The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Genetic Deletion or Pharmacological Inhibition of Dipeptidyl Peptidase-4 Improves Cardiovascular Outcomes After Myocardial Infarction in Mice
Open accessAbstract
OBJECTIVE: Glucagon-like peptide-1 (7-36)amide (GLP-1) is cleaved by dipeptidyl peptidase-4 (DPP-4) to GLP-1 (9-36)amide. We examined whether chemical inhibition or genetic elimination of DPP-4 activity affects cardiovascular function in normoglycemic and diabetic mice after experimental myocardial infarction. RESEARCH DESIGN AND METHODS: Cardiac structure and function was assessed by hemodynamic monitoring and echocardiography in DPP-4 knockout (Dpp4−/−) mice versus wild-type (Dpp4+/+) littermate controls and after left anterior descending (LAD) coronary artery ligation–induced myocardial infarction (MI). Effects of sustained DPP-4 inhibition with sitagliptin versus treatment with metformin were ascertained after experimental MI in a high-fat diet–streptozotocin model of murine diabetes. Functional recovery from ischemia-reperfusion (I/R) injury was measured in isolated hearts from Dpp4−/− versus Dpp4+/+ littermates and from normoglycemic wild-type (WT) mice treated with sitagliptin or metformin. Cardioprotective signaling in the murine heart was examined by RT-PCR and Western blot analyses. RESULTS: Dpp4 −/− mice exhibited normal indexes of cardiac structure and function. Survival post-MI was modestly improved in normoglycemic Dpp4−/− mice. Increased cardiac expression of phosphorylated AKT (pAKT), pGSK3β, and atrial natriuretic peptide (ANP) was detected in the nonischemic Dpp4−/− heart, and HO-1, ANP, and pGSK3β proteins were induced in nonischemic hearts from diabetic mice treated with sitagliptin or metformin. Sitagliptin and metformin treatment of wild-type diabetic mice reduced mortality after myocardial infarction. Sitagliptin improved functional recovery after I/R injury ex vivo in WT mice with similar protection from I/R injury also manifest in hearts from Dpp4−/− versus Dpp4+/+ mice. CONCLUSIONS: Genetic disruption or chemical inhibition of DPP-4 does not impair cardiovascular function in the normoglycemic or diabetic mouse heart.
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Cites
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Cited by
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Cardiovascular Actions of Incretin-Based Therapies
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Metadata
- Authors
- Sauvé, M., Ban, K., Momen, M. A., Zhou, Y.-Q., Henkelman, R. M., Husain, M., & Drucker, D. J.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2010-01-22
- Volume
- 59
- Issue
- 4
- Pages
- 1063-1073
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2167522349
- Cited by
- 264
- References
- 44
- FWCI
- 22.68
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Sauvé, M., Ban, K., Momen, M. A., Zhou, Y.-Q., Henkelman, R. M., Husain, M., & Drucker, D. J. (2010). Genetic Deletion or Pharmacological Inhibition of Dipeptidyl Peptidase-4 Improves Cardiovascular Outcomes After Myocardial Infarction in Mice. Diabetes. https://doi.org/10.2337/db09-0955
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