The role of parathyroid hormone-related protein (PTHrP) in the pathophysiology of diabetes mellitus.
Type 2 diabetes is characterized by hyperglycemia resulting from insulin resistance in the setting of inadequate beta-cell compensation. Impaired beta-cell function and possibly beta-cell mass appear to be reversible, particularly at early stages of the disease. Pancreatic beta-cells possess the potential to greatly expand their function and mass in both physiologic and pathologic states by several mechanisms, including hypertrophy and proliferation of existing beta-cells, increased insulin production and secretion, and formation of new beta-cells from progenitor cells. Recently a large number of factors controlling the differentiation of beta-cells has been identified and among them the parathyroid hormone-related protein (PTHrP) emerged as a strong candidate in beta-cell survival. In this review, we will highlight our current knowledge in PTHrP physiology implicating its role into the mechanisms of beta-cell mass regulation and consequently in diabetes. Further research into mechanisms will reveal the key modulators of beta-cell failure and thus identify possible novel therapeutic targets.[1]References
- The role of parathyroid hormone-related protein (PTHrP) in the pathophysiology of diabetes mellitus. Legakis, I. Mini. Rev. Med. Chem (2009) [Pubmed]
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