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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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    Figure 1

    Schematic diagram explaining the physiological (postprandial) secretion of GLP-1 from the gut, its binding to GLP-1 receptors (e.g., on pancreatic endocrine β-cells), and its degradation by the ubiquitous protease DPP-4 as well as its rapid renal elimination (A). Incretin mimetics are peptide GLP-1 receptor agonists more or less structurally similar to GLP-1, which bind and activate the GLP-1 receptor, but are not degraded by DPP-4 and have much slower elimination pharmacokinetics (B). DPP-4 inhibitors prevent the degradation/inactivation of the biologically active form of GLP-1 and, thereby, augment the biological activity of GLP-1 released from endogenous sources (C).

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  • Table 1

    Similarities of incretin-based therapies

    Properties/actionIncretin mimeticsDPP-4 inhibitors
    Glucose-dependent insulin secretionYesYes
    Glucose-dependent glucagonostatic effectYesYes
    Effect on fasting plasma glucose (reduction)By 1.4–3.4 mmol/lBy 1.0–1.4 mmol/l
    Effect on postprandial glucoseYesYes (but weaker)
    Effect on A1C (reduction)By 0.8–1.8%By 0.5–1.1%
    Effect on (pro)insulin biosynthesisYesYes (weaker?)
    Improved in vivo β-cell function (in humans)Yes*Yes*
    Beneficial cardiovascular effectsProbableNot proven
    • ↵*As determined while patients received treatment (lasting effects need to be proven after washing out treatment).

  • Table 2

    Differences of incretin-based therapies

    Properties/actionIncretin mimeticsDPP-4 inhibitors
    AdministrationSubcutaneousOral
    GLP-1 levels (or equivalent)Pharmacological (six- to tenfold)Physiological (two- to threefold)
    Main mechanism of GLP-1 receptor stimulationInteraction with receptors on target organs/cellsInteraction with receptors on afferent nerves (autonomous nervous system)
    Other mediatorsNoGIP, PACAP, others (questionable)
    Effects on gastric emptyingYesNo (hardly)
    Effects on appetiteReducedHardly influenced
    Effects on body weightWeight lossWeight neutrality
    Adverse eventsNausea, vomiting, antibodies (exenatide, relevance?), pancreatitis (causal relation?)Upper respiratory tract infections, elevations in liver enzymes (vildagliptin), skin reactions (sitagliptin)
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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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    • 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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