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Update on the Protective Molecular Pathways Improving Pancreatic Beta-Cell Dysfunction
Author(s) -
Alessandra Puddu,
Roberta Sanguineti,
François Mach,
Franco Dallegri,
Giorgio Luciano Viviani,
Fabrizio Montecucco
Publication year - 2013
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2013/750540
Subject(s) - diabetes mellitus , beta cell , glucose homeostasis , beta (programming language) , bioinformatics , homeostasis , function (biology) , medicine , insulin , extracellular , cell , biology , endocrinology , microbiology and biotechnology , insulin resistance , biochemistry , islet , computer science , programming language
The primary function of pancreatic beta-cells is to produce and release insulin in response to increment in extracellular glucose concentrations, thus maintaining glucose homeostasis. Deficient beta-cell function can have profound metabolic consequences, leading to the development of hyperglycemia and, ultimately, diabetes mellitus. Therefore, strategies targeting the maintenance of the normal function and protecting pancreatic beta-cells from injury or death might be crucial in the treatment of diabetes. This narrative review will update evidence from the recently identified molecular regulators preserving beta-cell mass and function recovery in order to suggest potential therapeutic targets against diabetes. This review will also highlight the relevance for novel molecular pathways potentially improving beta-cell dysfunction.

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