Modulation of Pancreatic Activity by Ghrelin and Its Potential Effects on Acute Pancreatitis

Ghrelin is a brain–gut peptide primarily secreted by the gastric fundus, which exhibits a range of physiological functions, including stimulating growth hormone (GH) release, regulating energy metabolism, and modulating appetite. It is also expressed in pancreatic tissue and participates in the regulation of both endocrine and exocrine pancreatic functions. This article reviews the expression characteristics of ghrelin in the pancreas, its effects on islet cell function, and its potential protective mechanisms in acute pancreatitis (AP). Studies have shown that ghrelin and its receptor, Growth Hormone Secretagogue Receptor (GHSR), are highly expressed during early pancreatic development and play a regulatory role in pancreatic islet ε-cells, β-cells, and acinar cells. Ghrelin, via GHSR-mediated signaling pathways, influences the secretion of insulin and glucagon, thereby contributing to the maintenance of glucose homeostasis. In models of AP, ghrelin exerts anti-inflammatory and tissue-protective effects through multiple mechanisms, including inhibition of the NF-κB pathway, modulation of calcium channel expression, attenuation of oxidative stress, regulation of macrophage polarization, and via sensory nerve-dependent pathways. Furthermore, ghrelin has been shown to improve pancreatic blood flow and promote tissue repair, highlighting its multi-target therapeutic potential. This review aims to systematically elucidate the role of ghrelin in pancreatic physiology and pathology, thereby providing a theoretical basis for its potential clinical application in pancreatic diseases such as pancreatitis.