cholecystokinin and Food-Hypersensitivity

Functional dyspepsia (FD) is a common disorder of yet uncertain etiology. Dyspeptic symptoms are usually meal related and suggest an association to gastrointestinal (GI) sensorimotor dysfunction. Cholecystokinin (CCK) is an established brain-gut peptide that plays an important regulatory role in gastrointestinal function. It inhibits gastric motility and emptying via a capsaicin sensitive vagal pathway. The effects on emptying are via its action on the proximal stomach and pylorus. CCK is also involved in the regulation of food intake. It is released in the gut in response to a meal and acts via vagal afferents to induce satiety. Furthermore CCK has also been shown to be involved in the pathogenesis of panic disorder, anxiety and pain. Other neurotransmitters such as serotonin and noradrenaline may be implicated with CCK in the coordination of GI activity. In addition, intravenous administration of CCK has been observed to reproduce the symptoms in FD and this effect can be blocked both by atropine and loxiglumide (CCK-A antagonist). It is possible that an altered response to CCK may be responsible for the commonly observed gastric sensorimotor dysfunction, which may then be associated with the genesis of dyspeptic symptoms.

Topics: Atropine; Cholecystokinin; Dyspepsia; Efferent Pathways; Food Hypersensitivity; Gastrointestinal Motility; Gastrointestinal Tract; Humans; Norepinephrine; Proglumide; Receptors, Adrenergic; Receptors, Serotonin; Serotonin; Stress, Psychological

The biologic clock that determines the temporal sequence of maturation of digestive and absorptive processes in the gastrointestinal tract is genetically predetermined, but may be modified by dietary, hormonal, or other factors. In general it may be said that the gastrointestinal tract of full-term neonates is capable of digesting and absorbing a nutritionally adequate quantity of dietary protein but capacity is limited. Very low birth weight preterm infants, who are surviving the early neonatal period in increasing numbers, have immaturity of a wide range of digestive and membrane-associated absorptive processes; in addition macromolecular absorption may be increased. Whether a limited capacity to digest food protein results in increased or altered antigenic stimulation of these immature infants remains speculative with present knowledge. Immaturity of intestinal lactase may lead to problems of lactose intolerance, but there is recent evidence that lactase activity may be inducible by milk feeding.

Topics: Absorption; Aging; Amino Acids; beta-Galactosidase; Biological Transport, Active; Cholecystokinin; Dietary Proteins; Digestion; Digestive System; Endopeptidases; Exopeptidases; Fetus; Food Hypersensitivity; Gastric Acid; Gastrins; Humans; Hydrolysis; Infant; Infant, Newborn; Infant, Premature; Intestinal Mucosa; Lactose Intolerance; Pancreas; Pepsin A; Peptide Hydrolases; Secretin; Stomach; Substrate Specificity

Undiagnosed food allergies have been proposed as possible causes of promoting and perpetuating irritable bowel syndrome . Our aim was to find out if sensitization could induce chronic functional motor disturbances in the intestine and the mechanisms implicated. Rats were sensitized to ovalbumin (OVA) following three hypersensitivity induction protocols, two parenteral and one oral. Rat mast cell protease II (RMCP II) release in response to OVA challenge and immunoglobulin E (IgE) concentration were measured in serum. At least 1 week after challenge, small intestinal motility was evaluated using strain gauges. Intestinal tissue samples from orally sensitized rats were checked for in vitro stimulation with OVA. Mucosal mast cells were counted from duodenum sections. All sensitized rats showed intestinal hypermotility. Only rats sensitized by parenteral procedure showed an increase in RMCP II after OVA challenge in serum. IgEs increased only in the Bordetella pertussis sensitized group. Small intestine sections from orally sensitized rats released more RMCP II than sections from control rats. All sensitized rats showed an increase in the number of mucosal mast cells in duodenum. In conclusion, hypersensitivity to food proteins induces chronic motor alteration that persists long after antigen challenge and an excited/activated state of sensitized mucosal mast cells.

Topics: Animals; Bordetella pertussis; Cholecystokinin; Duodenum; Food Hypersensitivity; Gastrointestinal Motility; Ileum; Immunoglobulin E; Immunohistochemistry; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Male; Mast Cells; Muscle Tonus; Ovalbumin; Rats; Rats, Sprague-Dawley; Serine Endopeptidases