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

In a study of seven type II diabetics the effects of the usual diabetic diet were compared with those of a cereal of whole-meal (both having the same energy content and nutrients proportions). The cereal gave a more even blood-glucose curve at a significantly lower level (maximal rise after the first breakfast with the cereal was 20 mg/100 ml, after the usual diabetic breakfast 75 mg/100 ml). In addition, in 12 metabolically healthy persons comparison was made of post-prandial blood-glucose and insulin levels after intake of raw and of heated wheat and corn whole-meal preparations. The raw wheat variant produced much flatter blood-glucose and insulin curves than the heated test meals (maximal rise of blood-glucose 6 vs 27-38 mg/100 ml; blood insulin 8 vs 35-50 microU/ml), while the raw corn (oat) variant achieved only a small flattening of the curve compared with that after the heat-treated preparation. Measurement of H2 exhalation provided no evidence for differential malabsorption between raw and heated test meals. Fresh-corn muesli with unheated wheat whole-meal is suitable in the diet of type II diabetics to counteract high postprandial levels of blood-glucose and thus improve the diabetic metabolic state.
 ...
PMID:[Blood glucose and insulin levels in healthy persons and diabetics after intake of coarse wholemeal preparations, especially fresh grain muesli]. 282 98

Glucomannan (Propol), a potent gel forming dietary fibre, was added to a carbohydrate rich breakfast in eight patients with previous gastric surgery suffering from postprandial hypoglycaemia. Addition of only 2.6 g and 5.2 g glucomannan to the meal dose dependently improved reactive hypoglycaemia from 2.3 (0.2) mmol/l to 3.3 (0.2) mmol/l (p less than 0.0005) after 2.6 g and 4.1 (0.2) mmol/l (p = 0.0005) after 5.2 g, and decreased postprandial rise in plasma insulin (p less than 0.05). Expiratory breath hydrogen excretion tended to decrease reflecting improvement of carbohydrate metabolism. Addition of glucomannan to an intraduodenal sucrose solution significantly raised plasma glucose nadirs, indicating glucomannan to be effective during the intestinal phase. It is concluded that small amounts of glucomannan may be beneficial to patients with reactive postprandial hypoglycaemia, without the disadvantage of unpalatability and carbohydrate malabsorption.
 ...
PMID:Glucomannan prevents postprandial hypoglycaemia in patients with previous gastric surgery. 284 Mar 65

Based upon the clinical finding that a Merck somatostatin-14 (S-14) analog induced steatorrhea in man, we sought to develop animal models to study the effects of S-14 and a series of synthetic analogs on absorption. Rats were trained to eat a diet (preweighed) containing 15% fat. Following the feeding period, the remaining diet was removed and the amount consumed recorded. This food conditioning of the rats was continued until the rats consumed approximately 15 g of the diet per day. Feces were collected and weighed prior to feeding periods. On test days, S-14 or analogs were administered sc to rats immediately prior to feeding. For each compound tested, fat absorption decreased in dose-dependent fashion. For example, S-14 at 0.5 mg/kg did not increase % of dietary fat in feces (% DFF). At 1.0 mg/kg, S-14 increased % DFF from 7.9 to 10.2 (p less than 0.01, pretest day vs test day), and at 10 mg/kg S-14, % DFF increased from 9.1 to 12.8 (p less than 0.001). For each analog, the subcutaneous dose required to decrease fat absorption in rats was several orders of magnitude higher than the intravenous dose required to inhibit insulin and glucagon. Moreover, the threshold for production of statistically significant increases in fecal fat differed among analogs when compared to their endocrine potencies. One analog administered in the model for 14 days was shown to produce consistent fat malabsorption throughout the entire test period; however, this lipid malabsorption was substantially more pronounced on the first three days of the treatment period. When the compound was not administered on day 15, the % DFF significantly decreased. In an attempt to develop a system more suitable for rapid screening, pancreatic secretagogues such as secretin or cholecystokinin, were administered intravenously to anesthetized rats whose duodena had been cannulated and perfused to enable collection of pancreatic secretions. Total amylase, lipase, and protein were determined in single animals in response to a secretagogue, both before and after iv pretreatment by S-14 or an analog. Pancreatic enzyme secretion in response to sequential secretagogue-stimulation was found to be reproducible for up to three injections and behaved in a dose-dependent fashion. In general, secretagogue-induced increases in amylase, lipase, and total protein were comparable. Pretreatment with the S-14 analogs substantially inhibited secretagogue-induced pancreatic exocrine secretion and was dose-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:The effects of somatostatin and selected analogs on lipid absorption in animals. 286 42

Parenteral somatostatin has been used to suppress growth hormone secretion in acromegalic patients, but long-term treatment is hampered by its short half-life of a few minutes in the circulation. An octapeptide analogue of somatostatin (SMS 201-995) has recently been developed that has greater potency and selectivity in suppressing growth hormone than the native hormone. In this study somatostatin and somatostatin octapeptide infusions were compared in 13 patients with active acromegaly. The octapeptide had a longer duration of action in the suppression of growth hormone than native somatostatin. A twice daily dose of 100 micrograms significantly suppressed growth hormone during the day. Prolactin was not suppressed, even in hyperprolactinaemic patients, and suppression of insulin was of short duration. Two patients had diarrhoea, but this disappeared when treatment with the octapeptide was stopped. Somatostatin is known to suppress pancreatic exocrine function, and it is therefore important to look for evidence of malabsorption during long-term treatment with the octapeptide. Somatostatin octapeptide is therefore useful in the treatment of acromegaly, but evidence of malabsorption should be watched for; nonparenteral routes of administration need to be assessed.
 ...
PMID:Somatostatin octapeptide (SMS 201-995) in the medical treatment of acromegaly. 287 97

Phenytoin (diphenylhydantoin) was used in doses of 300 mg/24 hours to treat severe motor diarrhoea in 5 diabetic patients. The patients had been insulin-dependent for 2 to 17 years and had advanced neuropathy. In each case, malabsorption, lesions of the colon or small bowel, endocrine tumour or parasitic, infectious and inflammatory causes could be excluded. Under phenytoin the diarrhoea ceased in all 5 patients within 24 to 48 hours. It recurred in 4 of them within 48 hours when treatment was withdrawn to disappear within the same length of time when it was reintroduced. No relapse was observed for periods of 3 months to 5 years under phenytoin maintenance treatment. The mechanism of action of phenytoin may suggest that diabetic diarrhoea is hormone-mediated or caused by an effect on the autonomous nervous system or on the peptidergic system, but no definite conclusion can be reached in the present state of our knowledge.
 ...
PMID:[Phenytoin treatment of motor diarrhea in diabetic patients]. 293 41

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
 ...
PMID:Consequences of phosphate imbalance. 306 Jan 61

Sixteen patients given total pancreatectomy were experienced, and the essential points of postoperative management were reported. The morbid states after total pancreatectomy consist of: a deficiency of pancreatic endocrine function, a deficiency of pancreatic exocrine function, loss of the duodenum and upper jejunum, the influence of partial or total gastrectomy, and the influence of dissection around the superior mesenteric artery. These states influence each other and become more complicated. The management period is divided into five parts as follows; a period of intravenous nutrition, the early half; water replacement period, the late half; hyperalimentation period, a period of intravenous and enteral nutrition, a period of enteral, intravenous and oral nutrition, a period of oral and enteral nutrition, and a period of oral nutrition. In each period, a special form of management is needed. The essential points of long-term management are as follows: The use of suitable doses of pancreatic enzyme and antidiarrheal agents for the cure of severe maldigestion and malabsorption. Also, intermittent IVH or elemental diet are effective for recovery from deteriorative malnutrition. For the prevention of hypoglycemic attack, training of the patients and the maintainance of good nutrition are important. These patients have a high incidence of infection, and so speedy treatment must be given if this occurs. Fatty liver must be treated by intermittent IVH or elemental diet. As total pancreatectomy imposes a severe burden on the patient, including self-injection of insulin, the indications of this operation must be decided carefully giving due consideration to its radicality.
 ...
PMID:[Postoperative management of total pancreatectomy]. 309 14

Acarbose delays the production of monosaccharides (notably glucose) by inhibiting the alpha-glucosidases associated with the brush-border membrane of the small intestine which are responsible for the digestion of complex polysaccharides and sucrose. In healthy subjects acarbose 100 to 200 mg significantly inhibits postprandial glucose, insulin and triglyceride responses, with some evidence of carbohydrate malabsorption with the higher dose. Clinical trials in patients with non-insulin-dependent diabetes mellitus showed that acarbose improved diabetic control, especially postprandial blood glucose levels, independent of whether the patients were receiving concomitant oral antidiabetic drugs in addition to dietary management. In comparative studies acarbose was significantly superior to placebo, and comparable to biguanides, when used alone or as an adjuvant to sulphonylurea therapy. Trials in patients requiring insulin to control their diabetes demonstrated that acarbose significantly reduced postprandial blood glucose concentrations, resulting in a smoother diurnal blood glucose-time curve and improved symptoms associated with nocturnal hypoglycaemia. Daily insulin requirements were sometimes reduced. In large multicentre trials acarbose up to 600 mg/day for 3 to 12 months improved glycaemic control in approximately 55% of patients with non-insulin-dependent or insulin-dependent diabetes mellitus. Apart from its use in diabetes, encouraging preliminary results have been obtained with acarbose in other therapeutic areas such as dumping syndrome, reactive hypoglycaemia, and types IIb and IV hyperlipoproteinaemias--however, further clinical experience is needed in these settings before clear conclusions can be drawn. No serious side effects have been reported during treatment with acarbose, although it is associated with a high incidence of troublesome gastrointestinal symptoms such as flatulence, abdominal distension, borborygmus and diarrhoea. The incidence of these reactions usually decreases with time. Thus, acarbose represents the first of a new class of oral antidiabetic drugs--the alpha-glucosidase inhibitors. It has proven useful for improving glycaemic control when used as an adjunct to standard therapy involving dietary restriction, oral antidiabetic drugs and/or subcutaneous insulin. That being the case, acarbose should provide the clinician with an interesting treatment option which can be used in a broad range of patients with diabetes mellitus in whom 'traditional' management approaches produce suboptimal glycaemic control.
 ...
PMID:Acarbose. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential. 328 12

Within 1 hr of intraperitoneal administration of 1 microgram 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg, lipoprotein lipase (LPL) activity was reduced 38% from initial levels in the adipose tissue of the guinea pig. Maximal depression was observed after 2 days and persisted throughout the 10-day observation period. Oral administration of glucose restored LPL activity in TCDD-treated animals after 1 day but only partially after 2 and 5 days, and had no effect after 10 days of exposure. Although initial (2-day) serum insulin levels were depressed, the inability of glucose to restore LPL activity after prolonged exposure was not due to malabsorption of glucose nor to changes in serum thyroxine or insulin concentration. TCDD also inhibited the lipolytic pathway in the adipocyte, but had no effect on hormone sensitive lipase (HSL). Since HSL and LPL are reciprocally regulated, it was concluded that TCDD acts on the adipocyte to uncouple HSL-LPL reciprocity as well as to reduce LPL production.
 ...
PMID:Reduction of adipose tissue lipoprotein lipase activity as a result of in vivo administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin to the guinea pig. 328 12

Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .01), and glycosylated hemoglobin and fasting level of glucose were lower (P less than .01 to .05) in the 31 patients with pancreatogenic diabetes than than in 35 otherwise comparable patients with type I (insulin-dependent) diabetes, yet daily insulin dose was similar in the two groups. Glucagon stimulated C-peptide was inversely correlated to glycosylated hemoglobin in insulin-dependent patients with pancreatogenic diabetes and in type I diabetes. Since body mass indices were identical in the two groups, better glucoregulation was not due to reduced food intake or malabsorption in pancreatogenic diabetes. Rather residual B cell function and/or different secretion of other pancreatic hormones in pancreatogenic diabetes may account for different metabolic control in type I IDDM compared with insulin-dependent pancreatogenic diabetes.
 ...
PMID:Metabolic control and B cell function in patients with insulin-dependent diabetes mellitus secondary to chronic pancreatitis. 330 47


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>