Liraglutide treatment improves postprandial lipid metabolism and cardiometabolic risk factors in humans with adequately controlled type 2 diabetes : A single-centre randomized controlled study

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Pysyväisosoite

http://hdl.handle.net/10138/308850

Lähdeviite

Matikainen , N , Söderlund , S , Björnson , E , Pietiläinen , K , Hakkarainen , A , Lundbom , N , Taskinen , M-R & Boren , J 2019 , ' Liraglutide treatment improves postprandial lipid metabolism and cardiometabolic risk factors in humans with adequately controlled type 2 diabetes : A single-centre randomized controlled study ' , Diabetes, obesity and metabolism , vol. 21 , no. 1 , pp. 84-94 . https://doi.org/10.1111/dom.13487

Julkaisun nimi: Liraglutide treatment improves postprandial lipid metabolism and cardiometabolic risk factors in humans with adequately controlled type 2 diabetes : A single-centre randomized controlled study
Tekijä: Matikainen, Niina; Söderlund, Sanni; Björnson, Elias; Pietiläinen, Kirsi; Hakkarainen, Antti; Lundbom, Nina; Taskinen, Marja-Riitta; Boren, Jan
Tekijän organisaatio: Clinicum
Diabetes and Obesity Research Program
Research Programs Unit
Department of Medicine
Endokrinologian yksikkö
University of Helsinki
HUS Abdominal Center
Faculty of Medicine
HUS Internal Medicine and Rehabilitation
Department of Diagnostics and Therapeutics
HUS Medical Imaging Center
Marja-Riitta Taskinen Research Group
HUS Heart and Lung Center
Päiväys: 2019-01
Kieli: eng
Sivumäärä: 11
Kuuluu julkaisusarjaan: Diabetes, obesity and metabolism
ISSN: 1462-8902
DOI-tunniste: https://doi.org/10.1111/dom.13487
URI: http://hdl.handle.net/10138/308850
Tiivistelmä: Aims Patients with type 2 diabetes and non-alcoholic fatty liver disease (NAFLD) exhibit considerable residual risk for cardiovascular disease (CVD). There is, therefore, increasing interest in targeting postprandial lipid metabolism and remnant cholesterol. Treatment with the glucagon-like peptide 1 (GLP-1) analogue liraglutide reduces CVD risk by mechanisms that remain unexplained in part. Here we investigated the effects of liraglutide intervention on ectopic fat depots, hepatic lipogenesis and fat oxidation, postprandial lipid metabolism and glycaemia in humans with type 2 diabetes. Methods The effect of liraglutide was investigated in 22 patients with adequately controlled type 2 diabetes. Patients were randomly allocated, in a single-blind fashion, to either liraglutide 1.8 mg or placebo once daily for 16 weeks. Because liraglutide is known to promote weight loss, the study included dietary counselling to achieve similar weight loss in the liraglutide and placebo groups. Cardiometabolic responses to a high-fat mixed meal were measured before and at the end of the liraglutide intervention. Results Weight loss at Week 16 was similar between the groups: -2.4 kg (-2.5%) in the liraglutide group and -2.1 kg (-2.2%) in the placebo group. HBA1c improved by 6.4 mmol/mol (0.6%) in the liraglutide group (P = 0.005). Liver fat decreased in both groups, by 31% in the liraglutide group and by 18% in the placebo group, but there were no significant changes in the rate of hepatic de novo lipogenesis or beta-hydroxybutyrate levels, a marker of fat oxidation. We observed significant postprandial decreases in triglycerides only in plasma, chylomicrons and VLDL, and remnant particle cholesterol after treatment in the liraglutide group. Fasting and postprandial apoCIII concentrations decreased after liraglutide intervention and these changes were closely related to reduced glycaemia. In relative importance analysis, approximately half of the changes in postprandial lipids were explained by reductions in apoCIII concentrations, whereas less than 10% of the variation in postprandial lipids was explained by reductions in weight, glycaemic control, liver fat or postprandial insulin responses. Conclusions Intervention with liraglutide for 16 weeks produces multiple improvements in cardiometabolic risk factors that were not seen in the placebo group, despite similar weight loss. Of particular importance was a marked reduction in postprandial atherogenic remnant particles. The underlying mechanism may be improved glycaemic control, which leads to reduced expression of apoCIII, a key regulator of hypertriglyceridaemia in hyperglycaemic patients.
Avainsanat: apolipoprotein C3
atherogenic dyslipidaemia
de novo lipogenesis
GLP-1-agonist
liraglutide
liver fat
postprandial lipids
remnant lipoproteins
FATTY LIVER-DISEASE
REMNANT CHOLESTEROL
VILDAGLIPTIN THERAPY
RECEPTOR AGONISTS
TRIGLYCERIDE
LIPOPROTEINS
METFORMIN
EXENATIDE
PARTICLES
PLACEBO
3121 General medicine, internal medicine and other clinical medicine
Vertaisarvioitu: Kyllä
Pääsyrajoitteet: openAccess
Rinnakkaistallennettu versio: publishedVersion


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