Vitamin B12 Emerges As Promising Therapeutic For Acute Pancreatitis

A recent study has highlighted the potential of vitamin B12 as a therapeutic agent in both the prevention and treatment of acute pancreatitis, a serious gastrointestinal condition affecting individuals of all ages. Acute pancreatitis (AP) is a leading cause of hospital admissions, with approximately 20% of patients developing moderate to severe forms of the disease, which are associated with high mortality and long-term complications that can severely impact quality of life.

Despite ongoing research, the optimal treatment strategies for acute pancreatitis remain elusive, particularly in the search for pharmacological agents that can prevent early organ injury in the pancreas.

Led by Dr. Chuanwen Fan from the Department of Gastrointestinal Surgery at West China Fourth Hospital, Sichuan University, and the Department of Biomedical and Clinical Sciences at Linköping University, the research team, under the guidance of Prof. Dr. Xianming Mo, has combined human genetic epidemiology with animal models to elucidate the role of vitamin B12 in combating acute pancreatitis.

The research began with meta-analyses of genome-wide association studies (GWAS), utilizing extensive genetic datasets related to pancreatitis. Through a Mendelian randomization approach, the team investigated the correlation between various nutrients involved in one-carbon metabolism and the risk of developing pancreatitis. The findings indicated a significant association between elevated serum levels of vitamin B12 and a decreased risk of various types of pancreatitis.

To assess the protective and therapeutic effects of vitamin B12, the researchers utilized CD320 knockout mice, which are genetically engineered to lack a gene essential for vitamin B12 absorption. Two experimental models were employed to observe early pancreatic injury responses and the progression of acute pancreatitis.

Results demonstrated that vitamin B12 directly protects acinar cells from necrosis in the initial stages of acute pancreatitis and reduces T lymphocyte infiltration. Notably, artificially elevating serum vitamin B12 levels prior to and following the induction of pancreatitis not only mitigated the severity of the condition but also enhanced tissue repair post-injury.

Contrary to earlier hypotheses suggesting that vitamin B12’s protective effects were linked to the reduction of homocysteine or the glutathione pathways, the study found that vitamin B12 actually enhances ATP production in pancreatic tissue. This increase in ATP levels contributed to reduced acinar cell necrosis and staved off disease progression.

Further experiments showed that ATP supplementation in CD320-deficient mice also alleviated pancreatic damage, supporting the notion that the protective benefits of vitamin B12 arise from improved cellular energy supply rather than merely regulating oxidative stress.

“These exciting findings provide compelling evidence that vitamin B12 can mitigate the severity of acute pancreatitis by elevating ATP levels in pancreatic tissue,” said Prof. Mo. “This research lays a solid groundwork for potential clinical applications of vitamin B12 in managing acute pancreatitis, offering new therapeutic strategies for this challenging condition.”