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Diabetes Progression, Prevention, and Treatment

Incretin-Based Therapies

Viewpoints on the way to consensus

  1. Michael. A. Nauck, MD1,
  2. Tina Vilsbøll, MD2,
  3. Baptist Gallwitz, MD3,
  4. Alan Garber, MD4 and
  5. Sten Madsbad, MD5
  1. 1Diabetes Center Bad Lauterberg, Bad Lauterberg im Harz, Germany;
  2. 2Department of Internal Medicine, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark;
  3. 3Department of Medicine IV, Eberhard-Karls University Tübingen, Tübingen, Germany;
  4. 4Division of Diabetes, Endocrinology & Metabolism, Baylor College of Medicine, Houston, Texas;
  5. 5Department of Endocrinology, Hvidovre University Hospital, University of Copenhagen, Copenhagen, Denmark.
  1. Corresponding author: Michael A. Nauck, m.nauck{at}diabeteszentrum.de.
Diabetes Care 2009 Nov; 32(suppl 2): S223-S231. https://doi.org/10.2337/dc09-S315
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Viewpoints on the way to consensus

INTRODUCTION (by M.A.N.)

Incretin mimetics and inhibitors of the protease dipeptidyl peptidase (DPP)-4 are new classes of antidiabetic agents first introduced in the years 2005 (exenatide) and 2007 (sitagliptin), respectively. Both use the antidiabetic properties of the incretin hormone, glucagon-like peptide (GLP)-1 (1). This gut-derived peptide hormone not only augments glucose-induced insulin secretion (required to fulfill the definition of an incretin hormone), but does so in a highly glucose-dependent manner (2), thus preventing GLP-1 alone from provoking hypoglycemia. Additional beneficial effects of GLP-1 on endocrine pancreatic islets are that it 1) supports the synthesis of proinsulin to replenish insulin stores in β-cells; 2) reduces the rate of β-cell apoptosis when islets are incubated in a toxic environment (glucotoxicity, lipotoxicity, cytotoxic cytokines); and 3) promotes differentiation of precursor cells with the ability to develop into β-cells and proliferation of β-cell lines, and in whole animals (rodent studies), this leads to an increased β-cell mass within a few days or weeks (1,3). Furthermore, GLP-1 can lower glucagon concentrations, i.e., induce α-cells to respond again to the inhibitory action of hyperglycemia, while leaving the counterregulatory glucagon responses undisturbed, as in the case of hypoglycemia (2,4). Additional activities of GLP-1 are the deceleration of gastric emptying (5), which slows the entry of nutrients into the circulation after meals, a reduction in appetite, and earlier induction of satiety (6), leading to weight reduction with chronic exposure (7). Renal effects (promotion of sodium and water excretion (8), as well as neuro- (9) and cardioprotective (10) properties of GLP-1, have also been described. While GLP-1 is perfectly suitable for lowering, or even stabilizing, glucose concentrations in short-term experiments, its short half-life (∼1–2 min for the intact, biologically active form) caused by rapid proteolytic degradation and inactivation through the ubiquitous enzyme DPP-4 and renal elimination (Fig. 1 …

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November 2009, 32(suppl 2)
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Incretin-Based Therapies
Michael. A. Nauck, Tina Vilsbøll, Baptist Gallwitz, Alan Garber, Sten Madsbad
Diabetes Care Nov 2009, 32 (suppl 2) S223-S231; DOI: 10.2337/dc09-S315

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Incretin-Based Therapies
Michael. A. Nauck, Tina Vilsbøll, Baptist Gallwitz, Alan Garber, Sten Madsbad
Diabetes Care Nov 2009, 32 (suppl 2) S223-S231; DOI: 10.2337/dc09-S315
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  • Article
    • INTRODUCTION (by M.A.N.)
    • DIFFERENT APPROACHES TO DIABETES THERAPY
    • ADVANTAGES OF INCRETIN MIMETICS AND DPP-4 INHIBITORS
    • INCRETIN MIMETICS AND DPP-4 INHIBITORS
    • CONCLUSIONS (by M.A.N.)
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Diabetes Progression, Prevention, and Treatment

  • Where Does Insulin Resistance Start?
  • Bile Acids and Metabolic Regulation
  • Goals of Treatment for Type 2 Diabetes
Show more Diabetes Progression, Prevention, and Treatment

Treatment

  • Where Does Insulin Resistance Start?
  • Bile Acids and Metabolic Regulation
  • Goals of Treatment for Type 2 Diabetes
Show more Treatment

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