Also called: GDF-15, R-Ketorolac and GDF-15 Inhibitors
GDF15 stands for growth differentiation factor 15. It is a natural chemical messenger that your body makes. It belongs to a big family of messengers called the TGF-beta family. Most organs in the body make small amounts of it. When an organ like the liver, kidney, heart, or lung gets hurt, the body makes much more of it.
Scientists have found that GDF15 can make animals and people eat less. In one mouse study, liver cells that made extra GDF15 caused the mice to stop eating as much. The mice also handled blood sugar better. GDF15 works by sending a 'stop eating' signal to the brain. It may also be a signal the body sends when it is sick or injured.
Researchers are studying GDF15 as a clue for diseases like cancer and lung scarring. High amounts may show that a tumor is making the body waste away. Most of the research so far has been done in lab animals, not people. We still do not know the best dose or if it is safe as a medicine. No product is approved for people to use today.
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News
Dated, sourced reporting that mentions GDF15.
A genome-wide association study published in Nature Communications has identified a genetic link between hyperemesis gravidarum (HG), a severe form of pregnancy sickness, and two specific genes: GDF15 and IGFBP7. The research found that variants at chr19p13.11 and chr4q12 loci are associated with the condition, implicating these genes which are known to influence placentation, appetite regulation, and cachexia. While further study is needed to prove causality, these findings suggest that hormonal signaling involving these peptides may drive the severe nausea and vomiting experienced in HG.
A review in Nature Reviews Disease Primers examines the biological underpinnings and clinical management of nausea and vomiting of pregnancy (NVP) and hyperemesis gravidarum (HG). It highlights recent genetic advances implicating the hormone GDF15 and the protein IGFBP7 as key drivers of the condition, acting through receptors in the brainstem. These findings suggest a placental origin for the disease and offer potential targets for future therapeutic development.
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