Cited by 297Fibroblast Growth Factor ResearchPancreatic function and diabetesDiabetes Treatment and Management

Fibroblast Growth Factor 21 Controls Glycemia via Regulation of Hepatic Glucose Flux and Insulin Sensitivity

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Berglund, Eric D., Li, Candice Y., Bina, Holly A., Lynes, Sara E., Michael, M. Dodson, Shanafelt, Armen B., Kharitonenkov, Alexei, Wasserman, David H.·2009·Endocrinology

Abstract

Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator shown to improve glycemic control. However, the molecular and functional mechanisms underlying FGF21-mediated improvements in glycemic control are not completely understood. We examined FGF21 effects on insulin sensitivity and glucose fluxes upon chronic (daily injection for 8 d) and acute (6 h infusion) administration in ob/+ and ob/ob mice. Results show that chronic FGF21 ameliorated fasting hyperglycemia in ob/ob mice via increased glucose disposal and improved hepatic insulin sensitivity. Acute FGF21 suppressed hepatic glucose production, increased liver glycogen, lowered glucagon, and improved glucose clearance in ob/+ mice. These effects were blunted in ob/ob mice. Neither chronic nor acute FGF21 altered skeletal muscle or adipose tissue glucose uptake in either genotype. In conclusion, FGF21 has potent glycemic effects caused by hepatic changes in glucose flux and improved insulin sensitivity. Thus, these studies define mechanisms underlying anti-hyperglycemic actions of FGF21 and support its therapeutic potential.

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Crossref · 10.1210/en.2009-0221

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  • The decrease in plasma glucose occurs primarily through increased peripheral glucose disposal, although decreases in hepatic glucose production have also been observed.

    “This decrease in plasma glucose levels occurs primarily through increased peripheral glucose disposal41,56,65, although decreases in hepatic glucose production have also been observed66.”

    From Metabolic messengers: FGF21 (2021) · cites this paper as [66]

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Authors
Berglund, E. D., Li, C. Y., Bina, H. A., Lynes, S. E., Michael, M. D., Shanafelt, A. B., Kharitonenkov, A., & Wasserman, D. H.
Affiliations
  • National Institutes of Health (US)
  • Eli Lilly (United States) (US)
Corresponding author
Berglund, Eric D.
Venue
Endocrinology
Published
2009-05-21
Volume
150
Issue
9
Pages
4084-4093
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W1977516373
Cited by
297
References
35
Citations by year
2026: 6 · 2025: 14 · 2024: 15 · 2023: 18 · 2022: 18 · 2021: 11 · 2020: 19 · 2019: 15 · 2018: 13 · 2017: 20 · 2016: 19 · 2015: 23 · 2014: 27 · 2013: 21 · 2012: 26
FWCI
7.66
Type
journal article
Language
en
Open access
Locations
  • Endocrinology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Vanderbilt University
  • National Institutes of Health (DK-59637, U24 DK59637)
  • National Institute of Diabetes and Digestive and Kidney Diseases (U24DK59637, R01 DK-50277, T32DK07563, U24DK059637, R01DK050277, T32DK007563)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
FGF21, glycemic control, insulin sensitivity, hepatic glucose production, liver glycogen, glucagon, glucose clearance, fasting hyperglycemia, ob/ob mice, obesity, glucose disposal
MeSH terms
Animals, Blood Glucose, Fasting, Fibroblast Growth Factors, Glucagon, Insulin Resistance, Liver, Liver Glycogen, Male, Mice, Obese, Mice

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