Higher fasting plasma FGF21 concentration is associated with lower ad libitum soda consumption in humans.
FGF21
ad libitum energy intake
macronutrient intake
soda intake
sugar consumption
Journal
The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027
Informations de publication
Date de publication:
04 10 2021
04 10 2021
Historique:
received:
13
02
2021
accepted:
28
05
2021
pubmed:
24
6
2021
medline:
26
10
2021
entrez:
23
6
2021
Statut:
ppublish
Résumé
The hepatokine fibroblast growth factor 21 (FGF21) influences eating behavior and sugar consumption in rodent models. However, whether circulating FGF21 concentration is associated with food and soda intake in humans is still unclear. We investigated whether fasting plasma FGF21 concentration is associated with objective measures of ad libitum food intake and soda consumption. Healthy individuals [n = 109; 69 men, aged 34 ± 10 y; BMI (kg/m2): 30.4 ± 7.7; body fat by DXA: 30.5% ± 8.9%] with available plasma for hormonal measurements participated in an inpatient cohort study to objectively quantify ad libitum food and soda intake for 3 d using an automated and reproducible vending machine paradigm. Fasting plasma FGF21 concentration was measured by ELISA prior to ad libitum feeding. Fasting FGF21 concentration was inversely associated with daily soda intake (R = -0.22, P = 0.02 adjusted for demographics and anthropometrics), such that an interindividual difference of 200 pg/mL was associated with an average lower soda consumption by 68 kcal/d. Conversely, no associations were observed with total daily energy intake or macronutrient intake (all P > 0.17). Higher plasma fasting FGF21 concentration is associated with lower ad libitum soda intake. Although this inverse correlation does not imply causation, the present results support the putative role of FGF21 in the reward pathways regulating sugar consumption in humans. This trial was registered at www.clinicaltrials.gov as NCT00342732.
Sections du résumé
BACKGROUND
The hepatokine fibroblast growth factor 21 (FGF21) influences eating behavior and sugar consumption in rodent models. However, whether circulating FGF21 concentration is associated with food and soda intake in humans is still unclear.
OBJECTIVE
We investigated whether fasting plasma FGF21 concentration is associated with objective measures of ad libitum food intake and soda consumption.
METHODS
Healthy individuals [n = 109; 69 men, aged 34 ± 10 y; BMI (kg/m2): 30.4 ± 7.7; body fat by DXA: 30.5% ± 8.9%] with available plasma for hormonal measurements participated in an inpatient cohort study to objectively quantify ad libitum food and soda intake for 3 d using an automated and reproducible vending machine paradigm. Fasting plasma FGF21 concentration was measured by ELISA prior to ad libitum feeding.
RESULTS
Fasting FGF21 concentration was inversely associated with daily soda intake (R = -0.22, P = 0.02 adjusted for demographics and anthropometrics), such that an interindividual difference of 200 pg/mL was associated with an average lower soda consumption by 68 kcal/d. Conversely, no associations were observed with total daily energy intake or macronutrient intake (all P > 0.17).
CONCLUSIONS
Higher plasma fasting FGF21 concentration is associated with lower ad libitum soda intake. Although this inverse correlation does not imply causation, the present results support the putative role of FGF21 in the reward pathways regulating sugar consumption in humans. This trial was registered at www.clinicaltrials.gov as NCT00342732.
Identifiants
pubmed: 34159373
pii: S0002-9165(22)00480-4
doi: 10.1093/ajcn/nqab204
pmc: PMC8488863
doi:
Substances chimiques
FGF21 protein, human
0
Fibroblast Growth Factors
62031-54-3
Banques de données
ClinicalTrials.gov
['NCT00342732']
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1518-1522Informations de copyright
Published by Oxford University Press on behalf of the American Society for Nutrition 2021.
Références
Hum Mol Genet. 2013 May 1;22(9):1895-902
pubmed: 23372041
Int J Obes (Lond). 2014 Feb;38(2):243-51
pubmed: 23736368
Cell Rep. 2018 Apr 10;23(2):327-336
pubmed: 29641994
Cell Metab. 2016 Feb 9;23(2):335-43
pubmed: 26724858
Am J Clin Nutr. 2019 Sep 1;110(3):593-604
pubmed: 31172178
Nature. 1963 Jan 5;197:79-80
pubmed: 13975629
Diabetes. 2014 Dec;63(12):4064-75
pubmed: 25024372
J Acad Nutr Diet. 2014 Mar;114(3):444-449
pubmed: 24321742
Mol Metab. 2014 Oct 08;4(1):51-7
pubmed: 25685689
Metabolism. 2018 May;82:65-71
pubmed: 29305947
Hepatology. 2010 Jun;51(6):1961-71
pubmed: 20301112
J Clin Endocrinol Metab. 2015 Aug;100(8):3011-20
pubmed: 26086330
Diabetes. 2020 Feb;69(2):181-192
pubmed: 31712321
Cell Rep. 2019 Jun 4;27(10):2934-2947.e3
pubmed: 31167139
Obesity (Silver Spring). 2019 May;27(5):691-699
pubmed: 31012296
Semin Cell Dev Biol. 2016 May;53:85-93
pubmed: 26428296
Diabetes. 2019 Feb;68(2):318-323
pubmed: 30257977
Cell Metab. 2016 Feb 9;23(2):344-9
pubmed: 26724861
J Endocrinol Invest. 2018 Jan;41(1):83-89
pubmed: 28741280
Cell Metab. 2017 May 2;25(5):1045-1053.e6
pubmed: 28467924
Mol Metab. 2016 Nov 16;6(1):22-29
pubmed: 28123934
Am J Clin Nutr. 1997 Apr;65(4 Suppl):1220S-1228S; discussion 1229S-1231S
pubmed: 9094926
Am J Clin Nutr. 2010 Feb;91(2):343-8
pubmed: 19923376
Diabetes. 2015 Nov;64(11):3680-9
pubmed: 26185280
Cell Metab. 2017 Apr 4;25(4):935-944.e4
pubmed: 28380381
Am J Clin Nutr. 2013 Jun;97(6):1395-402
pubmed: 23636237
Curr Obes Rep. 2020 Jun;9(2):121-135
pubmed: 32248352