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Adv Exp Med Biol. 2010;654:515-35. doi: 10.1007/978-90-481-3271-3_23.

Clinical approaches to preserve beta-cell function in diabetes.

Author information

1
Endocrine Service and Diabetes and Heart Center of the Heart Institute, Hospital das, Clinicas of The University of São Paulo Medical School, São Paulo, SP 05403-000, Brazil. bernarwaj@globo.com

Abstract

In type 2 diabetes (DM2) there is progressive deterioration in beta-cell function and mass. It was found that islet function was about 50% of normal at the time of diagnosis and reduction in beta-cell mass of about 60% at necropsy (accelerated apoptosis). Among the interventions to preserve the beta-cells, those to lead to short-term improvement of beta-cell secretion are weight loss, metformin, sulfonylureas, and insulin. The long-term improvement was demonstrated with short-term intensive insulin therapy of newly diagnosed DM2, the use of antiapoptotic drugs such as glitazones, and the use of glucagon-like peptide-1 receptor agonists (GLP-1 mimetics), not inactivated by the enzyme dipeptidyl peptidase 4 and/or to inhibit that enzyme (GLP-1 enhancers). The incretin hormones are released from the gastrointestinal tract in response to nutrient ingestion to enhance glucose-dependent insulin secretion from the pancreas and overall maintenance of glucose homeostasis. From the two major incretins, GLP-1 and GIP (glucose-dependent insulinotropic polypeptide), only the first one or its mimetics or enhancers can be used for treatment. The GLP-1 mimetics exenatide and liraglutide as well as the DPP 4 inhibitors (sitagliptin and vildagliptin) were approved for treatment of DM2.

PMID:
20217513
DOI:
10.1007/978-90-481-3271-3_23
[Indexed for MEDLINE]

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