Abstract
Type 2 diabetes (T2DM) is frequently associated with elevated levels of lipids, in particular plasma free fatty acids and toxic lipid metabolites in muscle, liver, adipocytes, pancreatic islets and arterial tissues, contributing to insulin resistance and pancreatic islet β-cell dysfunction. The pathophysiology of T2DM is increasingly being linked with inflammatory mediators such as cytokines and chemokines as well as with changes in the number and activation state of macrophages/monocytes leading to β-cell dysfunction and subsequently to insulin insufficiency. The prevalent product of the cyclooxygenase 2 (COX-2) enzyme PGE2, controls numerous physiological functions through a family of cognate G proteincoupled receptors (EP1-EP4). The EP3 receptor which is selectively upregulated in islets of T2DM individuals, is upregulated under lipotoxic conditions and is involved in β-cell dysfunction and demise. This EP3 target presents a new approach to delay the progression of T2DM disease by preserving the pancreatic β-cells.
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