The gastrointestinal peptides and nutrition
Gastrointestinal (GI) peptides have been identified in endocrine cells and nerve fibres throughout the GI tract. They play both a direct and indirect role in the regulation of food intake, digestion, and absorption. The rate at which food is absorbed is dependent upon the rates of gastric emptying, intestinal transit, membrane transport, and enzymatic degradation. The control of pepsin secretion is intimately linked to that of acid secretion and stimulatory peptides, e.g., gastrin and bombesin. Inhibitors of acid secretion such as gastric inhibitory polypeptide (GIP), vasoactive intestinal peptide (VIP), secretin, and glucagon also control pepsin secretion. Powerful inhibitory reflexes, both nervous and hormonal, operate from the duodenum to slow gastric emptying and the most compelling evidence exists for the involvement of neurally released VIP. However, a unifying concept for the role of peptides in the control of intestinal motility is lacking. It is well established that the enzyme component of pancreatic secretion is controlled by the peptide cholecystokinin (CCK) and the aqueous component by secretin. Nutrient absorption can be affected by the endocrine pancreas and by somatostatin. Control of luminal enzyme secretion is increased by CCK, secretin, GIP, VIP, glucagon, and gastrin. Peptides influence the rate and direction of electrolyte and attendant water movement. The secretory actions of VIP are well documented. Peptides, again notably VIP, probably influence digestion and absorption via blood flow changes. Evidence has accumulated that gut hormones stimulate insulin release from the pancreas. The peptide, GIP, has been demonstrated to be a hormone involved in this mechanism and has been hypothesized to be a causal agent in disease states involving hyperinsulinemta, e.g., obesity and maturity onset diabetes. The hypothalamus is recognized to be the major regulatory area for appetite. It receives rich peptidergic innervation as well as being influenced by exogenous peptides. CCK has been shown to inhibit food intake. The presence of this peptide in the brain as well as the gut has led to the suggestion that it is a satiety hormone. However, problems with experimental design render equivocal the role of CCK and other peptides in the control of food intake.