Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouth-caecum transit time (M-CTT) of a lactulose labelled liquid test meal has been measured in 27 coeliac patients and 10 healthy controls using the breath hydrogen technique. Although all patients were urged to maintain a gluten free diet, not all did, and there was, therefore, a wide range in the severity of fat malabsorption within the patient group. Gastric emptying of a 113Indium DTPA-labelled liquid test meal was also assessed in separate studies on six healthy controls and 11 of the coeliac patients. Fasting breath hydrogen concentrations and the response to lactulose, as assessed both by the rate of rise, and the peak breath hydrogen concentration reached, showed no difference between coeliacs and controls, regardless of the presence or absence of steatorrhoea. Mouth-caecum transit time in the 16 coeliac patients with steatorrhea (faecal fat greater than 7 g/24 h) was, however, significantly prolonged being 158 +/- 18 minutes (mean +/- SEM), compared with 70 +/- 9 minutes for the controls (p less than 0.02), and 83 +/- 15 minutes for the 11 coeliacs without steatorrhoea (p less than 0.002). Mouth-caecum transit time in the coeliac patients was linearly related to the 24 hour faecal fat excretion, r = 0.55, n = 27, p less than 0.01. Slow mouth-caecum transit in the coeliacs with steatorrhoea was not caused by delayed gastric emptying as the t1/2 for coeliacs with steatorrhoea was within the normal range. Coeliacs with delayed mouth-caecum transit had impaired insulin release but the postprandial profiles of the other peptides measured (cholecystokinin, GIP, secretin, motilin, neurotensin, enteroglucagon, and peptide YY) were all within the normal range in this group of partially treated coeliac patients.
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PMID:Delayed mouth-caecum transit of a lactulose labelled liquid test meal in patients with steatorrhoea caused by partially treated coeliac disease. 367 57

A major barrier to the widespread clinical use of an alpha-glucosidase inhibitor such as Acarbose, is the unpleasant gastrointestinal symptoms of carbohydrate malabsorption associated with its use. Acarbose is usually administered as a tablet and eaten with the first mouthful of the meal, making its uniform distribution through the meal unlikely. In the present study, Acarbose was crushed to a powder and mixed through a test meal before it was consumed. Six healthy young men consumed test meals containing 75 g carbohydrate either as whole brown rice or as ground brown rice. When Acarbose was uniformly mixed through a ground rice meal prior to digestion it produced dose-dependent reductions in the postprandial glucose, insulin and GIP responses which were evident at doses as low as 12.5 mg. The responses to whole brown rice were intermediate between those to 12.5 and 25 mg Acarbose in ground brown rice. In tablet form Acarbose was only one quarter as effective in flattening the post prandial glucose and insulin responses as it was in powder form. These results highlight the importance of uniform distribution of Acarbose through a carbohydrate meal in order to achieve maximum effectiveness in delaying digestion and absorption and yet not promoting carbohydrate malabsorption.
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PMID:Optimum effectiveness of intestinal alpha-glucosidase inhibitors: importance of uniform distribution through a meal. 388 43

The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
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PMID:Gastric inhibitory polypeptide. 610 91

Malnutrition may cause to the damage intestinal epithelium and pancreas resulting in overt signs of malabsorption syndrome. The diet protein, fats and carbohydrates stimulate secretion, CCK-P, GIP, and gastrin release and effect insulin and HGH release. The amounts of the hormones released depends on intestinal absorption and pancreas secretory function. Therefore, in undernourished children with malabsorption syndrome on impaired function of the hormonal entero-insular axis is likely. In 30 children hormonal component of malnutrition was studied. Digestion and absorption were assayed by glycemic levels and FFA, with hydroxyprolinuria studies following administration of the mixed test meal. HGH and IRI levels were measured following mixed test meal stimulation. Hormonal studies data were correlated with digestion and absorption indices. In undernourished children low levels of HGH and IRI were frequently found. In certain patients with malnutrition the administration of anabolic drugs seems to be advisable.
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PMID:[Food stimulated release of IRI and HGH in children with malabsorption (author's transl)]. 610 40

Several problems are associated with gastric resection, including the dumping syndrome, reflux esophagitis, and malabsorption. A better understanding of the pathophysiological changes will shed light on new and improved therapy. Serum levels of seven circulating gastrointestinal hormones following a standardized solid meal and a brief score of symptoms were evaluated in 10 patients after partial distal gastrectomy and 12 patients after total gastrectomy, both groups reconstructed by Billroth II anastomosis, and 9 age-matched healthy controls. Patients underwent resection for gastric cancer and were studied 45 +/- 10 months after surgery. At the time of study, the patients had adapted well to surgery and no longer exhibited the severe symptoms of dumping seen immediately post-operatively. In contrast, the total gastrectomy patients exhibited the symptoms of reflux esophagitis. The gastrointestinal hormone changes could be divided into three patterns; obtunded responses (gastrin, PP), normal release (motilin, GIP) and increased secretion (CCK, neurotensin, PYY). In these, the early reaction of neurotensin correlated with the scores of late dumping syndrome and reflux esophagitis. In the literature, many gastrointestinal hormones have been shown to respond as an enhancement rather than adaptation. In other gastrointestinal hormones, secretin belonged to the obtunded type and enteroglucagon were classified in the increased type. However, pathophysiological significance of these hormonal changes remained uncertain. The late adaptive changes in gastrointestinal hormone secretion may help to compensate for loss of gastric motor function which accompanies gastric resection. On the other hand, these hormonal changes may exacerbate the esophageal reflux following gastrectomy.
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PMID:Gastrointestinal hormone in dumping syndrome and reflux esophagitis after gastric surgery. 940 15