Journal
CELL METABOLISM
Volume 23, Issue 2, Pages 335-343Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2015.12.003
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Funding
- American Diabetes Association [7-13-JF-49]
- Edward Mallinckrodt Jr. Foundation
- National Institutes of Health (NIH) [R01DK106104, T32 GM067795, P30 DC004657]
- Fraternal Order of Eagles Diabetes Research Center
- University of Iowa Carver College of Medicine
- Novo Nordisk Foundation Center for Basic Metabolic Research
- Novo Nordisk scholarship
- Lundbeck Foundation
- Danish Research Council
- Novo Nordisk Foundation
- NNF Center for Basic Metabolic Research [Gillum Group] Funding Source: researchfish
- Novo Nordisk Fonden [NNF15SA0018486, NNF14OC0009525] Funding Source: researchfish
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The liver is an important integrator of nutrient metabolism, yet no liver-derived factors regulating nutrient preference or carbohydrate appetite have been identified. Here we show that the liver regulates carbohydrate intake through production of the hepatokine fibroblast growth factor 21 (FGF21), which markedly suppresses consumption of simple sugars, but not complex carbohydrates, proteins, or lipids. Genetic loss of FGF21 in mice increases sucrose consumption, whereas acute administration or overexpression of FGF21 suppresses the intake of both sugar and non-caloric sweeteners. FGF21 does not affect chorda tympani nerve responses to sweet tastants, instead reducing sweet-seeking behavior and meal size via neurons in the hypothalamus. This liver-to-brain hormonal axis likely represents a negative feedback loop as hepatic FGF21 production is elevated by sucrose ingestion. We conclude that the liver functions to regulate macronutrient-specific intake by producing an endocrine satiety signal that acts centrally to suppress the intake of sweets.''
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