Endogenous glucagon‐like peptide‐1 system response is impaired during ST‐elevation myocardial infarction in type 2 diabetes patients
We previously demonstrated increased glucagon‐like peptide‐1 (GLP‐1) secretion during acute ST elevation myocardial infarction (STEMI) in non‐diabetic (ND) patients. Whether the endogenous GLP‐1 system response is different in patients with type 2 diabetes (T2D) during STEMI is unknown. Patients wit...
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Published in | Diabetes, obesity & metabolism Vol. 21; no. 1; pp. 194 - 198 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.01.2019
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | We previously demonstrated increased glucagon‐like peptide‐1 (GLP‐1) secretion during acute ST elevation myocardial infarction (STEMI) in non‐diabetic (ND) patients. Whether the endogenous GLP‐1 system response is different in patients with type 2 diabetes (T2D) during STEMI is unknown. Patients with STEMI (20 ND, 13 T2D) and 3 control groups (non‐STEMI [14 ND, 13 T2D], stable angina pectoris [SAP] [8 ND, 10 T2D] patients and healthy subjects) (n = 25) were studied. Plasma levels of total and active GLP‐1 and soluble dipeptidyl peptidase‐4 (sDPP4) were estimated by enzyme‐linked immunosorbent assay on admission and at 24 and 48 hours after percutaneous coronary intervention in all patients. Sharply elevated levels of total and active GLP‐1 were found in ND STEMI patients at 24 h (P < 0.05 and P < 0.005, respectively), but not in T2D STEMI patients. All patients demonstrated decreased sDPP4 levels compared with healthy controls (P < 0.0005) accompanied by increased active/total GLP‐1 ratio regardless of their ischemic state. These data demonstrate that T2D patients fail to further upregulate their endogenous GLP‐1 system during STEMI. This may underlie their worse cardiovascular outcome. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1462-8902 1463-1326 1463-1326 |
DOI: | 10.1111/dom.13490 |