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Hepc1基因敲除小鼠的铁过载并未损害葡萄糖稳态。

Iron overload in Hepc1(-/-) mice is not impairing glucose homeostasis.

作者信息

Ramey G, Faye A, Durel B, Viollet B, Vaulont S

机构信息

Institut Cochin, Département Endocrinologie Métabolisme et Cancer, Paris, F-75014, France.

出版信息

FEBS Lett. 2007 Mar 6;581(5):1053-7. doi: 10.1016/j.febslet.2007.02.002. Epub 2007 Feb 12.

DOI:10.1016/j.febslet.2007.02.002
PMID:17316628
Abstract

Diabetes Mellitus is found with increasing frequency in iron overload patients with hemochromatosis. In these conditions, the pancreas shows predominant iron overload in acini but also islet beta-cells. We assess glucose homeostasis status in iron-overloaded hepcidin-deficient mice. These mice presented with heavy pancreatic iron deposits but only in the acini. The beta-cell function was found unaffected with a normal production and secretion of insulin. The mutant mice were not diabetic, responded as the control group to glucose and insulin challenges, with no alteration of insulin signalling in the muscle and the liver. These results indicate that, beta-cells iron deposits-induced decreased insulin secretory capacity might be of primary importance to trigger diabetes in hemochromatosic patients.

摘要

糖尿病在患有血色素沉着症的铁过载患者中越来越常见。在这些情况下,胰腺在腺泡以及胰岛β细胞中均表现出主要的铁过载。我们评估了铁过载且铁调素缺乏的小鼠的葡萄糖稳态状态。这些小鼠胰腺有大量铁沉积,但仅存在于腺泡中。发现β细胞功能未受影响,胰岛素的产生和分泌正常。突变小鼠未患糖尿病,在葡萄糖和胰岛素刺激下的反应与对照组相同,肌肉和肝脏中的胰岛素信号传导没有改变。这些结果表明,β细胞中铁沉积导致的胰岛素分泌能力下降可能是引发血色素沉着症患者糖尿病的主要因素。

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