GFRAL is the receptor for GDF15 and the ligand promotes weight loss in mice and nonhuman primates
Abstract
Growth differentiation factor 15 (GDF15), a distant member of the transforming growth factor (TGF)-β family, is a secreted protein that circulates as a 25-kDa dimer. In humans, elevated GDF15 correlates with weight loss, and the administration of GDF15 to mice with obesity reduces body weight, at least in part, by decreasing food intake. The mechanisms through which GDF15 reduces body weight remain poorly understood, because the cognate receptor for GDF15 is unknown. Here we show that recombinant GDF15 induces weight loss in mice fed a high-fat diet and in nonhuman primates with spontaneous obesity. Furthermore, we find that GDF15 binds with high affinity to GDNF family receptor α-like (GFRAL), a distant relative of receptors for a distinct class of the TGF-β superfamily ligands. Gfral is expressed in neurons of the area postrema and nucleus of the solitary tract in mice and humans, and genetic deletion of the receptor abrogates the ability of GDF15 to decrease food intake and body weight in mice. In addition, diet-induced obesity and insulin resistance are exacerbated in GFRAL-deficient mice, suggesting a homeostatic role for this receptor in metabolism. Finally, we demonstrate that GDF15-induced cell signaling requires the interaction of GFRAL with the coreceptor RET. Our data identify GFRAL as a new regulator of body weight and as the bona fide receptor mediating the metabolic effects of GDF15, enabling a more comprehensive assessment of GDF15 as a potential pharmacotherapy for the treatment of obesity.
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GDF-15 binds exclusively to GFRAL and not to other TGF-β receptors or other GDNF family receptors.
“Metformin increases the secretion of GDF-15, which binds exclusively to glial cell-derived neurotrophic factor family receptor alpha-like (GFRAL).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [41]
Exogenous administration of recombinant murine or human GDF-15 induces weight loss in different animal models.
“In line with these studies, exogenous administration of recombinant murine or human GDF-15 induced weight loss in different animal models (26, 32, 40, 41, 107).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [41]
GFRAL expression is limited to the brainstem and Gfral mRNA is highly expressed in the area postrema of mouse, rat, monkey and human.
“Unlike Gdf-15 which is expressed in diverse tissues, including kidney, liver, gut, muscle, adipose, and placenta, GFRAL expression is limited to the brainstem and Gfral mRNA is highly expressed in the area postrema of mouse, rat, monkey and human (39–41).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [41]
Blocking RET by inhibitor or mRNA depletion prevents GDF-15-mediated signaling in neuroblastoma cells.
“Blocking RET by inhibitor or mRNA depletion could also prevent GDF-15-mediated signaling in neuroblastoma cells (41).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [41]
GDF-15 and GFRAL have emerged as regulators of energy balance and body weight.
“In addition to these functions, GDF-15 and its tissue-specific brainstem receptor, the glial cell-derived neurotrophic factor (GDNF) family receptor alpha-like (GFRAL), have emerged as regulators of energy balance and body weight (39–41).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [41]
Experimental and clinical data support a role for GDF15 in regulating body weight and energy homeostasis.
“Experimental and clinical data have supported its role in regulating body weight and energy homeostasis [[210], [211], [212], [213]] (Figure 2).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [212]
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- Authors
- Mullican, S. E., Lin-Schmidt, X., Chin, C.-N., Chavez, J. A., Furman, J. L., Armstrong, A. A., Beck, S. C., South, V. J., Dinh, T. Q., Cash-Mason, T. D., Cavanaugh, C. R., Nelson, S., Huang, C., Hunter, M. J., & Rangwala, S. M.
- Corresponding author
- Rangwala, Shamina M
- Venue
- Nature Medicine
- Published
- 2017-08-28
- Volume
- 23
- Issue
- 10
- Pages
- 1150-1157
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2748135921
- Cited by
- 774
- References
- 38
- Citations by year
- 2026: 82 · 2025: 88 · 2024: 119 · 2023: 81 · 2022: 96 · 2021: 96 · 2020: 93 · 2019: 65 · 2018: 39 · 2017: 14
- FWCI
- 50.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › GDF15 and Related Biomarkers
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Pharmacology › Apelin-related biomedical research
- Keywords
- GDF15, GFRAL, growth differentiation factor 15, receptor identification, obesity, weight loss, dietary intake, TGF-beta superfamily, area postrema, nucleus tractus solitarius, insulin resistance, diet-induced obesity, obesity pharmacotherapy, non-human primates
- MeSH terms
- Animals, Eating, Humans, Macaca fascicularis, Obesity, Weight Loss, Mice, Knockout, Glial Cell Line-Derived Neurotrophic Factor Receptors, Mice, Growth Differentiation Factor 15, Diet, High-Fat
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