Postprandial levels of GLP-1, GIP and glucagon after 2 years of weight loss with a Paleolithic diet: a randomised controlled trial in healthy obese women.


Journal

European journal of endocrinology
ISSN: 1479-683X
Titre abrégé: Eur J Endocrinol
Pays: England
ID NLM: 9423848

Informations de publication

Date de publication:
01 Jun 2019
Historique:
received: 05 02 2019
accepted: 30 04 2019
pubmed: 3 5 2019
medline: 31 5 2019
entrez: 3 5 2019
Statut: ppublish

Résumé

Objective To investigate how weight loss by different diets impacts postprandial levels of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon. Methods In this single-centre, parallel group 2-year trial, 70 healthy postmenopausal obese women were randomised to the Paleolithic diet or a healthy control diet based on Nordic Nutrition Recommendations. Both diets were without calorie restriction. The primary outcome was the change in fat mass. Here, secondary analyses on GLP-1, GIP and glucagon measured during an OGTT are described. Results In the Paleolithic diet group, mean weight loss compared to baseline was 11% at 6 months and 10% at 24 months. In the control diet group, mean weight loss was 6% after 6 and 24 months (P = 0.0001 and P = 0.049 for the comparison between groups at 6 and 24 months respectively). Compared to baseline, the mean incremental area under the curve (iAUC) for GLP-1 increased by 34 and 45% after 6 and 24 months in the Paleolithic diet group and increased by 59% after 24 months in the control diet group. The mean iAUC for GIP increased only in the Paleolithic diet group. The area under the curve (AUC) for glucagon increased during the first 6 months in both groups. The fasting glucagon increase correlated with the β-hydroxybutyrate increase. Conclusions Weight loss caused an increase in postprandial GLP-1 levels and a further rise occurred during weight maintenance. Postprandial GIP levels increased only after the Paleolithic diet. Reduced postprandial glucagon suppression may be caused by a catabolic state.

Identifiants

pubmed: 31042670
doi: 10.1530/EJE-19-0082
pii: EJE-19-0082.R1
pmc: PMC6528411
doi:
pii:

Substances chimiques

Biomarkers 0
Gastric Inhibitory Polypeptide 59392-49-3
Glucagon-Like Peptide 1 89750-14-1
Glucagon 9007-92-5

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

417-427

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Auteurs

Julia Otten (J)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Mats Ryberg (M)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Caroline Mellberg (C)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Tomas Andersson (T)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Elin Chorell (E)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Bernt Lindahl (B)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

Christel Larsson (C)

Department of Food and Nutrition, and Sport Science, University of Gothenburg, Gothenburg, Sweden.

Jens Juul Holst (JJ)

NNF Center for Basal Metabolic Research and Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.

Tommy Olsson (T)

Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.

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Classifications MeSH