Vitamin D: A Potential Star for Treating Chronic Pancreatitis

Abstract

Chronic pancreatitis (CP) is a chronic inflammatory and fibrotic disease of the pancreas. The incidence of CP is increasing worldwide but the effective therapies are lacking. Hence, it is necessary to identify economical and effective agents for the treatment of CP patients. Vitamin D (VD) and its analogues have been confirmed as pleiotropic regulators of cell proliferation, apoptosis, differentiation and autophagy. Clinical studies show that VD deficiency is prevalent in CP patients. However, the correlation between VD level and the risk of CP remains controversial. VD and its analogues have been demonstrated to inhibit pancreatic fibrosis by suppressing the activation of pancreatic stellate cells and the production of extracellular matrix. Limited clinical trials have shown that the supplement of VD can improve VD deficiency in patients with CP, suggesting a potential therapeutic value of VD in CP. However, the mechanisms by which VD and its analogues inhibit pancreatic fibrosis have not been fully elucidated. We are reviewing the current literature concerning the risk factors for developing CP, prevalence of VD deficiency in CP, mechanisms of VD action in PSC-mediated fibrogenesis during the development of CP and potential therapeutic applications of VD and its analogues in the treatment of CP.

The research progress of anti-inflammatory and anti-fibrosis treatment of chronic pancreatitis

“…VD can inhibit the development of CP mainly due to its anti-inflammatory, anti-fibrosis and immunomodulatory effects ( 128 ). In addition, VD can also inhibit the cell cycle of a variety of cells, inhibit cell proliferation, interfere with the dedifferentiation of tumor cells, and induce apoptosis ( 129 – 131 ), which is of great significance to prevent CP from developing into PC and the deterioration of PC ( 132 ).…”

Serum 25‐hydroxyvitamin D, vitamin D receptor, and vitamin D binding protein concentrations in dogs with acute pancreatitis compared to healthy control dogs

“…7 Additionally, it affects anti-inflammatory processes and immune regulation, 8,9 highlighting the importance of vitamin D in inflammatory diseases. Cholecalciferol (vitamin D3) absorbed from the intestine is transported to the liver by binding to circulating vitamin D-binding proteins (VDBP), 10,11 and hydroxylated into 25(OH)D. 8,9,12 In the kidneys, 25(OH)D is converted into 1,25-dihydroxyvitamin D, the biologically active form. 8,9,12 The active form of vitamin D binds to vitamin D receptors (VDR) expressed in various tissues, 13 and activated VDR regulates target genes, bringing about the biological effects of vitamin D. 12 Considering the important roles of VDR and VDBP in the functions of vitamin D, VDR expression and serum VDBP concentrations in inflammatory diseases are of interest.…”

“…Cholecalciferol (vitamin D3) absorbed from the intestine is transported to the liver by binding to circulating vitamin D-binding proteins (VDBP), 10,11 and hydroxylated into 25(OH)D. 8,9,12 In the kidneys, 25(OH)D is converted into 1,25-dihydroxyvitamin D, the biologically active form. 8,9,12 The active form of vitamin D binds to vitamin D receptors (VDR) expressed in various tissues, 13 and activated VDR regulates target genes, bringing about the biological effects of vitamin D. 12 Considering the important roles of VDR and VDBP in the functions of vitamin D, VDR expression and serum VDBP concentrations in inflammatory diseases are of interest. The association between VDR polymorphisms and increased inflammation has been reported in several inflammatory diseases, such as inflammatory bowel disease, asthma, and sepsis.…”

“…Additionally, it affects anti‐inflammatory processes and immune regulation, 8,9 highlighting the importance of vitamin D in inflammatory diseases. Cholecalciferol (vitamin D3) absorbed from the intestine is transported to the liver by binding to circulating vitamin D‐binding proteins (VDBP), 10,11 and hydroxylated into 25(OH)D 8,9,12 . In the kidneys, 25(OH)D is converted into 1,25‐dihydroxyvitamin D, the biologically active form 8,9,12 .…”

“…Cholecalciferol (vitamin D3) absorbed from the intestine is transported to the liver by binding to circulating vitamin D‐binding proteins (VDBP), 10,11 and hydroxylated into 25(OH)D 8,9,12 . In the kidneys, 25(OH)D is converted into 1,25‐dihydroxyvitamin D, the biologically active form 8,9,12 . The active form of vitamin D binds to vitamin D receptors (VDR) expressed in various tissues, 13 and activated VDR regulates target genes, bringing about the biological effects of vitamin D 12 …”