Digestion In the human digestive system, a bolus (a small rounded mass of chewed up food) enters the<unk>  through the esophagus via the lower esophageal sphincter. The<unk>  releases proteases (protein-digesting enzymes such as pepsin) and hydrochloric acid, which kills or inhibits bacteria and provides the acidic pH of 2 for the proteases to work. Food is churned by the<unk>  through muscular contractions of the wall called peristalsis – reducing the volume of the bolus, before looping around the fundus and the body of<unk>  as the boluses are converted into chyme (partially digested food). Chyme slowly passes through the pyloric sphincter and into the duodenum of the small intestine, where the extraction of nutrients begins. Gastric juice in the<unk>  also contains pepsinogen. Hydrochloric acid activates this inactive form of enzyme into the active form, pepsin. Pepsin breaks down proteins into polypeptides. Absorption Although the absorption in the human digestive system is mainly a function of the small intestine, some absorption of certain small molecules nevertheless does occur in the<unk>  through its lining. This includes: * Water, if the body is dehydrated * Medication, such as aspirin * Amino acids * 10–20% of ingested ethanol (e.g. from alcoholic beverages) *Caffeine * To a small extent water-soluble vitamins (most are absorbed in the small intestine) The parietal cells of the human<unk>  are responsible for producing intrinsic factor, which is necessary for the absorption of vitamin B12. B12 is used in cellular metabolism and is necessary for the production of red blood cells, and the functioning of the nervous system. Control of secretion and motility The movement and the flow of chemicals into the<unk>  are controlled by both the autonomic nervous system and by the various digestive hormones of the digestive system: Gastrin The hormone gastrin causes an increase in the secretion of HCl from the parietal cells and pepsinogen from chief cells in the<unk> . It also causes increased motility in the<unk> . Gastrin is released by G cells in the<unk>  in response to distension of the antrum and digestive products (especially large quantities of incompletely digested proteins). It is inhibited by a pH normally less than 4(high acid), as well as the hormone somatostatin. Cholecystokinin Cholecystokinin (CCK) has most effect on the gall bladder, causing gall bladder contractions, but it also decreases gastric emptying and increases release of pancreatic juice, which is alkaline and neutralizes the chyme. CCK is synthesized by I-cells in the mucosal epithelium of the small intestine. Secretin In a different and rare manner, secretin, which has the most effects on the pancreas, also diminishes acid secretion in the<unk> . Secretin is synthesized by S-cells, which are located in the duodenal mucosa as well as in the jejunal mucosa in smaller numbers. Gastric inhibitory peptide Gastric inhibitory peptide (GIP) decreases both gastric acid release and motility. GIP is synthesized by K-cells, which are located in the duodenal and jejunal mucosa. Enteroglucagon Enteroglucagon decreases both gastric acid and motility. Other than gastrin, these hormones all act to turn off the<unk>  action. This is in response to food products in the liver and gall bladder, which have not yet been absorbed. The<unk>  needs to push food into the small intestine only when the intestine is not busy. While the intestine is full and still digesting food, the<unk>  acts as storage for food. Other ;Effects of EGF Epidermal growth factor (EGF) results in cellular proliferation, differentiation, and survival. EGF is a low-molecular-weight polypeptide first purified from the mouse submandibular gland, but since then found in many human tissues including the submandibular gland, and the parotid gland. Salivary EGF, which also seems to be regulated by dietary inorganic iodine, also plays an important physiological role in the maintenance of oro-oesophageal and gastric tissue integrity. The biological effects of salivary EGF include healing of oral and gastroesophageal ulcers, inhibition of gastric acid secretion, stimulation of DNA synthesis, and mucosal protection from intraluminal injurious factors such as gastric acid, bile acids, pepsin, and trypsin and from physical, chemical, and bacterial agents.<unk>  as nutrition sensor The human<unk>  can "taste" sodium glutamate using glutamate receptors and this information is passed to the lateral hypothalamus and limbic system in the brain as a palatability signal through the vagus nerve. The<unk>  can also sense, independently of tongue and oral taste receptors, glucose, carbohydrates, proteins, and fats. This allows the brain to link nutritional value of foods to their tastes. ;Thyrogastric syndrome This syndrome defines the association between thyroid disease and chronic gastritis, which was first described in the 1960s. This term was coined also to indicate the presence of thyroid autoantibodies or autoimmune thyroid disease in patients with pernicious anemia, a late clinical stage of atrophic gastritis. In 1993, a more complete investigation on the<unk>  and thyroid was published, reporting that the thyroid is, embryogenetically and phylogenetically, derived from a primitive<unk> , and that the thyroid cells, such as primitive gastroenteric cells, migrated and specialized in uptake of iodide and in storage and elaboration of iodine compounds during vertebrate evolution. In fact, the<unk>  and thyroid share iodine-concentrating ability and many morphological and functional similarities, such as cell polarity and apical microvilli, similar organ-specific antigens and associated autoimmune diseases, secretion of glycoproteins (thyroglobulin and mucin) and peptide hormones, the digesting and readsorbing ability, and lastly, similar ability to form iodotyrosines by peroxidase activity, where iodide acts as an electron donor in the presence of H2O2. In the following years, many researchers published reviews about this syndrome.
Stomach
Large intestine
Small intestine
Gastrointestinal tract
Heart
Liver
Lung
Venom