Four weeks treatment with the GLP-1 receptor analogue liraglutide lowers liver fat and concomitantly circulating glucagon in individuals with overweight
Publikation: Bidrag til tidsskrift › Letter › Forskning › fagfællebedømt
We investigated the effect of pharmacologically induced weight loss on markers of glucagon resistance in individuals with overweight during treatment with the glucagon-like peptide-1 receptor agonist liraglutide. We performed an open-label study in 14 men with overweight (age 38 ± 11 years, BMI 32 ± 4 kg/m2) without simultaneously diabetes. Subjects were treated with liraglutide, initiated and titrated with 0.6 mg/day/week to reach the final dose of 3.0 mg/day. Subjects were examined at baseline, during titration (Week 4), after 2 weeks of steady state (Week 6) of final dosing of liraglutide and 3 weeks after discontinuation of liraglutide (follow-up). Study participants lost 3.3 ± 1.9 kg (3%) total body weight during the first 4 weeks of treatment with liraglutide. Simultaneously, liver fat content decreased from 12.4 ± 11.6% to 10.2 ± 11.1%, p = 0.025, whereas fat content in the spleen and subcutaneous tissue was unaltered. Markers of glucagon resistance, including plasma glucagon and the glucagon-alanine-index, also decreased significantly during treatment, but total and individual plasma amino acid concentrations did not. Insulin resistance (HOMA-IR) was unchanged during treatment, whereas insulin clearance increased. Treatment with the GLP-1 receptor analogue liraglutide decreased liver fat content, and simultaneously attenuated glucagon concentrations and the glucagon-alanine index in individuals with overweight without diabetes.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | International Journal of Obesity |
| Vol/bind | 46 |
| Udgave nummer | 11 |
| Sider (fra-til) | 2058–2062 |
| Antal sider | 8 |
| ISSN | 0307-0565 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
NJWA has received speaker fees from MSD and Mercodia and research support from Novo Nordisk A/S, Janssen Pharmaceuticals and Mercodia.CFD has received consultancy/lecture fees from Boehringer Ingelheim, Lilly, Merck/MSD, Novo Nordisk and Novartis. SM has received research grants from Novo Nordisk and Boehringer Ingelheim; lecture fees from AstraZeneca, Boehringer Ingelheim, Eli Lilly, Merck Sharp & Dohme, Novartis, Novo Nordisk and Sanofi Aventis; and is a member of advisory boards of AstraZeneca, Boehringer Ingelheim, Eli Lilly, Intarcia Therapeutics, Johnson & Johnson, Merck Sharp & Dohme, Novartis, Novo Nordisk and Sanofi Aventis. JJH has served on advisory panels for GlaxoSmithKline, Novo Nordisk, Zealand Pharma, AstraZeneca, MSD, Intarcia and Hanmi and acts as a consultant for Novo Nordisk, and has received research support from Merck, Sharp & Dohme. All other authors have nothing to disclosure.
Funding Information:
The study was supported by unrestricted grants from the Novo Nordisk Foundation and Rigshospitalet. NJWA is supported by NNF Excellence Emerging Investigator Grant – Endocrinology and Metabolism (Application No. NNF19OC0055001), EFSD Future Leader Award (NNF21SA0072746) and DFF Sapere Aude (1052-00003B). Novo Nordisk Foundation Center for Protein Research is supported financially by the Novo Nordisk Foundation (Grant agreement NNF14CC0001). The funders were not involved in the design of the study; the collection, analysis, and interpretation of data; writing the report; and did not impose any restrictions regarding the publication of the report.
Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Nature Limited.
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