Phosphodiesterases in the pathophysiology of diabetes mellitus
Journal Title: Journal of Analytical Bio-Science - Year 2011, Vol 34, Issue 5
Abstract
Diabetes Mellitus is a serious progressive disorder caused by an absence of or insufficient amount of insulin in the bloodstream. It is associated with risk of cardiovascular disease as well as specific microvascular complications [such as retinopathy, nephropathy and neuropathy]. Primarily there are two main types of diabetes classified as type 1 and type 2. Type 1 diabetes mellitus, is characterized by the inability of the pancreas to secrete insulin because of autoimmune destruction of the β-cells. Type 2 is insulin resistance and the most common form of diabetes, and most individuals with the disease are adults. Cyclic 3'5'-AMP (cAMP) is an important physiological amplifier of glucose-induced insulin secretion by the pancreatic islet β-cell. It is formed by the activity of adenylyl cyclase. Nine families of adenylyl cycylases catalyze the synthesis of the second messenger cAMP and protein kinases A. Cyclic nucleotide levels are regulated through catabolic processes directed by phosphodiesterases (PDEs) that breaks a phosphodiester bond in the second messenger molecules cAMP and cGMP. PDEs, which are ubiquitously distributed in mammalian tissues, contains at least 11 gene families. PDE inhibitors may be of value in preventing β-cell loss in both type 1 and type 2 diabetes. Comparative studies on PDEs would be very important to evaluate the involvement of each PDE in specific cellular function and to understand regulation of cyclic nucleotide signaling. In this overview, we highlight recent studies to define PDE expression and to provide evidence that PDE inhibitors may be effective agents in delay or in treatment of diabetes mellitus.
Authors and Affiliations
Mudigonda Saraswati
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