Literature DB >> 18292465

Targeting beta-cell mass in type 2 diabetes: promise and limitations of new drugs based on incretins.

Marzieh Salehi1, Benedikt A Aulinger, David A D'Alessio.   

Abstract

Progressive insulin secretory defects, due to either functional abnormalities of the pancreatic beta-cells or a reduction in beta-cell mass, are the cornerstone of type 2 diabetes. Incretin-based drugs hold the potential to improve glucose tolerance by immediate favorable effect on beta-cell physiology as well as by expanding or at least maintaining beta-cell mass, which may delay the progression of the disease. Long-term studies in humans are needed to elaborate on these effects.

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Year:  2008        PMID: 18292465      PMCID: PMC2528856          DOI: 10.1210/er.2007-0031

Source DB:  PubMed          Journal:  Endocr Rev        ISSN: 0163-769X            Impact factor:   19.871


  161 in total

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5.  Role of the vagus nerve in mediating proximal nutrient-induced glucagon-like peptide-1 secretion.

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Journal:  Endocrinology       Date:  1999-04       Impact factor: 4.736

6.  Glucose intolerance but normal satiety in mice with a null mutation in the glucagon-like peptide 1 receptor gene.

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7.  Insulinotropic hormone glucagon-like peptide-1 differentiation of human pancreatic islet-derived progenitor cells into insulin-producing cells.

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8.  Receptor gene expression of glucagon-like peptide-1, but not glucose-dependent insulinotropic polypeptide, in rat nodose ganglion cells.

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Review 9.  Decreased beta-cell mass in diabetes: significance, mechanisms and therapeutic implications.

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Journal:  Diabetologia       Date:  2004-02-07       Impact factor: 10.122

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Journal:  Metabolism       Date:  1987-07       Impact factor: 8.694

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Review 7.  The proteostasis boundary in misfolding diseases of membrane traffic.

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8.  Longitudinal changes in pancreatic and adipocyte hormones following Roux-en-Y gastric bypass surgery.

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