ArticleFrontiers in endocrinology2022
Obesity-resistance of UCP1-deficient mice associates with sustained FGF21 sensitivity in inguinal adipose tissue.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Pharmacological administration of FGF21 reverses obesity through a parabrachial-projecting neuron population in the hindbrain.Cell reports · 2026Article
- Polyphenol Compound 18a Modulates UCP1-Dependent Thermogenesis to Counteract Obesity.Biomolecules · 2024Article
- Leaf Extract ofNutrients · 2023Article
- FGF21 has a sex-specific role in calorie-restriction-induced beiging of white adipose tissue in mice.Aging biology · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Metabolic diseases represent the major health burden of our modern society. With the need of novel therapeutic approaches, fibroblast growth factor 21 (FGF21) is a promising target, based on metabolic improvements upon FGF21 administration in mice and humans. Endogenous FGF21 serum levels, however, are increased during obesity-related diseases, suggesting the development of FGF21 resistance during obesity and thereby lowering FGF21 efficacy. In uncoupling protein 1 knockout (UCP1 KO) mice, however, elevated endogenous FGF21 levels mediate resistance against diet-induced obesity. Here, we show that after long-term high fat diet feeding (HFD), circulating FGF21 levels become similarly high in obese wildtype and obesity-resistant UCP1 KO mice, suggesting improved FGF21 sensitivity in UCP1 KO mice. To test this hypothesis, we injected FGF21 after long-term HFD and assessed the metabolic and molecular effects. The UCP1 KO mice lost weight directly upon FGF21 administration, whereas body weights of WT mice resisted weight loss in the initial phase of the treatment. The FGF21 treatment induced expression of liver
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