Fig 1.

Diagram of the effects of protein maldigestion and putrefaction in the gut. A) Healthy protein digestion: I. Dietary protein enters the stomach. II. Protein in the stomach stimulates G-cells secrete gastrin. III. Gastrin stimulates enterochromaffin-like (ECL) cells, which releases histamine that stimulates parietal cells. Gastrin also stimulates chief cells to release pepsinogen. IV. HCl denatures the proteins and activates pepsinogen into pepsin. Pepsin begins cleaving proteins into smaller peptides. V. Cholecystokinin (CCK) and secretin released by the small intestine and stimulates the pancreas to release digestive enzymes and HCO₃. VI. The pancreas releases HCO₃ and enzymes (trypsinogen, chymotrypsinogen, procarboxypeptidase, etc.). Enterokinase (released by intestinal cells) activates trypsin, and trypsin activates chymotrypsinogen and procarboxypeptidase. VII. Amino acids and di-and tripeptides get absorbed into the enterocytes primarily in the jejunum. VIII. Primarily carbohydrates reach the colon and undergo fermentation releasing vitamins and short-chain fatty acids (SCFA). B) Incomplete protein digestion and pathogenesis: I. Decreased HCl limits protein denaturation and pepsin activation. II. Pancreatitis and pancreatic insufficiency result in decreased secretion of digestive enzymes. III. Inflammation in the intestine can impair CCK release and thus lower pancreatic secretion of proteases. IV. Protein escapes digestion and reaches the colon, which can promote microbial putrefaction. Colonic putrefaction produces toxic metabolites such as hydrogen sulfide, ammonia and p-cresol.