ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2022
LPS induces rapid increase in GDF15 levels in mice, rats, and humans but is not required for anorexia in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Levels of Growth Differentiation Factor 15 Correlated with Metabolic Dysfunction-Associated Steatotic Liver Disease in Children.International journal of molecular sciences · 2025Observational
- GDF15 links adipose tissue lipolysis with anxiety.Nature metabolism · 2025Article
- Growth Differentiation Factor-15 Knockout Mice Are Protected from Neonatal Hypoxic-Ischemic Injury in a Sex-Dependent Manner.Developmental neuroscience · 2025Article
- Proximate and ultimate causes of pregnancy sickness.Evolution, medicine, and public health · 2025Review
- Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024Review
- GDF15 Mediates the Effect of Skeletal Muscle Contraction on Glucose-Stimulated Insulin Secretion.Diabetes · 2023Article
- The GDF15-GFRAL axis mediates chemotherapy-induced fatigue in mice.Brain, behavior, and immunity · 2023Article
- Chronic intermittent hypoxia due to obstructive sleep apnea slightly alters nutritional status: a pre-clinical study.Frontiers in nutrition · 2023Article
- Brainstem ADCYAP1Nature · 2022Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Growth differentiation factor 15 (GDF15), a TGFβ superfamily cytokine, acts through its receptor, cell line-derived neurotrophic factorfamily receptor α-like (GFRAL), to suppress food intake and promote nausea. GDF15 is broadly expressed at low levels but increases in states of disease such as cancer, cachexia, and sepsis. Whether GDF15 is necessary for inducing sepsis-associated anorexia and body weight loss is currently unclear. To test this we used a model of moderate systemic infection in GDF15KO and GFRALKO mice with lipopolysaccharide (LPS) treatment to define the role of GDF15 signaling in infection-mediated physiologic responses. Since physiological responses to LPS depend on housing temperature, we tested the effects of subthermoneutral and thermoneutral conditions on eliciting anorexia and inducing GDF15. Our data demonstrate a conserved LPS-mediated increase in circulating GDF15 levels in mouse, rat, and human. However, we did not detect differences in LPS-induced anorexia between WT and GDF15KO or GFRALKO mice. Furthermore, there were no differences in anorexia or circulating GDF15 levels at either thermoneutral or subthermoneutral housing conditions in LPS-treated mice. These data demonstrate that GDF15 is not necessary to drive food intake suppression in response to moderate doses of LPS.
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Registered trials
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