A Hormonal Tug-of-War in Chronic Pancreatitis

January 7, 2024by Dr. S. F. Czar0

Secretin and Gastrin: 

Chronic pancreatitis is a debilitating inflammatory condition of the pancreas, characterized by recurrent episodes of pain and impaired digestion. While the exact cause of chronic pancreatitis remains elusive, a complex interplay of factors, including genetic predisposition, alcohol abuse, and autoimmune reactions, is believed to contribute to its development. In recent years, the hormonal tug-of-war between secretin and gastrin has emerged as a potential player in the pathogenesis and progression of this challenging disease.

Enter the Contenders: Secretin and Gastrin

  • Secretin: This 27-amino acid peptide hormone, produced by S cells in the duodenum, plays a crucial role in pancreatic and biliary ductal health. Upon encountering acidic chyme from the stomach, secretin is released into the bloodstream. It travels to the pancreas, where it stimulates the acinar cells to produce bicarbonate-rich fluid. This alkaline fluid neutralizes the acidic chyme, protecting the delicate pancreatic ducts from erosion and inflammation. 
  • Gastrin: Primarily produced by G cells in the stomach and duodenum, gastrin is a gastrointestinal peptide hormone responsible for stimulating gastric acid secretion and promoting gastric motility. It also exerts proliferative effects on the exocrine and endocrine cells of the pancreas. While essential for normal digestion, overproduction or dysregulated gastrin signaling can contribute to pancreatic inflammation and injury. 

The Hormonal Tug-of-War: Implications in Chronic Pancreatitis

In healthy individuals, a delicate balance exists between the protective actions of secretin and the pro-inflammatory effects of gastrin. This equilibrium ensures optimal pancreatic function and guards against inflammation. However, in chronic pancreatitis, this balance is disrupted, leading to a pathological tug-of-war between the two hormones.

  • Defective Secretin Secretion: Chronic inflammation and scarring in the duodenum can impair S cell function, leading to diminished secretin production. This, in turn, results in inadequate bicarbonate secretion, leaving the pancreatic ducts vulnerable to acidic injury and perpetuating inflammation. 
  • Gastrin Hyperactivity: Various factors, including duodenal inflammation and nerve damage, can trigger excessive gastrin release. This gastrin hyperactivity further stimulates acid secretion and promotes pancreatic cell proliferation, potentially contributing to fibrosis and ductal obstruction, hallmarks of chronic pancreatitis. 

Clinical Implications and Therapeutic Avenues

Understanding the intricate interplay between secretin and gastrin has opened up novel therapeutic avenues for chronic pancreatitis.

  • Secretin Analogues: Synthetic secretin analogues are being investigated as potential replacements for deficient endogenous secretin. These long-acting analogues can help neutralize duodenal acidity and protect the pancreatic ducts from further damage. 
  • Gastrin Receptor Antagonists: Medications that block the action of gastrin at its receptors have shown promise in managing chronic pancreatitis. By suppressing gastrin-induced acid secretion and cell proliferation, these drugs may help alleviate pain and slow disease progression. 
  • Combination Therapy: A combination of secretin analogues and gastrin receptor antagonists may offer a more comprehensive approach to managing chronic pancreatitis by addressing both arms of the hormonal tug-of-war.

Secretin vs. Gastrin: A Hormonal Tug-of-War in Chronic Pancreatitis

Chronic pancreatitis, a stubborn foe, thrives on inflammation and disharmony. In this battleground, two key hormones engage in a tug-of-war: secretin, the protector, and gastrin, the provocateur.

Secretin: The good guy, secretin, shields the delicate pancreatic ducts by neutralizing acidic stomach contents with bicarbonate-rich fluid. But chronic inflammation cripples his production, leaving the ducts vulnerable.

Gastrin: The troublemaker, gastrin, fuels the fire by over-producing stomach acid and promoting pancreatic cell growth. This excessive activity fuels inflammation and fibrosis, hallmarks of the disease.

The Tug-of-War:

  • Defective Secretin: Scarred intestines weaken secretin production, leaving ducts exposed.
  • Gastrin Hyperactivity: Inflammation and nerve damage trigger gastrin’s overdrive, worsening inflammation and fibrosis.

The Battlefield:

  • Pain: Both acidic attacks and ductal constriction scream out in pain.
  • Digestive Woes: Impaired enzyme secretion leads to malabsorption and malnutrition.

Hope on the Horizon:

  • Secretin Analogues: Like reinforcements, these synthetic versions bolster bicarbonate defenses.
  • Gastrin Receptor Antagonists: These blockers disarm gastrin, curbing acid attacks and cell growth.
  • Combined Arms: Merging therapies may offer a comprehensive attack, restoring balance and easing symptoms.


The delicate balance between secretin and gastrin plays a critical role in maintaining pancreatic health. Disruption of this equilibrium, as seen in chronic pancreatitis, sets the stage for a self-perpetuating cycle of inflammation and injury. By understanding the hormonal tug-of-war and its clinical implications, researchers are developing novel therapeutic strategies aimed at restoring balance and mitigating the debilitating effects of chronic pancreatitis. While further research is warranted, targeting the secretin-gastrin axis holds promise for improving the lives of individuals suffering from this challenging condition.

In conclusion, the hormonal tug-of-war between secretin and gastrin is a fascinating story unfolding in the battle against chronic pancreatitis. By unraveling the intricate interplay between these key players, we can unlock new therapeutic avenues and offer hope for a brighter future for individuals living with this debilitating disease.



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