We are analyzing https://link.springer.com/article/10.1186/1475-2840-12-154.

Title:
Dipeptidyl peptidase-4 inhibitors and GLP-1 reduce myocardial infarct size in a glucose-dependent manner | Cardiovascular Diabetology
Description:
The dipeptidyl peptidase-4 (DPP-4) inhibitors Sitagliptin and Vildagliptin lower blood glucose by augmenting endogenous levels of glucagon-like peptide-1 (GLP-1), an incretin which also confers cardioprotection. As such, we hypothesized that treatment with DPP-4 inhibitors are also cardioprotective. In ex vivo experiments: Male Sprague–Dawley rats were randomized to receive by oral gavage either Vildagliptin (20 mg/kg/day), Sitagliptin (100 mg/kg/day), or water for 2 weeks. Excised hearts were Langendorff-perfused with buffer containing either 5 mmol/L or 11 mmol/L glucose and subjected to 35 minutes ischaemia/120 minutes reperfusion. In in vivo experiments: Male young Wistar and Sprague–Dawley rats, middle aged Wistar and Goto-Kakizaki diabetic rats were randomized to receive by oral gavage either Sitagliptin (100 mg/kg/day), or water for 2 weeks. Rats were then subjected to 30 minutes ischaemia/120 minutes reperfusion and infarct size ascertained. Two weeks pre-treatment with either Vildagliptin or Sitagliptin reduced ex vivo myocardial infarction (MI) size in hearts perfused with buffer containing 11 mmol/L glucose but not 5 mmol/L glucose. This effect was abolished by Exendin 9–39 (GLP-1 receptor antagonist) and H-89 (PKA antagonist). Treatment of perfused hearts with native GLP-1 was also glucose-sensitive, reducing MI size, at glucose concentrations 7, 9, and 11 mmol/L but not at 5 mmol/L. Finally, Sitagliptin reduced in vivo MI size in middle aged Wistar (7-8 mmol/L glucose) and Goto-Kakizaki (9-10 mmol/L glucose) rats where blood glucose was elevated, but not in young Wistar (5 mmol/L glucose) or Sprague–Dawley (5 mmol/L glucose) rats, where blood glucose was normal. We find that chronic treatment with DPP-4 inhibitors reduced MI size, via the GLP-1 receptor-PKA pathway, in a glucose-dependent manner. Glucose-sensitive cardioprotection of endogenous GLP-1 in diabetic patients may in part explain why intensive control of serum glucose levels has been associated with increased cardiovascular risk.
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Keywords {🔍}

glucose, glp, myocardial, article, mmoll, pubmed, sitagliptin, google, scholar, size, infarct, heart, cas, vildagliptin, dpp, rats, hearts, risk, cardioprotection, control, blood, levels, diabetes, area, vivo, figure, infarction, perfused, buffer, reperfusion, inhibitors, wistar, pretreatment, effects, study, group, authors, patients, coronary, glucagonlike, peptide, treatment, effect, acute, rat, cardioprotective, reduced, receptor, pka, versus,

Topics {✒️}

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Questions {❓}

Hausenloy DJ, Maddock HL, Baxter GF, Yellon DM: Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?

Schema {🗺️}

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            Reperfusion
            Glucagon-like peptide 1
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            Diabetes
            Angiology
            Cardiology
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         Reperfusion
         Glucagon-like peptide 1
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         Vildagliptin
         Dipeptidyl peptidase-4 inhibitor
         Blood glucose
         Diabetes
         Angiology
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      name:The Hatter Cardiovascular Institute, UCL Institute of Cardiovascular Science and NIHR University College London Hospitals Biomedical Research Centre, London, UK
      name:The Hatter Cardiovascular Institute, UCL Institute of Cardiovascular Science and NIHR University College London Hospitals Biomedical Research Centre, London, UK
      name:The Hatter Cardiovascular Institute, UCL Institute of Cardiovascular Science and NIHR University College London Hospitals Biomedical Research Centre, London, UK
      name:Department of General Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands
      name:The Hatter Cardiovascular Institute, UCL Institute of Cardiovascular Science and NIHR University College London Hospitals Biomedical Research Centre, London, UK
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