FGF-21 as a novel metabolic regulator
Open accessAbstract
Diabetes mellitus is a major health concern, affecting more than 5% of the population. Here we describe a potential novel therapeutic agent for this disease, FGF-21, which was discovered to be a potent regulator of glucose uptake in mouse 3T3-L1 and primary human adipocytes. FGF-21-transgenic mice were viable and resistant to diet-induced obesity. Therapeutic administration of FGF-21 reduced plasma glucose and triglycerides to near normal levels in both ob/ob and db/db mice. These effects persisted for at least 24 hours following the cessation of FGF-21 administration. Importantly, FGF-21 did not induce mitogenicity, hypoglycemia, or weight gain at any dose tested in diabetic or healthy animals or when overexpressed in transgenic mice. Thus, we conclude that FGF-21, which we have identified as a novel metabolic factor, exhibits the therapeutic characteristics necessary for an effective treatment of diabetes.
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FGF21 stimulates uptake of glucose by adipocytes and inhibits production of glucose in the liver.
“In general, FGF21 stimulates the uptake of glucose by adipocytes and inhibits the production of glucose in the liver.”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Kharitonenkov et al., 2005
The Identification of FGF-21 in vitro bioactivity section reports that FGF-21 stimulated glucose uptake in mouse and human adipocytes. The Discussion proposes reduced glucagon secretion as a possible contributor to lower blood glucose, but does not establish that FGF-21 inhibits glucose production in the liver; that part of the claim is overstated. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFGF21 acts in the control of glucose and lipid homeostasis.
“FGF21 acts in the control of glucose and lipid homeostasis (Kharitonenkov et al., 2005).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Kharitonenkov et al., 2005
FGF21 appears to protect pancreatic β cells from cell death induced by glycotoxicity.
“In addition, FGF21 appears to protect pancreatic β cells from cell death induced by glycotoxicity (Kharitonenkov et al., 2005, 2007).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Kharitonenkov et al., 2005
The pancreatic-islet methods describe measurements of insulin and glucagon release, not β-cell survival. The Discussion reports no effect on insulin secretion; searches for glycotoxicity, β-cell death, and protection found no passage addressing whether FGF-21 prevents glycotoxicity-induced cell death. (LLM, conf=0.72)
Experimental — accuracy not yet measuredMice that overexpress FGF-21, a circulating FGF which is induced by a ketogenic diet, are lean and have increased brown fat, suggesting that the beneficial metabolic effects induced by a ketogenic diet are brought about in part by increases in BAT mass.
“Interestingly, mice that overexpress FGF-21, a circulating FGF which is induced by a ketogenic diet 106, are lean and have increased brown fat 107, suggesting that the beneficial metabolic effects induced by a ketogenic diet are brought about in part by increases in BAT mass.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [107]
FGF21 binding promotes formation of a dimeric FGFR1c-KLB complex, activates tyrosine kinase domains and propagates signalling through ERK phosphorylation.
“FGF21 binding promotes the formation of a dimeric FGFR1c–KLB signalling complex, which activates the intracellular tyrosine kinase domains of FGFR1c and propagates signalling through phosphorylation by the kinase ERK46,53,58,59”
From Metabolic messengers: FGF21 (2021) · cites this paper as [58]
Prolonged administration of FGF21 or FGF21 analogues decreases body weight in rodents and non-human primates, and has more modest effects on body weight in humans.
“prolonged administration of FGF21 or FGF21 analogues has important metabolic effects, including a marked decrease in body weight in rodents and non-human primates, and more modest effects on body weight in humans3,40,58,77,78.”
From Metabolic messengers: FGF21 (2021) · cites this paper as [58]
Overexpression of FGF21 is highly protective.
“overexpression of FGF21 is highly protective [135].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [135]
Activation of the FGF21/FGFR1c/KLB receptor complex results in phosphorylation of ERK1/2 and FRS2α.
“activation of the FGF21/FGFR1c/KLB receptor complex results in the phosphorylation of ERK1/2 and FRS2α [135].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [135]
Administering FGF21 to obese or diabetic rodents and primates markedly reduced body weight and significantly improved carbohydrate and lipid homeostasis.
“A myriad of studies ensued demonstrating that administering FGF21 to obese or diabetic rodents and primates markedly reduced body weight and significantly improved carbohydrate and lipid homeostasis (21, 64, 65, 141).”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
In rodents, pharmacological levels of FGF21 increase energy expenditure, which results in increased food intake.
“In rodents, pharmacological levels of FGF21 increase energy expenditure (64, 141), which results in increased food intake (54, 64).”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
FGF21 administration increases energy expenditure and the browning of adipose tissues in vivo.
“Since FGF21 administration increases energy expenditure and the browning of adipose tissues in vivo (21, 64, 141), it was hypothesized that FGF21 regulates adaptive thermogenesis in response to cold.”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
In diabetic and obese animal models, FGF21 administration decreases blood glucose levels and body weight, improves insulin and leptin sensitivity, improves plasma lipid profiles, and decreases hepatic steatosis.
“When administered to diabetic and obese animal models, FGF21 provides multiple metabolic benefits and has been shown to decrease blood glucose levels and body weight, improve insulin and leptin sensitivity, improve plasma lipid profiles, and decrease hepatic steatosis (21, 64, 141, 142).”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
In animal models, FGF21 treatment not only prevents but also reverses diabetes and obesity.
“Importantly, in animal models FGF21 treatment not only prevents (64) but also reverses diabetes and obesity (21, 141).”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
FGF21 enhances insulin sensitivity in primary brown adipocytes but not in primary white adipocytes.
“In addition, FGF21 enhances insulin sensitivity in primary brown adipocytes (86) but not in primary white adipocytes (64, 86).”
From Fibroblast Growth Factor 21: A Versatile Regulator of Metabolic Homeostasis (2018) · cites this paper as [64]
FGF21 reduces body weight, glucose levels, and lipid concentrations in models of obesity.
“FGF21’s ability to reduce body weight, glucose levels, and lipid concentrations in models of obesity generated substantial initial interest”
From FGF21 and the physiological regulation of macronutrient preference (2020) · cites this paper as [114]
FGF21 was first identified as a hepatokine and is necessary for adaptation to fasting.
“Fibroblast growth factor 21 (FGF21) was first identified as an hepatokine 61 and has been shown to be necessary for the adaptation to fasting 62, 63.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [61]
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- Authors
- Kharitonenkov, A., Shiyanova, T. L., Koester, A., Ford, A. M., Micanovic, R., Galbreath, E. J., Sandusky, G. E., Hammond, L. J., Moyers, J. S., Owens, R. A., Gromada, J., Brozinick, J. T., Hawkins, E. D., Wroblewski, V. J., Li, D.-S., Mehrbod, F., Jaskunas, S. R., & Shanafelt, A. B.
- Affiliations
- Eli Lilly (United States) (US)
- Corresponding author
- Kharitonenkov, Alexei
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2005-06-01
- Volume
- 115
- Issue
- 6
- Pages
- 1627-1635
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1088017
- OpenAlex
- W2000665430
- Cited by
- 2,125
- References
- 46
- Citations by year
- 2026: 72 · 2025: 99 · 2024: 111 · 2023: 120 · 2022: 137 · 2021: 138 · 2020: 116 · 2019: 136 · 2018: 147 · 2017: 135 · 2016: 142 · 2015: 155 · 2014: 124 · 2013: 125 · 2012: 115
- FWCI
- 8.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Hospital for Sick Children
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- FGF21, diabetes mellitus, glucose uptake, adipocytes, diet-induced obesity, transgenic mice, ob/ob mice, db/db mice, plasma glucose, triglycerides, metabolic regulation, diabetes treatment
- MeSH terms
- Animals, Blood Glucose, Cell Division, Cells, Cultured, Diabetes Mellitus, Fibroblast Growth Factors, Humans, Hyperglycemia, Hypoglycemic Agents, Mice, Obese, Mice, Transgenic, Triglycerides, Weight Gain, Adipocytes, Mice
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