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Effect of liraglutide on dietary lipid‐induced insulin resistance in humans

Effect of liraglutide on dietary lipid‐induced insulin resistance in humans INTRODUCTIONInsulin resistance is closely linked to a variety of conditions, including dyslipidaemia, hyperglycaemia, hypertension, inflammation and endothelial dysfunction. It can be rapidly induced by high‐fat Western diets in the absence of significant weight gain. Ingestion of high‐fat meals leads to postprandial rises in triglyceride‐rich lipoproteins and spillover release of fatty acids to adipose tissue, skeletal muscle and liver, interfering with insulin action on glucose metabolism. Fatty acids also impair vasodilatory action of insulin in the microvasculature, diminishing insulin delivery to skeletal muscle.Given the above, reducing postprandial lipid excursions may be an important strategy to prevent and/or reverse high‐fat‐diet‐induced insulin resistance. Glucagon‐like peptide 1 receptor (GLP‐1R) agonists decrease fasting and postprandial glucose concentrations through multiple mechanisms, including delayed gastric emptying, increased glucose‐induced insulin secretion, diminished glucagon secretion and increased satiety. Several of these same mechanisms and additional effects, such as reduction of intestinal apolipoprotein production and chylomicron movement into the lymph, have been implicated in the reduction of postprandial triglyceride‐rich lipoproteins by GLP‐1R agonists.Our recent studies with GLP‐1R agonists support these concepts; both a single dose and a 10‐day treatment with exenatide prior to high‐fat meals were found to markedly suppress typical postprandial rises in triglycerides, remnant lipoproteins and apolipoproteins, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetes Obesity & Metabolism Wiley

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References (43)

Publisher
Wiley
Copyright
© 2018 John Wiley & Sons Ltd
ISSN
1462-8902
eISSN
1463-1326
DOI
10.1111/dom.13037
pmid
28605158
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONInsulin resistance is closely linked to a variety of conditions, including dyslipidaemia, hyperglycaemia, hypertension, inflammation and endothelial dysfunction. It can be rapidly induced by high‐fat Western diets in the absence of significant weight gain. Ingestion of high‐fat meals leads to postprandial rises in triglyceride‐rich lipoproteins and spillover release of fatty acids to adipose tissue, skeletal muscle and liver, interfering with insulin action on glucose metabolism. Fatty acids also impair vasodilatory action of insulin in the microvasculature, diminishing insulin delivery to skeletal muscle.Given the above, reducing postprandial lipid excursions may be an important strategy to prevent and/or reverse high‐fat‐diet‐induced insulin resistance. Glucagon‐like peptide 1 receptor (GLP‐1R) agonists decrease fasting and postprandial glucose concentrations through multiple mechanisms, including delayed gastric emptying, increased glucose‐induced insulin secretion, diminished glucagon secretion and increased satiety. Several of these same mechanisms and additional effects, such as reduction of intestinal apolipoprotein production and chylomicron movement into the lymph, have been implicated in the reduction of postprandial triglyceride‐rich lipoproteins by GLP‐1R agonists.Our recent studies with GLP‐1R agonists support these concepts; both a single dose and a 10‐day treatment with exenatide prior to high‐fat meals were found to markedly suppress typical postprandial rises in triglycerides, remnant lipoproteins and apolipoproteins,

Journal

Diabetes Obesity & MetabolismWiley

Published: Jan 1, 2018

Keywords: ; ;

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