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肥胖与成年型糖尿病之间的发病机制关系

[Pathogenetic relationships between obesity and maturity-onset diabetes].

作者信息

Spanár E, Uhrín P, Levcík A, Záhradný V

出版信息

Z Gesamte Inn Med. 1977 Jun 1;32(11):suppl 170-1.

PMID:930174
Abstract

The influences of the biguanide therapy on the behaviour of the glucose tolerance and the reactive IRI-values in obese diabetics were investigated. Apart from this a group treated with sulfonylurea was compared. Here besides the IRI-values the fat parameters were tested. Apart from these investigations the half-life periods of insulin in obese diabetics were established before and after the treatment with biguanides and compared with the half-life period in diabetics treated with insulin. In a small group a tolbutamide test was carried out and the insulin secretion, the STH-values, and the cortisol values were examined. The investigations permitted the conclusion that the increased IRI-levels are to be explained by a hypertrophy of lipocytes, when at the same time the carbohydrate tolerance is reduced. The hypertrophic fat cell needs more insulin for the induction of glucose than the normal lipocyte. By this means also the improvement of the carbohydrate tolerance after reduction of weight is to be explained. Finally it is tried to interpret the behaviour of the fat parameters.

摘要

研究了双胍类疗法对肥胖糖尿病患者糖耐量行为及反应性IRI值的影响。除此之外,还对一组接受磺脲类治疗的患者进行了比较。在此,除了IRI值外,还检测了脂肪参数。除了这些研究外,还测定了肥胖糖尿病患者在接受双胍类治疗前后胰岛素的半衰期,并与接受胰岛素治疗的糖尿病患者的半衰期进行了比较。在一个小群体中进行了甲苯磺丁脲试验,并检测了胰岛素分泌、生长激素值和皮质醇值。这些研究得出的结论是,当碳水化合物耐受性同时降低时,IRI水平升高可由脂肪细胞肥大来解释。肥大的脂肪细胞比正常脂肪细胞诱导葡萄糖需要更多的胰岛素。通过这种方式,也可以解释体重减轻后碳水化合物耐受性的改善。最后尝试解释脂肪参数的行为。

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