In recent years, significant progress has been made in understanding the role and effects of neuropeptides in the bidirectional interaction between the brain and the gut, leading to the discovery of many new peptides such as Phoenixin (1). Phoenixin was initially found in brain nuclei involved in the regulation of food intake in the hypothalamus. Subsequent studies have identified the presence of Phoenixin and its receptors in various parts of the gastrointestinal system, including the esophagus, stomach, pancreas, spleen, jejunum, duodenum, ileum, and colon (2,3). It has been shown that Phoenixin is involved in bidirectional signaling of the brain-gut axis in the regulation of food intake and has orexigenic effects (4)

Phoenixin has been observed to contribute to the modulation of energy homeostasis and metabolism by regulating the function of pancreatic endocrine beta and alpha cells, which secrete key regulatory hormones of glucose and lipid metabolism. It controls the production/secretion of insulin following high glucose levels. The peptide's secretion is influenced by blood glucose and fatty acid levels. Phoenixin promotes white adipose tissue formation by contributing to the proliferation of preadipocyte cells and their differentiation into mature adipocytes. Additionally, it is known that blood levels of Phoenixin have a positive correlation with body mass index (5).

Given Phoenixin’s roles in stimulating food intake and thereby regulating energy metabolism, further research is needed on its regulatory effects on the brain-gut axis, as well as in the pancreas, intestines, and stomach. In conclusion, this review will examine and discuss the physiological and pathophysiological effects of Phoenixin in the brain-gut axis.