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Incretin physiology and its role in type 2 diabetes mellitus.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Svec, Frank |
| Copyright Year | 2010 |
| Abstract | Incretins are hormones that are released after ingestion of a meal and augment the secretion of insulin. Current research suggests that GLP-1 (glucagon-like peptide 1) is the most important. Their action is terminated by enzymes known as dipeptidyl peptidase-4 (DPP-4). The observation that the incretin response may be diminished in individuals with type 2 diabetes mellitus has led to advances in the management of this disease. Agents that act as incretin mimetics, such as exenatide and liraglutide, and DPP-4 inhibitors, such as sitagliptin phosphate and saxagliptin, improve glycated hemoglobin levels either as monotherapy or in combination with other agents. Importantly, these agents either lead to weight loss or are weight neutral and are associated with a low risk of hypoglycemia--properties that further contribute to their clinical utility. |
| File Format | PDF HTM / HTML |
| PubMed reference number | 20644202 |
| Journal | Medline |
| Volume Number | 110 |
| Issue Number | 7 |
| Alternate Webpage(s) | https://watermark.silverchair.com/s20.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAcUwggHBBgkqhkiG9w0BBwagggGyMIIBrgIBADCCAacGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMTaNb_VNMT6s9VzYjAgEQgIIBeFnIc3ZwWy29bLtwy6LAEYjE4I1ND7nqKg_VPSZ_IamH4UzPuzKgxtLGf6AhTasApI3TuPBrU0khW_lGc_1PVSA5FCQ6IS5PNwWYyF_iU5zpYlis6Unp6qqJrBWgLrJwVAnEJY9tRUoYWl4YF0m1wFsl6QzcXTlnQH6OGXmB8HA3qIUGJZy2Z2XYgYWmYEjw6Zrh28fblG-dFr6iQkvyF6fkI8DGjlE5PnG_srkGnalXJT3eWtrNrKMD6nR4e7LLIn1i1xsx7lPbJx6jjJ881GlzIdgebpyjpi94hp5L41J6tTxC9YCxlsHqpE_bczw8LbRvSA41033SoBYjDG0S5AIBY30Ei9kGjanWDWdoBAFFQiUOto6usIwkzCQOon_OjNUxknCn00z9Ljl3wXeZSyvnCaNgl4BUXlgbH7DraAswDbcudraxZGkJe7OQQS-trUnqa1VJmGmIG6dS83sUOtY6_cCQ5gNwYWnSoor0jWLu8BSzspdqFOU |
| Journal | The Journal of the American Osteopathic Association |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
