FGF21 and the Physiological Regulation of Macronutrient Preference.


Journal

Endocrinology
ISSN: 1945-7170
Titre abrégé: Endocrinology
Pays: United States
ID NLM: 0375040

Informations de publication

Date de publication:
01 03 2020
Historique:
received: 22 11 2019
accepted: 06 02 2020
pubmed: 13 2 2020
medline: 6 8 2020
entrez: 13 2 2020
Statut: ppublish

Résumé

The ability to respond to variations in nutritional status depends on regulatory systems that monitor nutrient intake and adaptively alter metabolism and feeding behavior during nutrient restriction. There is ample evidence that the restriction of water, sodium, or energy intake triggers adaptive responses that conserve existing nutrient stores and promote the ingestion of the missing nutrient, and that these homeostatic responses are mediated, at least in part, by nutritionally regulated hormones acting within the brain. This review highlights recent research that suggests that the metabolic hormone fibroblast growth factor 21 (FGF21) acts on the brain to homeostatically alter macronutrient preference. Circulating FGF21 levels are robustly increased by diets that are high in carbohydrate but low in protein, and exogenous FGF21 treatment reduces the consumption of sweet foods and alcohol while alternatively increasing the consumption of protein. In addition, while control mice adaptively shift macronutrient preference and increase protein intake in response to dietary protein restriction, mice that lack either FGF21 or FGF21 signaling in the brain fail to exhibit this homeostatic response. FGF21 therefore mediates a unique physiological niche, coordinating adaptive shifts in macronutrient preference that serve to maintain protein intake in the face of dietary protein restriction.

Identifiants

pubmed: 32047920
pii: 5734531
doi: 10.1210/endocr/bqaa019
pmc: PMC7053867
pii:
doi:

Substances chimiques

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

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK047348
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK105032
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM104940
Pays : United States
Organisme : NIDDK NIH HHS
ID : F32 DK115137
Pays : United States

Informations de copyright

© Endocrine Society 2020.

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Auteurs

Cristal M Hill (CM)

Pennington Biomedical Research Center, Baton Rouge, LA.

Emily Qualls-Creekmore (E)

Pennington Biomedical Research Center, Baton Rouge, LA.

Hans-Rudolf Berthoud (HR)

Pennington Biomedical Research Center, Baton Rouge, LA.

Paul Soto (P)

Pennington Biomedical Research Center, Baton Rouge, LA.

Sangho Yu (S)

Pennington Biomedical Research Center, Baton Rouge, LA.

David H McDougal (DH)

Pennington Biomedical Research Center, Baton Rouge, LA.

Heike Münzberg (H)

Pennington Biomedical Research Center, Baton Rouge, LA.

Christopher D Morrison (CD)

Pennington Biomedical Research Center, Baton Rouge, LA.

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