Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Colonic pseudo-obstruction (Ogilvie's syndrome) may occur in surgical patients, particularly those who have had orthopedic or blunt trauma, have uremia or diabetes, have complex metabolic or cardiac failure, have metastatic cancer involving the lymph nodes and neural tissue, or are addicted to narcotics. Although a single true cause has not been identified by fulfilling Koch's postulates, the clinical pattern has been recognized in a variety of surgical patients, and this pattern must be distinguished from true obstruction of the colon. Tumor or internal hernia may constitute an obstruction, but the important differential diagnosis of cecal volvulus must be excluded. Ischemic colitis may be confused with Ogilvie's syndrome or may follow it. Gangrene, infarction, and perforation may ensue as colon diameter increases and particularly if cecal distention reaches above 14 cm. This arbitrary number for cecal dilatation should not be awaited before treatment is instituted if signs of devitalization of the gut or peritoneal signs have developed in the patient. Treatment has changed recently with the widespread application of colonoscopy. Endoscopy is helpful in relieving distention but may also be dangerous in the patient with a massively distended colon, particularly at the level of the thin-walled cecum. Colonoscopy also appears to be associated with a high rate of treatment failure and recurrence. Surgical decompression may take the form of cecostomy or may require exteriorization or resection of the colon if infarction has occurred. A series of 12 patients has been presented. The patients were all referred to a single surgeon in a university medical center over a 4 1/2 year period with clinical patterns not suggestive of a common cause but a similar clinical evolution of Ogilvie's syndrome. The prognosis for such patients in whom the complication is recognized early and in whom decompression is performed endoscopically or surgically is encouraging. If recognition is late and particularly if perforation and gangrene result, mortality is nearly 50 percent.
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PMID:Colonic pseudo-obstruction in surgical patients. 397 Mar 26

Pressure activity in the stomach and upper intestine was studied in 104 patients referred to the Mayo Clinic for evaluation of functional symptoms (nausea, vomiting, upper abdominal pain, or other dyspeptic symptoms in the absence of structural gut abnormalities). Manometric abnormalities were found in 75 patients. Forty-three of these had gastric abnormalities and 32 patients had both gastric and intestinal abnormalities. In the stomach, decreased antral phasic pressure activity after a solid meal was the most common abnormality. In the upper intestine, unpropagated bursts of phasic and tonic contractile activity were a relatively frequent abnormality but a number of other altered manometric patterns also were observed. Digestive tract symptoms were not good predictors of the presence or site of the gastrointestinal manometric abnormalities. Patients with associated neurologic, urologic, or metabolic (diabetes) disease were more likely to exhibit manometric abnormalities than were those without evidence of disease outside the gut. Almost two-thirds of the patients with symptoms and normal manometry presented features suggestive of psychiatric disease. We conclude that in patients with severe functional-type symptoms gastrointestinal manometry is a useful technique to evidence the underlying gut motor disturbance that is present in a relatively high proportion of these patients.
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PMID:Manometric evaluation of functional upper gut symptoms. 397 47

The small intestine can utilize endogenous substrates for triglyceride synthesis. In diabetes mellitus, potential endogenous substrates are elevated. This study was designed to investigate whether intestinal triglyceride production utilizing endogenous substrates contributes to the pathogenesis of hyperlipidemia in diabetes. Intestinal fatty acid esterification as well as activities of acyl-CoA synthetase and acyl-CoA monoglyceride acyltransferase are the same in diabetic and control rats when the results are expressed per milligram protein. However, due to marked intestinal hypertrophy these activities are increased when the results are expressed as per centimeter gut length. In the mesenteric lymph fistula rat model, we found that during fasting diabetic rats have a greater than twofold increase in triglyceride output that is carried mainly by very low-density lipoproteins (VLDL). During lipid infusion, total triglyceride fatty acid output was not different between diabetic and control rats, although there were significant differences in the patterns of partition of endogenous and exogenous triglyceride into chylomicrons and VLDL. Endogenous triglyceride production did not increase in diabetic rats during lipid infusion. In contrast, there was a substantial increase in endogenous triglyceride production in the control group to a level comparable with that of the diabetic rats. There was a significant reduction in incorporation of exogenous triglyceride into chylomicrons in diabetic rats.
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PMID:Role of small intestine in pathogenesis of hyperlipidemia in diabetic rats. 402 44

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

Immunoreactive somatostatin (IRS) was measured in extracted plasma obtained from the hepatic portal vein (PV) and inferior vena cava (IVC) of acute, untreated, spontaneously diabetic Wistar rats (BBL), insulin-treated diabetic rats, and nondiabetic controls. Acetic acid extracts of the pancreas and entire gastrointestinal tract were assayed for IRS, and the volume density of pancreatic D-, A-, and B-cells was determined by quantitative morphometry. The concentration of IRS in the PV and IVC of the untreated diabetic rats was significantly elevated compared with controls, with a much greater percent increase in the IVC compared with the PV. Insulin treatment for 4-6 wk restored the elevated PV and IVC levels to control values. The pancreatic content of IRS and the volume density of D-cells was severely reduced in the diabetic groups whereas gut IRS was unchanged. These data suggest that the elevated blood levels are secondary to insulin deficiency and result from altered peripheral metabolism and/or increased secretion of IRS most probably from the gut. The increased peripheral blood concentration of IRS raises the possibility of an endocrine role of circulating somatostatin in diabetes. The reduction in pancreatic IRS found in this model is probably secondary to insulitis and contrasts with the D-cell augmentation reported in streptozotocin-diabetic rats.
Diabetes 1980 Sep
PMID:Elevated portal and peripheral blood concentration of immunoreactive somatostatin in spontaneously diabetic (BBL) Wistar rats: suppression with insulin. 610 76

The effect of gut glucagon-like immunoreactivity (GLI) devoid of pancreatic glucagon was studied in piglets. All glucagon-like peptides with an accessible C-terminal were removed from the gut extract by specific antibodies reacting with the C-terminal of the glucagon molecule. Endogenous secretion of pancreatic and gut glucagon was blocked by somatostatin infusion, and then the purified gut glucagon preparation was infused. The latter prevented the hypoglycemia resulting from somatostatin infusion, and increased the glucagon level detectable by C-terminal specific antibodies in the blood of the animals. This rise was significant statistically from the 30th min of GLI administration (26.7 +/- 7.2 pg/ml versus 137.0 +/- 67.0 pg/ml; P less than 0.05) and increased until the end of the infusion (90th min, 218 +/- 60 pg/ml; P less than 0.005). It has been suggested that, owing to the in vivo enzymatic degradation of the infused gut glucagon, biologically active "pancreatic" glucagon fractions are formed extracellularly.
Diabetes 1981 Sep
PMID:Evidence for transformation of glucagon-like immunoreactivity of gut into pancreatic glucagon in vivo. 611 89

The widespread role of somatostatin (SRIF) as a mediator of function in the brain and gut has stimulated interest in it mechanism of action. We have examined the mode of action of SRIF in stimulus-secretion coupling in the pancreatic islet beta-cell to determine whether SRIF antagonizes the glucose-induced decrease in K+ permeability (PK). The influence of SRIF on 86Rb fluxes and insulin release in cultured rat islet cells, and also the electrical events recorded from cultured islets and microdissected mouse islets, was examined. In cultured islets, 100 ng/ml SRIF in the presence of 16.7 mM glucose inhibited the incidence of spike activity and evoked hyperpolarization. This effect was counteracted by 0.1 mM quinine and 20 mM tetraethylammonium (TEA), drugs that inhibit the Ca2+-sensitive or voltage-sensitive increase in PK, respectively. These agents also counteracted the inhibitory influence of SRIF on glucose-induced insulin release in cultured islets. SRIF disrupted the typical glucose-induced oscillatory pattern of electrical activity (burst activity) during continuous microelectrode recordings in mouse beta-cells, resulting in a transient 5mV hyperpolarization and a decrease in the frequency of generation of burst activity. The presence of 20 mm TEA prevented the influence of SRIF on the electrical activity. SRIF had no effect on the accumulation of 86Rb into islet cells obtained in the presence of 16.7 mM glucose. However, SRIF enhanced the rate of 86Rb efflux from cells exposed to glucose. SRIF-induced enhancement of 86Rb efflux was antagonized by TEA or quinine. These results indicate that SRIF may activate PK as its primary mode of action, an event that may be sufficient to reduce the accumulation of intracellular Ca2+ thereby disrupting glucose-induced stimulus-secretion coupling.
Diabetes 1981 Oct
PMID:Somatostatin: mechanism of action in pancreatic islet beta-cells. 611 84

In the present study we have attempted to assess the functional status of somatostatin cells in relation to the function of the other islet cell types (B, A, and PP cells) in the BB Wistar rat. Somatostatin-like immunoreactivity (SLI), glucagon, and insulin were measured in extracted plasma obtained from the hepatic portal vein (PV) and inferior vena cava (IVC) of acutely diabetic untreated rats, insulin-treated diabetic rats and nondiabetic controls. Extracts of the pancreas were assayed for SLI, glucagon, and insulin, and the pancreatic populations of A, B, D, and PP cells were evaluated by morphometry. Extrapancreatic somatostatin changes were assessed by measurement of SLI in extracts of the whole gut, hypothalamus, and retina. Direct studies of SLI, glucagon, and insulin secretion in response to glucose, arginine, and theophylline were carried out using the isolated perfused pancreases of two separate groups of untreated diabetic and nondiabetic rats. Our results showed that in the severely insulin deficient BB Wistar rat (1) pancreatic concentrations of SLI, glucagon, and insulin were reduced; (2) the B cells are virtually eliminated and the D cells severely reduced early in diabetes; A and PP cells are resistant initially but eventually sustain major losses as observed in terminal islets; (3) retinal SLI is reduced, but SLI in gut and brain appears unchanged; (4) the secretion of SLI, glucagon, and insulin from the perfused pancreas is diminished 60%, 36%, and 99%, respectively; (5) PV and IVC blood levels of SLI and glucagon are elevated despite decreased pancreatic secretion; (6) The trans-hepatic gradient of SLI is reduced; and (7) Insulin treatment normalizes the elevated PV and IVC levels of SLI and glucagon. It is concluded that the elevated PV and IVC levels of SLI are secondary to insulin deficiency and result from increased SLI secretion most probably from the gut and from diminished hepatic metabolism. The origin of the hyperglucagonemia is less certain, but as in the case of SLI, important contributions from extra-pancreatic secretion appears likely.
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PMID:Alterations in somatostatin and other islet cell functions in the spontaneously diabetic BB Wistar rat: biochemical and morphological characterization. 613 36

Delayed augmented mitogenic reactivity follows mast-cell secretion in mesentery and skin in streptozotocin-diabetic rats with 4-week insulin-deficiency (Norrby 1982; Norrby et al. 1982; Norrby 1983). In such rats the basal proliferation is essentially unchanged in the mesentery and skin, whereas it is significantly increased in the small gut and significantly decreased in the kidney. On treating rats with 4-week-old diabetes with very-long-acting insulin for over 3 days (16 U/kg X 2 daily) the basal proliferation of the small gut and the kidney apparently became normal, the body weight increased, and the blood glucose concentration dropped substantially and progressively. However, insulin-treatment did not affect the mast-cell-dependent mitogenesis in the mesentery following intraperitoneal injection of the mast-cell secretagogue compound 48/80, as judged by specific DNA activity and mitosis counting. We conclude that some metabolic or cellular feature of diabetes which is not restored by 3-day insulin treatment, and not insulin deficiency itself, is the cause of the delayed increased mitogenic reactivity that follows mast-cell secretion in diabetic rat.
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PMID:The effect of insulin on delayed augmented mast-cell mediated mitogenesis in diabetic rats. 614 62

We reported previously that pancreatic somatostatin and glucagon content and D and A cells are reduced in spontaneously diabetic BB rats while portal plasma levels of these hormones are elevated but normalized by insulin therapy. Presently, we have characterized the basal and stimulated (glucose, theophylline, arginine) release of islet hormones from perfused pancreases of three groups: nondiabetic, untreated diabetic, and insulin-treated diabetic rats. Maximal glucagon and somatostatin release were significantly reduced in untreated diabetics. Treatment normalized glucagon but further reduced somatostatin secretion. Thus, hyperglucagonemia and hypersomatostatinemia cannot result from pancreatic hypersecretion but are of extrapancreatic (probably gut) origin. A theophylline-induced paradoxical inhibition of somatostatin secretion that was normalized by insulin was found in insulin-openic diabetic rats. This likely represents a secondary effect of insulin deficiency. One animal with the rare finding of spontaneous recovery from insulin-dependent diabetes was characterized as normoglycemic, hypoinsulinemic, hypersomatostatinemic, and normoglucagonemic. Normal basal and hyperglycemic insulin release was exhausted by more potent secretagogues. Somatostatin release was markedly exaggerated, whereas secretagogues had no significant effect on elevated basal glucagon output.
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PMID:Somatostatin, glucagon, and insulin secretion from perfused pancreas of BB rats. 614 95


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