After eating, there is a rapid increase in spike and contractile activity in the colon18-20. The calorific content appears to have a more important effect on the degree of motility than the size or pH of the meal. Fat is a more important stimulant of motility than either carbohydrate or protein. Ingestion of fat alone produces both an early (10 to 40 min) and late (70 to 90 min) increase in colonic motility19. The late response can be abolished by the simultaneous ingestion of protein, and both responses are inhibited by the ingestion of amino acids. This colonic response to feeding is known as the gastrocolic reflex, and must be an integrated response to both fat and protein induced mediators. The gastrocolic response is initiated by a sensory receptor in the gastroduodenal mucosa20.
Three components have been identified in the response of the colon to the ingestion of a meal: an initial cholinergic propulsive reflex, followed by a cholinergic segmenting reflex and finally a noradrenergic segmenting reflex21. Intravenous infusion of anticholinergic drugs prior to a meal abolishes the early colonic effects, thus supporting a cholinergic neural mechanism for mediation of the early response to eating. It is possible that there may also be a humoral component to this early response, in that the release of gastrointestinal hormones may be responsible for stimulating the cholinergic neural pathways. The late response, however, is unaffected by pre-treatment with anticholinergic drugs, thus implicating an essentially humoral pathway which may involve release of gastrin, cholecystokinin (CCK) or another gastrointestinal hormone. A postprandial increase in gastrin levels has been observed and CCK is released from the duodenum in the presence of fat. CCK stimulates gall bladder contraction and increases motility in both the small intestine and colon. Gastrin, in the G17 short chain form, and CCK stimulate colonic motility at serum concentrations within the physiological range22. Intravenous and intraduodenal amino acids stimulate the release of pancreatic glucagon, which has been shown to be a potent inhibitor of colonic myoelectric and motor activity. Enkephalins, endogenous pentapeptides, have been implicated since the response to a meal can be blocked by naloxone, an opiate antagonist20. Met-enkephalin analogues inhibit colonic motility through a peripheral mechanism thought to involve the myenteric cholinergic plexus whereas leu-enkephalins stimulate motility through a centrally-acting mechanism20 23.
Despite this almost immediate colonic motor response to eating in normal subjects, the right colon does not empty soon after a meal, although this phenomenon can be seen in patients with the irritable bowel syndrome24. Studies to elucidate this apparent anomaly have shown that non-propagating motor activity increases in all colonic segments immediately after eating a 1000 kcal meal. When propagating contractions do occur postprandially these are associated with a rapid movement of intraluminal contents25. The greatest increase in motor activity is seen in the descending colon26 and this is often associated with retrograde movement of colonic contents from the descending to the transverse colon25.
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