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Editorial

Novel Factors in the Regulation of ß-Cell Function

¹ INSERM U342, St. Vincent de Paul Hospital, Paris, France
² Department of Endocrinology & Metabolism, Hebrew University Hadassah Medical Center, Jerusalem, Israel
³ Department of Molecular Medicine, Division of Endocrinology & Diabetes, Karolinska Hospital, Stockholm, Sweden
⁴ Department of Physiology, Endocrinology-Metabolism, Université Catholique de Louvain, Brussels, Belgium
⁵ Department of Biochemistry and Molecular Biology, and Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois
⁶ Metabolism Unit, CNR Institute of Clinical Physiology, University of Pisa, Pisa, Italy

The first 300 words of the full text of this article appear below.

Insulin secretion and ß-cell biology are the focus of the Servier-IGIS Symposia that have been held yearly since 2000 in St. Jean Cap Ferrat in southern France (1). This volume, the fourth of a series published in Diabetes (1–3), collects the proceedings of the fourth Servier-IGIS Symposium, which focused on novel factors involved in islet biology and ß-cell function. Special emphasis was placed on nuclear receptors, new genes that are associated with type 2 diabetes, and the role of mitochondria and lipid modulators in islet function. This symposium offers a striking example of how better knowledge of ß-cell biology and the introduction of genetic tools to explore the pathophysiology of type 2 diabetes complement each other to improve our understanding of glucose homeostasis.

Section I details the role of nuclear receptors in islet function, with special emphasis on peroxisome proliferator-activated receptors (PPARs). PPAR was cloned in 1990; related receptors were subsequently cloned, namely PPAR (or ß) and PPAR. They form heterodimers with retinoid X receptor (RXR); their natural ligands are fatty acids and lipid-derived substrates. These receptors are major regulators of lipid metabolism, linking availability of glucose and lipids and long-term metabolic adaptation. Most importantly, they are targeted by key drugs used in treatment of hyperlipidemias and diabetes, namely fibrates and thiazolidinediones. Thiazolidinediones are synthetic PPAR agonists developed to improve glucose tolerance by enhancing insulin sensitivity and restoring ß-cell function. Patients with dominant-negative PPAR mutations develop severe hyperglycemia, and PPAR gene variants have been associated with type 2 diabetes. Besides the many actions of PPAR agonists on the transcription of genes controlling insulin sensitivity in adipose tissue, they increase glucose sensing in liver and in ß-cells. In the latter, PPAR also enhances growth and prevents apoptosis.

PPAR (the target of fibrates) controls lipid . . . [Full Text of this Article]

Address correspondence and reprint requests to E. Ferrannini, MD, Department of Internal Medicine, University of Pisa, Via Roma 67, 56126 Pisa, Italy. E-mail: ferranni@ifc.cnr.it

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