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The GPCR Action Group

Insulin secretion from pancreatic β-cells is regulated by both metabolic pathways (glucose, amino acids, free fatty acids) and extracellular signals (hormones, free fatty acids, neurotransmitters and various small molecules) acting predominantly via G-protein coupled receptors (GPCRs). Signals from both metabolic pathways and cell surface receptors characteristically converge at the level of both plasmalemmal and ion channels, which modulate electrical activity and thereby influence transmembrane Ca2+-fluxes, and intracellular second messenger systems (MAPKs) that modulate ultimately insulin secretion. Thus type 2 diabetes results from impaired insulin secretion and action.

GPCRs (a family of seven transmembrane spanning receptors) are one of the largest known families in the human genome. Analysis of the human genome (with the roughly 865 GPCRs) has revealed that approximately 139 GPCRs still have unknown natural ligands. These receptors are known as orphan GPCRs. Our preliminary data indicate that a number of these orphan GPCRs are also expressed in human pancreatic islets. Approximately 35 % of all drugs on the market target these receptors. It has also been shown that some identified GPCRs function as sensors of extracellular signals, mediating metabolic information from the environment (body) into the β-cell, thereby modifying insulin secretion. We have already identified a few of GPCRs, which are of high importance for β-cell function and type 2 diabetes. Moreover, based on our preliminary results we have reason to believe that some of these identified GPCRs might play a role in mitochondrial function.

Group members

Albert Salehi (Coordinator)
Holger Luthman (Vice coordinator)
Maria Gomez
Åke Lernmark
Fariba Vaziri Sani
Lina Åkesson
Bo Ahrén
Jenny Wikman
Avinash Abhyankar
Frank Sundler
Niels Wierup
Corrado Cilio

Lund University Diabetes Centre, CRC, SUS Malmö, Entrance 72, House 91:12. SE-205 02 Malmö. Telephone: +46 40 39 10 00