文章摘要
付 麒,王知笑,唐 伟,杨 涛,胡 勇.代谢综合征及高危人群空腹血糖与胰岛功能的关系[J].南京医科大学学报,2013,(9):1237~1242
代谢综合征及高危人群空腹血糖与胰岛功能的关系
The relationship between fasting plasma glucose and β-cell function of population with metabolic disorders
投稿时间:2013-02-27  
DOI:10.7655/NYDXBNS20130912
中文关键词: 空腹血糖  胰岛功能  糖尿病
英文关键词: fasting plasma glucoes  β-cell function  type 2 diabetes
基金项目:江苏省科技支撑计划(社会发展)重点项目(BE2009687);江苏省科技支撑计划(社会发展)重大项目(BE2009613)
作者单位
付 麒 南京医科大学第一附属医院内分泌科,江苏 南京 210029 
王知笑 南京医科大学第一附属医院内分泌科,江苏 南京 210029 
唐 伟 南京医科大学第一附属医院内分泌科,江苏 南京 210029 
杨 涛 南京医科大学第一附属医院内分泌科,江苏 南京 210029 
胡 勇 南京理工大学医院,江苏 南京 210094 
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中文摘要:
      目的:分析不同空腹血糖水平胰岛功能特点及变化趋势。方法:选取南京理工大学社区及江苏高邮地区非确诊糖尿病人群1 068例,标准化问卷?人体测量及生化分析分别获取病史资料?体格特征和生化数据,口服75 g葡萄糖耐量(OGTT)及胰岛素释放试验0?30?120 min分别采血测定血糖?胰岛素水平。Matsuda ISI指数评价胰岛素敏感性,0~30 min和0~120 min胰岛素曲线下面积(AUCINS30和AUCINS120)及其与血糖曲线下面积之比(胰岛素释放指数,INSR30和INSR120)评估β细胞胰岛素分泌能力,INSR30和INSR120与MatsudaISI的乘积作为处置指数(DI30和DI120),反应β细胞相对于胰岛素抵抗的代偿能力。结果:与空腹血糖< 4.6 mmol/L相比,在空腹血糖处于4.6~5.6 mmol/L时,INSR30和INSR120已出现显著下降,在空腹血糖≥7.0 mmol/L时AUCINS30和AUCINS120出现显著下降。胰岛素敏感性指标Matsuda ISI随着空腹血糖升高逐渐减低,胰岛素抵抗指数HOMAIR随着空腹血糖升高逐渐增大,处置指数DI30和DI120随着空腹血糖升高稳步减低。体质指数(BMI)分组后,在各种血糖水平,肥胖者胰岛素曲线下面积和释放指数均高于非肥胖者,胰岛素敏感性则低于非肥胖者,处置指数在两者间无差别。结论:在空腹血糖正常高界时胰岛功能已经出现减低,尽管其胰岛素释放量尚可维持在一定水平,但β细胞相对于胰岛素抵抗水平的代偿能力已经出现降低。
英文摘要:
      Objective:To investigate the relationship between β-cell function and fasting plasma glucose. Methods:History taking,physical examination,laboratory tests,75-g oral glucose tolerance tes(OGTT) and insulin secretion test were performed on 1 068 sujects without confirmed diabetes from Gaoyou district and Nanjing University of Science and Technology community of Jiangsu Province. Venous blood samples were collected at 0,30 and 120 min of OGTT to measure plasma glucose and serum insulin. MatsudaISI and HOMAIR were used to determine insulin sensitivity. The area under curve (AUC) of insulin during 0 to 30 min and 0 to 120 min(AUCINS30 and AUCINS120),together with the ratio of AUC of insulin to the AUC of glucose(i.e. insulin release indices,including INSR30 and INSR120) were calculated as surrogate indices of β-cell insulin secretion function. To evaluate the compensatory response of β-cell to insulin resistance,we used the products of insulin release indices multiplied by Matsuda ISI as disposition indices (DI30 and DI120). Results:When fasting plasma glucose (FPG) level was in the rang of 4.6~5.6 mmol/L,INSR30 and INSR120 decreased significantly. AUCINS30 and AUCINS120 decreased significantly when FPG≥7.0 mmol/L. Matsuda ISI always attenuated along with FPG increased,while HOMAIR was enhanced. Interestingly,DI30 and DI120 decreased steadily even at the normal glucose. After grouped by BMI,AUCINS30,AUCINS120,INSR30 and INSR120 of obese subjects were larger than non-obese,but the insulin sensitivity was less than non-obese. There was no difference between obese and non-obese subjects on DI30 and DI120. Conclusion:β-cell function was already impaired when the FPG was in high normal range,although the sum of insulin secretion is not reduced,the compensatory response of β-cell to insulin resistance has already decreased.
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