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胎球蛋白-A水平与体重依赖性胰岛素抵抗及2型糖尿病的关系。

Relationship of fetuin-A levels to weight-dependent insulin resistance and type 2 diabetes mellitus.

作者信息

Erdmann Johannes, Salmhofer Hermann, Knauß Amelie, Mayr Martina, Wagenpfeil Stefan, Sypchenko Oleg, Luppa Peter, Schusdziarra Volker

机构信息

Department of Nutritional Medicine, Technical University of Munich, Germany.

出版信息

Regul Pept. 2012 Oct 10;178(1-3):6-10. doi: 10.1016/j.regpep.2012.02.004. Epub 2012 Feb 28.

Abstract

OBJECTIVE

Weight gain and obesity are of substantial importance for the development of insulin-resistance and type-2 diabetes mellitus. Fetuin-A, a liver-derived glycoprotein, may also play a role in these alterations. Several studies have demonstrated an association between fetuin-A and body weight which, however, was within a fairly small range at the border of overweight to obesity. The present study examines the relationship between fetuin-A and a wide range of BMI, together with basal insulin, and HOMA-IR. In addition, matched groups of non-diabetic patients and those with type-2 diabetes mellitus were compared.

METHODS

We examined the relationship between fetuin-A and BMI, insulin, HOMA-IR, glucose and HbA1c in a cohort of 445 non-diabetic obese subjects and 150 obese patients with type-2-diabetes mellitus (DM2).

RESULTS

In relation to quintiles of fetuin-A a significant increase of BMI, basal insulin and HOMA-IR was observed between the 1st and 2nd quintile with no further change thereafter. Correspondingly, fetuin-A levels increased significantly only between the 1st and 2nd quintile of BMI, insulin or HOMA-IR, respectively. When patients with type 2 diabetes were compared with non-diabetic subjects matched for BMI, insulin, and age median fetuin-A levels were not significantly different.

CONCLUSION

At the early stage of weight gain fetuin-A could be of relevance for the development of insulin resistance. For the further progressive resistance with increasing weight in the obesity range the present data do not support a role of fetuin-A. Similarly its contribution to the resistance of type-2 diabetes seems to be of minor importance.

摘要

目的

体重增加和肥胖对于胰岛素抵抗和2型糖尿病的发展至关重要。胎球蛋白-A是一种肝脏来源的糖蛋白,可能也在这些改变中发挥作用。多项研究已证明胎球蛋白-A与体重之间存在关联,然而,这种关联处于超重至肥胖边界的相当小范围内。本研究考察了胎球蛋白-A与广泛的体重指数(BMI)、基础胰岛素以及胰岛素抵抗稳态模型评估(HOMA-IR)之间的关系。此外,还比较了非糖尿病患者和2型糖尿病患者的匹配组。

方法

我们在一组445名非糖尿病肥胖受试者和150名2型糖尿病(DM2)肥胖患者中考察了胎球蛋白-A与BMI、胰岛素、HOMA-IR、血糖和糖化血红蛋白(HbA1c)之间的关系。

结果

就胎球蛋白-A的五分位数而言,在第1和第2五分位数之间观察到BMI、基础胰岛素和HOMA-IR显著增加,此后没有进一步变化。相应地,胎球蛋白-A水平仅在BMI、胰岛素或HOMA-IR的第1和第2五分位数之间分别显著增加。当将2型糖尿病患者与BMI、胰岛素和年龄匹配的非糖尿病受试者进行比较时,胎球蛋白-A的中位数水平没有显著差异。

结论

在体重增加的早期阶段,胎球蛋白-A可能与胰岛素抵抗的发展有关。对于肥胖范围内体重增加导致的进一步渐进性抵抗,目前的数据不支持胎球蛋白-A发挥作用。同样,它对2型糖尿病抵抗的贡献似乎也不太重要。

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