Abstract
Type 2 diabetes is characterized by hyperglycemia resulting from insulin resistance in the setting of inadequate beta-cell compensation. Recent studies indicate that for attaining a well-functioning ß-cell mass, parathyroid hormone-related protein (PTHrP) is a very promising candidate among several insulinotropic peptides. In order to elucidate its role, we determine the levels of PTHrP, insulin and c-peptide in type 2 diabetics and in normal subjects in the fasting state. We enrolled 28 patients (16 men and 12 postmenopausal women) with type 2 diabetes and twenty eight aged-matched healthy individuals as control subjects (15 men and 13 women). PTHrP was statistically significant correlated with glucose in type 2 diabetes and in normal subjects in the fasting state. Additionally, PTHrP serum levels exhibited a significant increase in type 2 diabetes compared to control subjects. Interestingly, PTHrP showed a positive correlation with insulin levels only among healthy individuals presumably due to defective glucose stimulated insulin secretion known to occur in type 2 diabetics. In conclusion, the strong positive relation of PTHrP with glucose in the fasting state in patients with type 2 diabetes mellitus raises several questions for further experimentation concerning its exact role and physiological significance.
Highlights
Blood glucose homeostasis is controlled by the endocrine cells of the pancreas, located in the islets of Langerhans
A statistical significant increase was detected in both PTH-related peptide (PTHrP) and glucose levels in women and men with type 2 diabetes compared with control subjects
In recent years, a large number of factors controlling the differentiation of ß-cells have been identified, and among them the PTHrP emerged as a strong candidate in ß-cell survival
Summary
Blood glucose homeostasis is controlled by the endocrine cells of the pancreas, located in the islets of Langerhans. The islet cells monitor the concentration of glucose in the blood and secrete hormones with opposite effects. Failure of ß-cell survival is critical to the etiology of diabetes mellitus as well as in the setting of islet transplantation [1, 2]. A large number of factors controlling the differentiation of beta-cells have been identified. They are classified into the following main categories: growth factors, cytokine and inflammatory factors, and hormones, such as PTH-related peptide (PTHrP) and glucagon-like peptide (GLP-1) [3,4,5]. Treatment with these external stimuli can restore a functional beta-cell mass in diabetic animals, but further studies are required before it can be applied to humans
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