P<0.01),与HOMA-IR负相关(r=-0.41,P<0.01);脂联素/瘦素比值进性行降低,与HOMA-IR负相关(r=-0.53,P<0.01)。结论T2DM一级亲属在NGT时即存在瘦素水平升高和脂联素水平明显下降。脂联素/瘦素比值下降趋势与IR和糖调节受损的严重程度密切相关,推测该比值的变化可能是糖尿病一级亲属存在的固有遗传缺陷的一种表现,可能在IR和T2DM的发生发展中起重要作用,因而渴望作为预测T2DM发病的早期观察指标。Objective To study the association of serum leptin and adiponectin with insulin resistance in first-degree relatives of type 2 diabetes mellitus (T2DM), and to investigate the role of leptin and adiponectin in development of T2DM. Methods Serum levels of adiponectin and leptin were measured by ELISA in 71 patients with newly diagnosed T2DM, 55 subjects with IGT/IFG and 174 NGT from first-degree relatives of T2DM, and 114 subjects of NGT without T2DM family history as control group (NC). Insulin resistance was evaluated by HOMA-IR. Results The serum levels of leptin were progressively increased from NC to NGT, to IGT/IFG and to T2DM groups, and positively correlated with HOMA-IR (r=0.35, P〈0.01). The serum levels of adiponectin were progressively decreased from NC to NGT, to IGT/IFG and to T2DM groups, and negatively correlated with HOMA-IR(r=-0.41, P〈0. 001). The adiponectin/leptin ratio was progressively reduced in groups of diabetic pedigree from NGT to IFG/IGT and to T2DM groups, and correlated with HOMA-IR significantly(r=-0.53, P〈0.01). Conclusions Decreased serum adiponectin level and increased leptin level, in parallel with increased insulin resistance, are already present in NGT pedigrees of T2DM, and the decreased ratio of adeponectin/leptin levels is associated with the severity degree of IR and IGR. We speculate the change of adiponectin/leptin ratio may be a reflection of genetic deficiency in T2DM pedigrees, and play an important role in the pathogenesis of insulin resistance and T2DM, thus the adiponectin/leptin ratio may be potent to be an early predicator of T2DM.
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