A spectrum of treatment (from bleeding to liver transplantation [

A spectrum of treatment (from bleeding to liver transplantation [64]) is available. Clinical and molecular investigations, leading to adapted treatment options are mandatory, because HH may lead Nivolumab to various organ dysfunctions (notably heart failure [65]) or to the development of hepatocarcinoma [66]. Iron overload is observed as secondary to many disorders and can be classified in different groups of diseases. In the first group, the “iron-loading anemias”, disorders such thallassemic syndromes, sideroblastic anemia, chronic hemolytic anemia, aplastic anemia, and pyruvate kinase

deficiency are observed. In the “chronic liver diseases”, several pathologies are encountered: hepatitis C infection, nonalcoholic fatty liver disease (NASH), alcoholic liver disease, or porphyria cutanea tarda. Finally, accumulation of iron may be secondary to red blood cell Torin 1 manufacturer transfusion, long-term hemodialysis with iron substitution, or to orphan diseases such as acerulopasminemia, African iron overload or neonatal iron overload [67]. In all these diseases, the consequences of

iron overload should be carefully determined. Type 2 diabetes (T2D) is a worldwide health burden considering that over 370 million individuals are today affected by the disease. T2D is responsible for a substantial morbidity and increased mortality. Iron homeostasis is closely linked to glucose homeostasis [68], [69] and [70]. Iron toxicity observed in hereditary hemochromatosis or during transfusional iron overload is associated with high prevalence of secondary diabetes [71]. Conversely, iron deficiency is associated with obesity which is the

most common risk factor for developing T2D. How can iron contribute to abnormal glucose homeostasis? In the experimental model of iron overload that mimics hemochromatosis, mice have a decreased glucose-stimulated insulin secretion and increased insulin sensitivity [72]. Insulin resistance occurs later during the disease in mice and these animals have an increased oxidative stress detected in pancreatic islets resulting to an excess of β-cell apoptosis. In contrast to the experimental Calpain mice models of hemochromatosis, both insulin deficiency and insulin resistance are present in human hemochromatosis [73]. However, the β-cell failure observed in humans with hemochromatosis is probably the primary and prerequisite abnormality for developing T2D. This is emphasized by the observation that insulin sensitivity is restored after bloodletting and insulin secretory abilities are only partially improved in patients with hemochromatosis who undergo phlebotomy [73] and [74]. The pathogenesis of T2D in patients with iron overload (hemochromatosis) compared to diabetic patients with elevated iron levels (inflammatory state and/or elevated iron intake) is probably not similar.

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