How B12 Prevents, Heals Acute Pancreatitis

Through genetic analysis and mouse model experiments, researchers showed that higher vitamin B12 levels can significantly reduce the severity of this often-deadly condition, the journal MedComm reported.

Acute pancreatitis (AP) is a serious gastrointestinal condition that affects people of all ages and is a leading cause of hospital admissions worldwide. Around 1 in 5 patients develop moderate to severe forms of the disease, which are linked to high rates of death and long-term disability. Even those who survive often face lasting complications that significantly reduce their quality of life. Despite its impact, there is still no clear consensus on the best way to treat acute pancreatitis. In particular, there is an urgent need for medications that can prevent early damage to the pancreas.

To address this, a research team led by Dr. Chuanwen Fan, from West China Fourth Hospital at Sichuan University and Linköping University in Sweden, conducted a study under the supervision of Prof. Dr. Xianming Mo at Sichuan University’s West China Hospital. Their goal was to explore whether vitamin B12 could help prevent or reduce the severity of acute pancreatitis by using both human genetic data and animal models.

The researchers began by analyzing large-scale genome-wide association studies (GWAS) to identify genetic links to pancreatitis. They then used Mendelian randomization, a method that leverages genetic variation to study the effects of specific nutrients, to examine whether one-carbon metabolism nutrients were connected to pancreatitis risk. Their results showed a strong association between higher blood levels of vitamin B12 and a lower risk of developing several forms of pancreatitis.

Next, the team determined whether vitamin B12 displayed protective and potential therapeutic effects using experimental models of pancreatitis in CD320 knockout mice, which lack a key gene responsible for vitamin B12 absorption. Two distinct models of pancreatitis were used in the study: one to observe early pancreatic injury responses, and the other to track the pathological progression of acute pancreatitis.

The results revealed that VB12 directly protects acinar cells from necrosis during the early stages of acute pancreatitis and subsequently reduces T lymphocyte infiltration. Notably, artificially increasing serum B12 levels before and after the induction of pancreatitis not only reduced the severity of the condition but also promoted tissue repair after pancreatic injury.

Interestingly, despite vitamin B12’s known role in the one-carbon metabolism pathway, its protective effects in pancreatitis were not mediated through the reduction of homocysteine or the glutathione (GSH) pathways, as was previously hypothesized. Instead, vitamin B12 was found to enhance ATP production in pancreatic tissue, thereby reducing acinar cell necrosis and preventing disease progression. ATP supplementation in CD320-deficient mice also alleviated pancreatic damage, further supporting the hypothesis that vitamin B12’s protective effects result from improved cellular energy supply rather than oxidative stress regulation.

“These exciting new findings add to the growing evidence that vitamin B12 can reduce the severity of acute pancreatitis by increasing ATP levels in pancreatic tissue, offering novel insights into potential therapeutic strategies for this disease. This study lays a robust foundation for future clinical applications of vitamin B12 in managing acute pancreatitis,” Prof. Mo concludes.

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