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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic ketoacidosis is an acute medical emergency that requires immediate diagnosis and treatment. Diagnosis may be established rapidly by measurement of urinary glucose and ketones, arterial blood pH and blood gases, and serum ketones. Rapid infusion of large volumes of fluids and electrolytes, together with continuous infusion of low doses of insulin, provides effective restoration of fluid and electrolyte balance and correction of metabolic derangements. Hyperosmolar nonketotic coma is characterized by marked hyperglycemia in the absence of ketoacidosis and occurs usually in patients with mild adult-onset diabetes. Symptoms develop more slowly than in diabetic ketoacidosis. Treatment is the same for both conditions. In alcoholic ketoacidosis, hyperketonemia is present without hyperglycemia. The syndrome differs from diabetic ketoacidosis in that blood glucose levels are lower and glycosuria is absent. Treatment consists of intravenous administration of dextrose in water and, if necessary, of sodium bicarbonate. Insulin administration usually is not necessary.
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PMID:Combating diabetic ketoacidosis and other hyperglycemic-ketoacidotic syndromes. 0 17

Factors that influence hemoglobin (Hb)A(Ic) synthesis by intact erythrocytes were studied in vitro. After incubation cells were lysed, and hemoglobins were separated by isoelectric focusing on polyacrylamide slab gels and quantitated by microdensitometry. HbA(Ic) increased with time, glucose concentrations (5-500 mM), and incubation temperature (4 degrees -37 degrees C). Low temperatures allowed prolonged incubations with minimal hemolysis. At 4 degrees C HbA(Ic) increased linearly with time for 6 wk; after incubation at the highest glucose concentration, HbA(Ic) comprised 50% of total hemoglobin. Insulin (1 and 0.1 mU/ml) did not affect HbA(Ic) synthesis in vitro. In addition to glucose, galactose and mannose, but not fructose, served as precursors to HbA(Ic). A good substrate for hexokinase (2-deoxyglucose) and a poor hexokinase substrate (3-O-methylglucose), were better precursors for HbA(Ic) synthesis than glucose, suggesting that enzymatic phosphorylation of glucose is not required for HbA(Ic) synthesis. Autoradiography after erythrocyte incubation with (32)P-phosphate showed incorporation of radioactivity into HbA(Ia1) and A(Ia2), but not HbA(Ib), A(Ic), or A. Acetylated HbA, generated during incubation with acetylsalicylate, migrated anodal to HbA(Ic) and clearly separated from it. Erythrocytes from patients with insulinopenic diabetes mellitus synthesized HbA(Ic) at the same rate as controls when incubated with identical glucose concentrations. Likewise, the rate of HbA(Ic) synthesis by erythrocytes from patients with cystic fibrosis and congenital spherocytosis paralleled controls. When erythrocytes from cord blood and from HbC and sickle cell anemia patients were incubated with elevated concentrations of glucose, fetal Hb, HbC, and sickle Hb decreased, whereas hemoglobins focusing at isoelectric points near those expected for the corresponding glycosylated derivatives appeared in proportionately increased amounts.
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PMID:Synthesis of hemoglobin Aic and related minor hemoglobin by erythrocytes. In vitro study of regulation. 3 12

Isolated, small intestinal microvillous membranes from normal and acutely diabetic rats were compared with respect to D-glucose transport. D-Glucose was accumulated to a greater extent by diabetic membrane vesicles when supplied with energy in the form of a NaC1 or a NaSCN gradient across the vesicle membrane. The difference appeared to be caused by an ability of the diabetic membranes to maintain a higher driving force for active D-glucose transport and not by changes in the glucose "carrier." Increasing the glucose-independent Na-+-conductance of the membrane with monactin or gramicidin D reduced the active accumulation of D-glucose by membrane preparations from both control and diabetic groups. Concentrations of monactin and gramicidin D in the incubation medium of membrane vesicles from diabetic animals could be adjusted so that their D-glucose transport became indistinguishable from that of membranes from normal animals not treated with ionophores. These observatins suggest the microvillous membranes as one site where changes occur in acute diabetes. In addition, the change in the transport properties of the isolated membranes offer a rational explanation for the simultaneous elevation of active intestinal sugar, amino acid, and bile salt transport observed for intact intestinal tissue.
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PMID:Diabetes mellitus: changes in the transport properties of isolated intestinal microvillous membranes. 4 51

Calcium distribution in B cells of the isolated perfused rat pancreas was examined by the pyroantimonate precipitation technique in relation to the insulin secretory pattern of the perfused pancreas in response to 3 mM or 20 mM D-glucose or 20 mM D-glucose in calcium-depleted ethylene glycol tetra-acetic acid (EGTA) medium. Perfusion fixation after various time intervals from 3 to 30 min allowed appropriate relation to secretory phases. Qualitative and quantitative evaluation of the precipitation patterns revealed a significant increase in cell membrane associated percipitates after 3--5 min of perfusion with 20 mM glucose compared with the results after perfusion with 3 mM glucose. After 10--30 min of perfusion with 20 mM glucose there was an additional significant increase in precipitates located in the cytoplasm and the halos of the secretory granules. Perfusion with 20 mM glucose in calcium-deprived EGTA medium strongly reduced the number of precipitates within the B cells. The results suggest that cell membrane associated calcium may be involved in exocytosis, and by its sudden increase may trigger the first phase of insulin secretion. The calcium stores in the cytoplasm and the granules may be of importance for long-term regulation of insulin release.
Diabetes 1979 Jun
PMID:Ultracytochemical calcium distribution in B cells in relation to biphasic glucose-stimulated insulin release by the perfused rat pancreas. 10 39

Abdominal aortic aneurysmectomy is being performed with progressively lower operative mortality and morbidity. Three hundred thirty seven patients have had elective aneurysm repair since 1954. Factors affecting mortality and morbidity in the last 108 cases are analyzed. Seventy-four per cent of patients had pre-existing disease, either cardiac, pulmonary, renal, cerebrovascular, diabetes mellitus, or hypertension. Six patients died following operation, a mortality rate of 5.5%. One died of pulmonary and 5 of cardiac causes. No patient died of renal failure or required dialysis. A signficant feature of management is the regimen of fluid therapy using dextrose in lactated Ringer's solution during and after operation to minimize hypotensive and renal complications. No patient developed a wound infection, graft infection, wound dehiscence, stroke, or intestinal ischemia. Serious postoperative complications were largely cardiac or pulmonary. Despite recent liberalization of indications for operation, comparative figures show continued reduction in operative mortality from 17% during 1954-1961, or 7.4% during 1962-1967, to 5.5% in the 1968-1974 era. This declining mortality is related to earlier diagnosis using non-invasive methods (sonogram), simplified operative techniques, improvement in fluid management, innovations in cardiopulmonary therapy, and recognition and proper handling of unusual manifestations of aortic aneurysms.
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PMID:Surgical management of abdominal aortic aneurysms: factors influencing mortality and morbidity--a 20-year experience. 12 60

Both alloxan and streptozotocin produce beta-cell necrosis in the rat. Previous studies have shown protection against alloxan toxicity by D-glucose, D-mannose, and the nonmetabolized analogue 3-0-methyl-D-glucose and removal of this protective effect by D-mannoheptulose. The effect of several agents (i.v. infusion) against the beta-cell toxic effect of streptozotocin (60 mg./kg. i.v. in 24-hour-fasted 200-gm. male rats) was studied. Protection was determined by plasma glucose concentrations 24 and 48 hours later and, in certain experiments, by histologic examination of the islets. D-glucose and D-mannose provided no protection. Similarly, D-galactose, D-fructose, alpha-methyl-D-glucoside, D-L-glyceraldehyde, D-xylose, and D-glucosamine had no effect. However, 3-0-methyl-D-glucose administered immediately before streptozotocin resulted in progressive inhibition of beta-cell toxicity with complete protection at 0.83 mMoles per rat. The protective effect of 3-0-methyl-D-glucose was not altered by mannoheptulose. 2-Deoxy-D-glucose, which has no effect against alloxan, provided nearly complete protection against streptozotocin at 2.2 mMoles per rat. The effects of 3-0-methyl-D-glucose and 2-deoxy-D-glucose were additive and were not altered by glucose. Furthermore, the 3-0-methyl-D-glucose as well as 2-deoxy-D-glucose protective effects were still present, albeit attenuated, when these agents were given following the administration of streptozotocin. This is in contrast to alloxan, against which 3-0-methyl-D-glucose provides protection only when given before alloxan. 3-0-Methyl-D-glucose is the only carbohydrate protective against both streptozotocin and alloxan in the rat. However, several silent differences seem to exist between the mechanisms of beta-cytotoxic effects of these two diabetogenic compounds.
Diabetes 1976 Jul
PMID:Studies on streptozotocin diabetes. 13 82

Multiple small injections of streptozotocin produce a delayed, progressive increase in plasma glucose in mice within 5-6 days after the injections, in association with pronounced insulitis and induction of type C viruses within beta cells. Multiple subdiabetogenic doses of streptozotocin in rats and multiple injections of another beta cell toxin, alloxan, in mice did not induce insulitis although hyperglycemia followed the injection of larger quantities of both agents. In mice, the prior injection of 3-O-methyl-D-glucose (3-OMG) or nicotinamide attenuated the diabetic syndrome produced by streptozotocin; however, 3-OMG was more protective. Rabbit antimouse lymphocyte serum, alone, provided partial protection but, when given together with either 3-OMG or nicotinamide, effectively prevented the streptozotocin-induced diabetic syndrome. Cessation of these preventive treatments was followed by the appearance of insulitis and diabetes. These findings suggest that multiple injections of streptozotocin induce, in susceptible hosts, the triad of direct beta cell cytotoxicity, virus induction within beta cells, and cell-mediated autoimmune reaction. These factors, acting separately or in concert, appear to induce a destructive insulitis and severe diabetes. The relative importance of each component and the factors governing host susceptibility remain to be clarified.
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PMID:Studies of streptozotocin-induced insulitis and diabetes. 14 53

D-glucose in the pyranose (ring) form exists as two anomers. The alpha-anomer is more effective than the beta-anomer in promoting insulin secretion, suppressing that of glucagon, and protecting beta-cells against alloxan toxicity. Streptozotocin (SZ), a beta cell toxin, is composed of a cytotoxic moiety, 1-methyl 1-nitrosourea, attached to carbon-2 of glucose and exists as either of two anomers in the pyranose form. In 24-hour-fasted male rats, predominantly alpha- or predominantly beta-SZ was injected intravenously and plasma glucose levels were obtained 48 hours later. The alpha-anomer produced significantly greater beta-cell necrosis at doses of 30, 35, and 40 mg./kg. body weight. At higher doses, no differences between the alpha and beta anomers were observed. 3-O-Methyl glucose (3-OMG) protected against both SZ anomers; however, the alpha-SZ remained more toxic. Larger doses of glucose protected against the lower doses of SZ and, under such conditions, the individual glucose anomers appeared equally potent. Finally, mannitol at comparable molar concentrations was ineffective in protecting against the SZ toxicity. This study suggests that streptozotocin's beta cell toxicity is mediated through recognition by the beta cell. In addition, 3-OMG and, to a lesser but significant extent, glucose were shown to protect against the streptozotocin toxicity, whereas mannitol did not.
Diabetes 1977 Dec
PMID:Pancreatic beta cell toxicity by streptozotocin anomers. 14 86

Pancreatic islets isolated from rats infused with glucose for twenty-four hours incorporated 3H-leucine into protein at higher rates than islets isolated from normoglycemic rats. Incorporation into proinsulin-insulin showed a thirteenfold increase. The effect on other islet proteins was fourfold. Exposure of islets from normoglycemic rats to high glucose in vitro for twenty and ninety minutes and subsequent incubation with 3H-leucine at low glucose showed a twofold and fivefold increase in proinsulin biosynthesis. In the in vitro system pre-exposure of the islets to mannose and dibutyryl-cyclic AMP induced a much smaller increase in proinsulin biosyntheses.
Diabetes 1975 Feb
PMID:Persisting enhanced proinsulin-insulin and protein biosynthesis (3H-leucine incorporation) by pancreatic islets of the rat after glucose exposure. 16 98

Standardization of a technic for isolating large numbers of pancreatic islets is described. This procedure employed collagenase digestion of rat pancreatic tissue in a cylindrical wire screen in order to separate isolated islets from undigested pancreas. From this basic protocol the following conditions were established: (1) the duration of the initial digestion period was found to be optimal at six minutes; (2) three subsequent digestions of one minute each effected maximum islet yield; (3) the optimal initial collagenase concentration was found to be 1,000 U. (Worthington)/ml.; and (4) proper reductions of collagenase concentrations during the three subsequent digestions were found to be 50 per cent of each preceding incubation period. This method, combined with Ficoll gradient separation, yielded a mean of 800 islets per two rat pancreases. The isolated islets appeared morphologically intact, contained 0.36 +/- 0.05 mug. protein/islet, and demonstrated a normal biphasic release of insulin in response to stimulative levels of D-glucose. The present method provides a means for obtaining a large mass of viable islet cell tissue in a short time.
Diabetes 1976 Aug
PMID:Standardization fo a digestion-filtration method for isolation of pancreatic islets. 18 6


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