β-Cell Glucose Non-sensing in Patients with Thalassemia major and Glucose Intolerance
Diabetes mellitus (DM), a relatively frequent complication in patients with thalassemia major (β-thal), is usually attributed to insulin deficiency due to islet β-cell loss because of toxic effects of iron deposited in the pancreatic islets [1–4]. There is also evidence for insulin resistance in peripheral tissues that precedes the development of diabetes [5–8]. A prospective long-term study of ours (6 years) of 60 patients with β-thal (unpublished data) agrees with previous data in the literature  showing that insulin resistance becomes evident in the pubertal period and progressively increases with age. Since in type-I and type-II DM the earliest finding in the prediabetic state is the diminished first-phase response of insulin to glucose infusion (IVGTT), while the insulin response to i.v. arginine, i.v. glucagon, oral glucose tolerance (OGTT) and i.v. tolbutamide is preserved or slightly impaired, this has been interpreted as decreased β-cell glucose non-sensing . The purpose of this study was to investigate the possibility that there is also β-cell glucose nonsensing in the prediabetic state in β-thal.
KeywordsInsulin Response Thalassemia Major Prediabetic State Cell Glucose Pubertal Period
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