Differential effects of protein intake versus intake of a defined oligopeptide on FGF-21 in obese human subjects in vivo.


Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
02 2021
Historique:
received: 14 04 2020
revised: 13 05 2020
accepted: 07 06 2020
pubmed: 1 7 2020
medline: 24 8 2021
entrez: 1 7 2020
Statut: ppublish

Résumé

FGF-21 is described as a powerful metabolic regulator with beneficial effects including glucose-lowering and improvement of insulin sensitivity without hypoglycaemia. On the other hand, FGF-21 is activated when muscle and other tissues are stressed by external effects or internal cellular pathogens that lead to shortcomings in metabolic balance. Previous results suggested that FGF-21 could be a promising target to develop future metabolic therapeutics. The present study was performed to gain deeper insight into the regulation of FGF-21 by protein metabolism in obese human subjects. FGF-21 serum concentrations were measured in a cohort of n = 246 obese humans ± type 2 diabetes mellitus (T2DM) (median age 53.0 [46.0; 60.0] years and BMI 40.43 [35.11; 47.24] kg/m In the cohort analysis, FGF-21 serum concentrations were significant lower with higher protein intake in obese subjects without T2DM but not in obese subjects with T2DM. Furthermore, relative methionine intake was inversely related to FGF-21. While global protein intake in obesity was inversely associated with FGF-21, incubation of HepG2 cells with a β-casein oligopeptide increased FGF-21 expression in vitro. This stimulatory effect was also present in vivo, since in the clinical intervention study treatment of obese subjects with the β-casein oligopeptide for 8 weeks significantly increased FGF-21 serum levels from W0 = 23.86 pg/mL to W8 = 30.54 pg/mL (p < 0.001), while no increase was found for placebo. While the total nutritional protein intake is inversely associated with FGF-21 serum levels, a purified and well characterised oligopeptide is able to induce FGF-21 serum levels in humans. These findings suggest a differential role of various components of protein metabolism on FGF-21, rather than this factor being solely a sensor of total nutritional protein intake.

Sections du résumé

BACKGROUND
FGF-21 is described as a powerful metabolic regulator with beneficial effects including glucose-lowering and improvement of insulin sensitivity without hypoglycaemia. On the other hand, FGF-21 is activated when muscle and other tissues are stressed by external effects or internal cellular pathogens that lead to shortcomings in metabolic balance. Previous results suggested that FGF-21 could be a promising target to develop future metabolic therapeutics.
PURPOSE
The present study was performed to gain deeper insight into the regulation of FGF-21 by protein metabolism in obese human subjects.
METHODS
FGF-21 serum concentrations were measured in a cohort of n = 246 obese humans ± type 2 diabetes mellitus (T2DM) (median age 53.0 [46.0; 60.0] years and BMI 40.43 [35.11; 47.24] kg/m
MAIN FINDINGS
In the cohort analysis, FGF-21 serum concentrations were significant lower with higher protein intake in obese subjects without T2DM but not in obese subjects with T2DM. Furthermore, relative methionine intake was inversely related to FGF-21. While global protein intake in obesity was inversely associated with FGF-21, incubation of HepG2 cells with a β-casein oligopeptide increased FGF-21 expression in vitro. This stimulatory effect was also present in vivo, since in the clinical intervention study treatment of obese subjects with the β-casein oligopeptide for 8 weeks significantly increased FGF-21 serum levels from W0 = 23.86 pg/mL to W8 = 30.54 pg/mL (p < 0.001), while no increase was found for placebo.
CONCLUSION
While the total nutritional protein intake is inversely associated with FGF-21 serum levels, a purified and well characterised oligopeptide is able to induce FGF-21 serum levels in humans. These findings suggest a differential role of various components of protein metabolism on FGF-21, rather than this factor being solely a sensor of total nutritional protein intake.

Identifiants

pubmed: 32600859
pii: S0261-5614(20)30296-X
doi: 10.1016/j.clnu.2020.06.006
pii:
doi:

Substances chimiques

Caseins 0
Dietary Proteins 0
Oligopeptides 0
fibroblast growth factor 21 0
Fibroblast Growth Factors 62031-54-3

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

600-607

Informations de copyright

Copyright © 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Déclaration de conflit d'intérêts

Conflicts of interest No potential conflicts of interest relevant to this article were reported.

Auteurs

Daniela Fangmann (D)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Corinna Geisler (C)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Kristina Schlicht (K)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Katharina Hartmann (K)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Jana Köpke (J)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Anika Tiede (A)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Ute Settgast (U)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Kathrin Türk (K)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Dominik M Schulte (DM)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany.

Karina Altmann (K)

Max Rubner-Institute, Federal Research Institute of Nutrition and Food, Department of Safety and Quality of Milk and Fish Products, Kiel, 24103, Germany.

Ingrid Clawin-Rädecker (I)

Max Rubner-Institute, Federal Research Institute of Nutrition and Food, Department of Safety and Quality of Milk and Fish Products, Kiel, 24103, Germany.

Peter Ch Lorenzen (PC)

Max Rubner-Institute, Federal Research Institute of Nutrition and Food, Department of Safety and Quality of Milk and Fish Products, Kiel, 24103, Germany.

Stefan Schreiber (S)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany; Institute of Clinical Molecular Biology, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24118, Germany.

Karin Schwarz (K)

University of Kiel, Department of Food Technology, University of Kiel, Kiel, 24118, Germany.

Matthias Laudes (M)

Division of Endocrinology, Diabetes and Clinical Nutrition, Department of Internal Medicine 1, University Hospital Schleswig-Holstein, Campus Kiel, University of Kiel, Kiel, 24105, Germany. Electronic address: matthias.laudes@uksh.de.

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Classifications MeSH