The association between plasma adiponectin and insulin sensitivity in humans depends on obesity

The association between plasma adiponectin and insulin sensitivity in humans depends on obesity
复制标题

DOI:
10.1038/oby.2005.206
复制
发表时间:
2005-10-01
期刊:
OBESITY RESEARCH
影响因子:
--
通讯作者:
Stefan, N
Stefan, N
中科院分区:
其他
文献类型:
--
作者:
Kantartzis, K;Fritsche, A;Stefan, N

文献摘要

被引文献

相似文献

目的:在人类中,低血浆脂联素浓度先于胰岛素敏感性降低,并独立于肥胖预测2型糖尿病。然而,有可能脂联素对胰岛素敏感性的贡献在整个肥胖范围内并不相同。研究方法和程序:我们研究了在不同体脂含量(以体脂百分比(PFAT)表示)范围内血浆脂联素水平与胰岛素敏感性之间的横断面关联,研究对象为900名正常葡萄糖耐受性受试者。所有受试者都进行了口服葡萄糖耐量试验(OGTT), 299名受试者另外进行了正糖高胰岛素钳夹。在纵向分析中,在108名受试者的亚组中研究了基线时脂联素与胰岛素敏感性变化的关系。结果:在横断分析中,血浆脂联素和胰岛素敏感性之间的关联,根据年龄、性别和PFAT进行了调整,取决于受试者是瘦还是肥胖[脂联素X PFAT的相互作用p < 0.001 (OGTT)和0.002 (clamp)]。按PFAT四分位数分层,最低PFAT四分位数受试者的脂联素与胰岛素敏感性不显著相关(R-2 = 0.10, p = 0.13, OGTT; R-2 = 0.10, p = 0.57, clamp),而最高PFAT四分位数受试者的相关性很强(R-2 = 0.36, p < 0.0001, OGTT; R-2 = 0.48, p = 0.003, clamp)。在纵向分析中,基线时的血浆脂联素先于肥胖者(n = 54, p = 0.03)的胰岛素敏感性改变,而非瘦人(n = 54, p = 0.68)。讨论:这些数据表明,脂联素在维持肥胖患者的胰岛素敏感性方面尤其重要。因此,通过增加脂联素浓度来降低胰岛素抵抗的干预措施可能对肥胖、胰岛素抵抗的个体特别有效。
Objective: In humans, low plasma adiponectin concentrations precede a decrease in insulin sensitivity and predict type 2 diabetes independently of obesity. However, it is possible that the contribution of adiponectin to insulin sensitivity is not equally strong over the whole range of obesity.Research Methods and Procedures: We investigated the cross-sectional association between plasma adiponectin levels and insulin sensitivity in different ranges of body fat content [expressed as percentage of body fat (PFAT)] in a large cohort of normal glucose-tolerant subjects (n = 900). All individuals underwent an, oral glucose tolerance test (OGTT), and 299 subjects additionally a euglycemic hyper-insulinemic clamp. In longitudinal analyses, the association of adiponectin at baseline with change in insulin sensitivity was investigated in a subgroup of 108 subjects.Results: In cross-sectional analyses, the association between plasma adiponectin and insulin sensitivity, adjusted for age, gender, and PFAT, depended on whether subjects were lean or obese [p for interaction adiponectin X PFAT < 0.001 (OGTT) and 0.002 (clamp)]. Stratified by quartiles of PFAT, adiponectin did not correlate significantly with insulin sensitivity in subjects in the lowest PFAT quartile (R-2 = 0.10, p = 0.13, OGTT; and R-2 = 0.10, p = 0.57, clamp), whereas the association in the upper PFAT quartile was rather strong (R-2 = 0.36, p < 0.0001, OGTT; and R-2 = 0.48, p = 0.003, clamp). In longitudinal analyses, plasma adiponectin at baseline preceded change in insulin sensitivity in obese (n = 54, p = 0.03) but not in lean (n = 54, p 0.68) individuals.Discussion: These data suggest that adiponectin is especially critical in sustaining insulin sensitivity in obese subjects. Thus, interventions to reduce insulin resistance by increasing adiponectin concentrations may be effective particularly in obese, insulin-resistant individuals.