Circulating concentrations of GLP-1 are associated with coronary atherosclerosis in humans

Abstract

BackgroundGLP-1 is an incretine hormone which gets secreted from intestinal L-cells in response to nutritional stimuli leading to pancreatic insulin secretion and suppression of glucagon release. GLP-1 further inhibits gastric motility and reduces appetite which in conjunction improves postprandial glucose metabolism. Additional vasoprotective effects have been described for GLP-1 in experimental models. Despite these vasoprotective actions, associations between endogenous levels of GLP-1 and cardiovascular disease have yet not been investigated in humans which was the aim of the present study.MethodsGLP-1 serum levels were assessed in a cohort of 303 patients receiving coronary CT-angiography due to typical or atypical chest pain.ResultsGLP-1 was found to be positively associated with total coronary plaque burden in a fully adjusted model containing age, sex, BMI, hypertension, diabetes mellitus, smoking, triglycerides, LDL-C (low density lipoprotein cholesterol), hsCRP (high-sensitive C-reactive protein), and eGFR (estimated glomerular filtration rate) (OR: 2.53 (95% CI: 1.12 – 6.08; p = 0.03).ConclusionCirculating GLP-1 was found to be positivity associated with coronary atherosclerosis in humans. The clinical relevance of this observation needs further investigations.

GLP-1 Secretion Is Increased by Inflammatory Stimuli in an IL-6–Dependent Manner, Leading to Hyperinsulinemia and Blood Glucose Lowering

“…This does suggest an inflammation-dependent regulation of GLP-1 secretion to be present in humans. Consistently, others have reported circulating GLP-1 to be increased in states of chronic inflammatory disease, including the metabolic syndrome, coronary artery disease, or heart failure (36)(37)(38).…”

Does Glucagon-like Peptide-1 Ameliorate Oxidative Stress in Diabetes? Evidence Based on Experimental and Clinical Studies

“…The anti-inflammatory action of GLP-1 has recently gained considerable interest as endogenous GLP-1 has been found to be increased in patients with chronic inflammatory diseases, where OS is implicated, as systolic heart failure (bearing in mind that atherosclerosis can cause heart failure) and to be associated with coronary plaque burden in patients [18, 19, 70]. Moreover, GLP-1 intervention has been shown to decrease inflammation in both preclinical in vivo [21, 71-74] and clinical studies [75-77].…”

“…Lately, a beneficial role of GLP-1 in inflammation has gained increasing interest as reports have shown that it is released in an interleukin-6 (IL-6) dependent manner [16, 17]. GLP-1 levels has been found to be increased in both atherosclerosis [18] and patients with ventricular systolic dysfunction [19] indicating that GLP-1 could be induced as a compensatory mechanism during disease progression where OS may also play a role. Experimental [20-22] and clinical [23, 24] studies have indicated, that GLP-1 can reduce OS under a variety of conditions making it important to investigate if these effects are dependent or independent of GLP-1’s effects on glucose homeostasis (insulinotropic and glucose-lowering effects).…”

Increased plasma dipeptidyl peptidase-4 activities are associated with high prevalence of subclinical atherosclerosis in Chinese patients with newly diagnosed type 2 diabetes: A cross-sectional study

“…First, this study is an epidemiological cross-sectional study and somehow it fails to address the causal role of DPP4 in the pathogenesis of subclinical atherosclerosis which is needed to be elucidated by further prospective and basic investigation. Second, some other risk factors related to DPP4 activity such as glucagon-like peptide-1 (GLP-1) [50], which could also be associated with the development of subclinical atherosclerosis as well, was not evaluated in this study. Finally, the lack of a control group without diabetes is an important weakness of the study, although most common confounders have been adjusted in our analysis, additional unmeasured confounders in type 2 diabetes might also had some impact on the independent relationship between DPP4 activity and subclinical atherosclerosis, however, one of our previous studies conducted in subjects with normal glucose tolerance (NGT) for evaluating the proinflammatory role of DPP4 activity and subclinical atherosclerosis might partly make up this limitation, this study also proved the same independent relationship in NGT subjects with less potential confounders.…”