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Effect of liraglutide on estimates of lipolysis and lipid oxidation in obese patients with stable coronary artery disease and newly diagnosed type 2 diabetes: A randomized trial
Author(s) -
Anholm Christian,
Kumarathurai Preman,
Samkani Amirsalar,
Pedersen Lene R.,
Boston Raymond C.,
Nielsen Olav W.,
Kristiansen Ole P.,
Fenger Mogens,
Madsbad Sten,
Sajadieh Ahmad,
Haugaard Steen B.
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.13761
Subject(s) - nefa , liraglutide , lipolysis , metformin , medicine , endocrinology , type 2 diabetes , insulin resistance , placebo , insulin , diabetes mellitus , adipose tissue , alternative medicine , pathology
Elevated levels of non‐esterified fatty acids (NEFA) play a role in insulin resistance, impaired beta‐cell function and they are a denominator of the abnormal atherogenic lipid profile that characterizes obese patients with type 2 diabetes (T2DM). We hypothesized that the GLP‐1 receptor agonist liraglutide, in combination with metformin, would reduce lipolysis. In a randomized, double‐blind, placebo‐controlled, cross‐over trial, 41 T2DM patients with coronary artery disease were randomized and treated with liraglutide‐metformin vs placebo‐metformin during 12‐ + 12‐week periods with a wash‐out period of at least 2 weeks before and between the intervention periods. NEFA kinetics were estimated using the Boston Minimal Model of NEFA metabolism, with plasma NEFA and glucose levels measured during a standard 180‐minute frequently sampled intravenous glucose tolerance test. Liraglutide‐metformin reduced estimates of lipolysis. Furthermore, placebo‐metformin increased estimates of lipid oxidation, while treatment with liraglutide eliminated this effect. We conclude that liraglutide exerts a clinically relevant reduction in estimates of lipolysis and lipid oxidation which is explained, in part, by improved insulin secretion, as revealed by an intravenous glucose tolerance test.