The DOI matches its Crossref record; 175 of the 175 references it cites were found in a registry or an index.
Enhancing Incretin Action for the Treatment of Type 2 Diabetes
Open accessAbstract
OBJECTIVE—To examine the mechanisms of action, therapeutic potential, and challenges inherent in the use of incretin peptides and dipeptidyl peptidase-IV (DPP-IV) inhibitors for the treatment of type 2 diabetes. RESEARCH DESIGN AND METHODS—The scientific literature describing the biological importance of incretin peptides and DPP-IV inhibitors in the control of glucose homeostasis has been reviewed, with an emphasis on mechanisms of action, experimental diabetes, human physiological experiments, and short-term clinical studies in normal and diabetic human subjects. RESULTS—Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) exert important effects on β-cells to stimulate glucose-dependent insulin secretion. Both peptides also regulate β-cell proliferation and cytoprotection. GLP-1, but not GIP, inhibits gastric emptying, glucagon secretion, and food intake. The glucose-lowering actions of GLP-1, but not GIP, are preserved in subjects with type 2 diabetes. However, native GLP-1 is rapidly degraded by DPP-IV after parenteral administration; hence, degradation-resistant, long-acting GLP-1 receptor (GLP-1R) agonists are preferable agents for the chronic treatment of human diabetes. Alternatively, inhibition of DPP-IV–mediated incretin degradation represents a complementary therapeutic approach, as orally available DPP-IV inhibitors have been shown to lower glucose in experimental diabetic models and human subjects with type 2 diabetes. CONCLUSIONS—GLP-1R agonists and DPP-IV inhibitors have shown promising results in clinical trials for the treatment of type 2 diabetes. The need for daily injections of potentially immunogenic GLP-1–derived peptides and the potential for unanticipated side effects with chronic use of DPP-IV inhibitors will require ongoing scrutiny of the risk-benefit ratio for these new therapies as they are evaluated in the clinic.
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Cites
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Cited by
Kendall, D. M., Riddle, M. C., Rosenstock, J., Zhuang, D., Kim, D. D., Fineman, M. S., & Baron, A. D. (2005) · Diabetes Care · doi:10.2337/diacare.28.5.1083 · Cited by 1,177
Heine, R. J., Van Gaal, L. F., Johns, D., Mihm, M. J., Widel, M. H., Brodows, R. G., & for the GWAA Study Group* (2005) · Annals of Internal Medicine · doi:10.7326/0003-4819-143-8-200510180-00006 · Cited by 795
Gastric Bypass for Obesity: Mechanisms of Weight Loss and Diabetes Resolution
Cummings, D. E., Overduin, J., & Foster-Schubert, K. E. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0433 · Cited by 503
DeFronzo, R. A., Hissa, M. N., Garber, A. J., Luiz Gross, J., Yuyan Duan, R., Ravichandran, S., Chen, R. S., & for the Saxagliptin 014 Study Group (2009) · Diabetes Care · doi:10.2337/dc08-1984 · Cited by 416
Butterfield, D. A., Di Domenico, F., & Barone, E. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.06.010 · Cited by 402
Metadata
- Authors
- Drucker, D. J.
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2003-10-01
- Volume
- 26
- Issue
- 10
- Pages
- 2929-2940
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W2108771199
- Cited by
- 579
- References
- 175
- FWCI
- 20.63
- Type
- journal article
- Language
- en
- Open access
- bronze
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