Which cells secrete intrinsic factor

Parietal cells contain an extensive secretory network called canaliculi from which the HCl is secreted by active transport into the stomach.

The resulting highly-acidic environment causes proteins from food to unfold or denature , exposing the peptide bonds that link together amino acids. HCl also activates pepsin , allowing it to help digestion by breaking specific peptide bonds, a process known as proteolysis. Furthermore, the sudden increase in gastric acid secretion following a meal can causes a physiological phenomenon called the alkaline tide , which is due to the production and export of bicarbonate from parietal cells.

Parietal cells secrete acid in response to three types of stimuli :. Upon stimulation, adenylate cyclase is activated within the parietal cells. This increases intracellular cyclic AMP , which leads to activation of protein kinase A.

The pH of the secreted fluid can fall 'by' 0. Parietal cells also produce intrinsic factor. Intrinsic factor is required for the absorption of [[Cyanocobalamin vitamin B Template:Ssub ]] in the diet. Atrophic Gastritis, in particular in the elderly, will cause an inability to absorb B12 and can lead to deficiencies. Physiology of the gastrointestinal system. Swallowing Vomiting. Saliva Gastric acid. Enterogastrone Cholecystokinin I cells Secretin S cells.

Intestinal juice. Segmentation contractions Migrating motor complex Borborygmus Defecation. Submucous plexus Myenteric plexus. Bile Pancreatic juice. Enterohepatic circulation. Peritoneal fluid. Hypochlorhydria or achlorhydria, whether medically induced or not, may impair cobalamin uptake. The cobalamin-R-protein complex is split by pancreatic enzymes in the duodenum, where cobalamin is bound to intrinsic factor. Pancreatic insufficiency may lead to cobalamin deficiency.

Lack of intrinsic factor is the commonest cause of cobalamin deficiency; very rarely, aberrant forms of intrinsic factor are produced, but the clinical syndrome is similar. Gram-negative anaerobe bacteria bind the cobalamin-intrinsic factor complex, and bacterial overgrowth of the small intestine diminishes cobalamin resorption.

Parasitic infections with fish tape-worm and Giardia lamblia are also associated with cobalamin malabsorption. Canaliculi intrude into the cytoplasm, with multiple microvilli protruding from them. There are a variety of pathologies that affect parietal cell gastric acid secretion, as well as intrinsic factor secretion. The most common cause of gastric pathology worldwide is Helicobacter pylori infection.

Prostaglandins are responsible for protecting the gastric mucosa from injuries caused by hydrochloric acid. NSAIDs cause gastritis by inhibiting the production of prostaglandins, which gets mediated by inhibition of cyclo-oxygenase. Helicobacter pylori infection is one of the most common infections worldwide, and it is the leading global cause of gastritis.

Nonetheless, recent studies have shown its prevalence is declining in the developed world. Most of the cases are asymptomatic; only some might present as functional dyspepsia and gastroesophageal reflux disease. Autoimmune gastritis symptoms vary throughout the disease, and patients with this disease do not have a higher risk of developing gastric or duodenal ulcers in comparison with acute gastritis.

Pernicious anemia can arise as a late complication of autoimmune gastritis, which normally precedes the former by at least 10 to 20 years. Common symptoms include pallor, fatigue, dizziness, shortness of breath, tachycardia, loss of appetite, weight loss, and diarrhea. Kressin M, Oxyntic cell differentiation during physiological cell renewal in abomasal mucosa of adult cattle. Anatomy and embryology. Ogata T,Yamasaki Y, Ultra-high-resolution scanning electron microscopy of the continuity of cytoplasmic and luminal membranes in frog oxyntic cells.

The Anatomical record. Annual review of physiology. World journal of gastroenterology. Bailliere's clinical gastroenterology. The American journal of physiology.