Premium
Endogenous glucagon‐like peptide‐1 system response is impaired during ST‐elevation myocardial infarction in type 2 diabetes patients
Author(s) -
ElbazGreener Gabby,
Bloch Olga,
Kumets Ilya,
Blatt Alex,
Rapoport Micha J.
Publication year - 2019
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.13490
Subject(s) - medicine , myocardial infarction , type 2 diabetes , percutaneous coronary intervention , cardiology , unstable angina , endogeny , diabetes mellitus , angina , dipeptidyl peptidase 4 , glucagon like peptide 1 , endocrinology
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.