title: Plasma levels of glucagon like peptide-1 associate with diastolic function in elderly men.
abstract: OBJECTIVE
  Congestive heart failure is a major cause of morbidity and mortality in diabetes. Besides the glycaemic effects of glucagon-like peptide 1 (GLP-1) mimetics, their effects on the heart are of interest.
  
  
  METHODS
  We aimed to investigate longitudinal relationships between plasma levels of fasting GLP-1 (fGLP-1), 60-min oral glucose tolerance test-stimulated GLP-1 levels (60GLP-1), and the dynamic GLP-1 response after oral glucose tolerance test (ΔGLP-1 = 60GLP-1 - fGLP-1) and incidence of hospitalized congestive heart failure, during a follow-up time of a maximum of 9.8 years in 71-year-old men. We also investigated, cross-sectionally, the association between GLP-1 and left ventricular function as estimated by echocardiography. R: During the follow-up period, 16 of 290 participants with normal glucose tolerance experienced a congestive heart failure event (rate 0.7/100 person-years at risk), as did eight of 136 participants (rate 0.8/100 person-years at risk) with impaired glucose tolerance and nine of 72 participants (rate 1.7/100 person-years at risk) with Type 2 diabetes mellitus. Although GLP-1 concentrations did not predict congestive heart failure (fGLP-1: HR 0.98, 95% CI 0.4-2.4; 60GLP-1: HR 1.1, 95% CI 0.4-2.6; ΔGLP-1: HR 0.9, 95% CI 0.3-2.3), there was an association between left ventricular diastolic function (E/A ratio) and fGLP-1 (r = 0.19, P = 0.001), 60GLP-1 (r = 0.20, P < 0.001) and ΔGLP-1 (r = 0.18, P = 0.004). There was a lack of differences in plasma levels of GLP-1 between the groups with Type 2 diabetes and normal glucose tolerance.
  
  
  CONCLUSIONS
  There were no longitudinal associations between GLP-1 levels and incidence of hospitalization for congestive heart failure. However, without any causality proven, GLP-1 levels did correlate, cross-sectionally, with left ventricular diastolic function in this cohort, suggesting that pathways including GLP-1 might be involved in the regulation of cardiac diastolic function.
authors.affiliation: Department of Clinical Science and Education, Unit for Diabetes Research, Södersjukhuset AB, Sweden. david.nathanson@sodersjukhuset.se
authors.forename: D
authors.initials: D
authors.lastname: Nathanson
authors.forename: B
authors.initials: B
authors.lastname: Zethelius
authors.forename: C
authors.initials: C
authors.lastname: Berne
authors.forename: L
authors.initials: L
authors.lastname: Lind
authors.forename: B
authors.initials: B
authors.lastname: Andrén
authors.forename: E
authors.initials: E
authors.lastname: Ingelsson
authors.forename: J J
authors.initials: JJ
authors.lastname: Holst
authors.forename: T
authors.initials: T
authors.lastname: Nyström
mesh_terms: D000369:Aged, 80 and over; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology / Q000503:physiopathology; D003971:Diastole / Q000502:physiology*; D005215:Fasting / Q000502:physiology; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D015309:Glucose Clamp Technique; D005951:Glucose Tolerance Test; D006333:Heart Failure / Q000097:blood* / Q000401:mortality / Q000503:physiopathology; D006801:Humans; D008297:Male; D011446:Prospective Studies; D016019:Survival Analysis
chemical_list: D052216:Glucagon-Like Peptide 1