FGF21 Is a Hormonal Mediator of the Human "Thrifty" Metabolic Phenotype.
Journal
Diabetes
ISSN: 1939-327X
Titre abrégé: Diabetes
Pays: United States
ID NLM: 0372763
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
23
06
2018
accepted:
17
09
2018
pubmed:
28
9
2018
medline:
6
8
2019
entrez:
28
9
2018
Statut:
ppublish
Résumé
Fibroblast growth factor 21 (FGF21) regulates energy expenditure (EE) and influences weight change during low-protein overfeeding in rodent models. The change in EE after a low-protein overfeeding diet is a predictor of weight change in humans and a feature of the "thrifty" metabolic phenotype. However, there are no studies showing an association between circulating FGF21 and diet-related EE in humans. We assessed the changes in plasma FGF21 concentrations after 24 h of seven dietary interventions with different macronutrient content while in a whole-room indirect calorimeter in 64 healthy subjects with normal glucose regulation. Plasma FGF21 concentration consistently increased by threefold only after the two low-protein (3%) overfeeding diets, one high in carbohydrate (75%) and the other high in fat (46%), with larger increases in FGF21 being associated with greater increases in 24-h EE. Subjects with smaller increases in FGF21 after the low-protein high-fat diet gained more weight after 6 months in free-living conditions. Therefore, the individual predisposition to weight gain over time can be assessed by 24-h overfeeding a low-protein diet and measurements of plasma FGF21 concentrations. Individuals with a blunted FGF21 response to a low-protein diet have a thrifty metabolism and are at risk for future weight gain.
Identifiants
pubmed: 30257977
pii: db18-0696
doi: 10.2337/db18-0696
pmc: PMC6341300
doi:
Substances chimiques
fibroblast growth factor 21
0
Fibroblast Growth Factors
62031-54-3
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Langues
eng
Pagination
318-323Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2018 by the American Diabetes Association.
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