Adropin is a protein encoded by the energy homeostasis-associated gene ENHO in humans[5] and is highly conserved across mammals.[6]
The biological role of adropin was first described in mice by Andrew Butler's team. They identified it as a protein hormone (hepatokine) secreted from the liver, playing a role in obesity and energy homeostasis. The name "Adropin" is derived from the Latin words "aduro" (to set fire to) and "pinguis" (fat).[7] Adropin is produced in various tissues, including the liver, brain, heart, and gastrointestinal tract.[8]
In animals, adropin regulates carbohydrate and lipid metabolism[9] and influences endothelial function.[10][11] Its expression in the liver is controlled by feeding status, macronutrient content,[9] as well as by the biological clock.[12] Liver adropin is upregulated by estrogen[13] via the estrogen receptor alpha (ERα).[14]
In humans, lower levels of circulating adropin are linked to several medical conditions, including the metabolic syndrome, obesity, and inflammatory bowel disease.[15] and inflammatory bowel disease.[16] The brain exhibits the highest levels of adropin expression,[17] In the brain, adropin has been shown to have a potential protective role against neurological disease,[18] where it may play a protective role against neurological diseases, brain aging, cognitive decline, and acute ischemia.[19][20] as well as following acute ischemia.[21]
The orphan G protein-coupled receptor GPR19 has been proposed as a receptor for adropin.[22][23]
^Kolben Y, Weksler-Zangen S, Ilan Y (February 2021). "Adropin as a potential mediator of the metabolic system-autonomic nervous system-chronobiology axis: Implementing a personalized signature-based platform for chronotherapy". Obesity Reviews. 22 (2): e13108. doi:10.1111/obr.13108. PMID32720402. S2CID220841405.
^Soltani S, Kolahdouz-Mohammadi R, Aydin S, Yosaee S, Clark CC, Abdollahi S (March 2022). "Circulating levels of adropin and overweight/obesity: a systematic review and meta-analysis of observational studies". Hormones. 21 (1): 15–22. doi:10.1007/s42000-021-00331-0. PMID34897581. S2CID245119139.