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

A patient with a history of diabetes mellitus and congestive heart failure was taking furosemide and metolazone as diuretics. Diabetic ketoacidosis developed, and the patient became lethargic and confused. Initial biochemical determinations showed an alkalemic pH, serum and urine ketones with an anion gap, and hyperventilation. The hyperventilation was appropriate for the degree of ketoacidosis but it was grossly inappropriate for the alkalemia. This could be explained by a direct effect of ketones on the respiratory center or a sudden increase in hydrogen ion concentration superimposed on previously chronic alkalemic pH due to the potent combination of furosemide and metolazone.
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PMID:Alkalemia in diabetic ketoacidosis. 643 81

Diabetes mellitus is associated with the enhanced uptake of several nutrients. The purpose of this study was to use an established in vitro technique to examine the uptake of bile acids into jejunum, ileum, and colon of control (CON) and streptozotocin-diabetic rats (DM). When the bulk phase was stirred to reduce the effective thickness of the unstirred layer, the ileal uptake of 1.5-15 mM cholic (C), glycocholic (GC), taurocholic (TC), chenodeoxycholic (CDC), glycochenodeoxycholic (GCDC), and deoxycholic (DC) acid was similar in CON and DM. The relative values of the maximal transport rates (Jdm) were CDC greater than GC greater than GCDC greater than C greater than TC = DC, and similar relative values were observed for the Michaelis constants (Km). The values of Jdm and Km for each bile acid were similar in CON and in DM. In CON and at pH 7.4 an inverse linear relationship was noted between the number of hydrogen bonds in the bile acids and the natural logarithm of the permeability coefficient (Pd) times the square root of the molecular weight of the bile acid. This slope reflected the incremental change in free energy, delta delta Fw leads to I, associated with the uptake of bile acids; the value of delta delta Fw leads to I was similar for jejunum, ileum, and colon of CON, but was lower in jejunum of DM than CON. Thus, DM is associated with a greater relative permeability of the jejunum but not the ileum or the colon to a series of bile acids.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 Oct
PMID:Uptake of bile acids into rat intestine. Effect of diabetes mellitus. 661 19

Metabolic acidosis with a normal anion gap results from either bicarbonate loss or a urine acidification defect. The bicarbonate loss may be via the gastrointestinal tract or the urine, or may be indirect due to excretion of the sodium and potassium as opposed to the ammonium salts of ketone body anions. Defects in urine acidification in the diabetic have several etiologies: first, hydrogen ion secretion may be decreased because of an intrinsic defect in the hydrogen ion pump (i.e., diseases of the renal medulla); second, there may be a failure to augment hydrogen ion secretion by a favorable electrical gradient (e.g., reduced mineralocorticoids); and third, there may be a failure to generate a favorable chemical gradient to augment hydrogen ion secretion (e.g., reduced urine ammonia). Reduced levels of aldosterone associated with hyporeninemia has been termed type IV RTA, and these patients have specific therapeutic needs.
Diabetes 1981 Sep
PMID:Selected aspects of the pathophysiology of metabolic acidosis in diabetes mellitus. 679 Mar 25

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.
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PMID:Serum potassium concentration in acidemic states. 679 Oct 40

Acarbose (Bay g 5421) is a powerful alpha-glucoside hydrolase inhibitor of potential value in the treatment of diabetes and hypoglycemic dumping syndrome after gastric surgery. The extent of its use may be limited by symptoms produced by carbohydrate malabsorption. To minimize these, the action of low doses of acarbose on 24-h blood glucose profiles and hydrogen evolution have been studied on four ambulant volunteers on control diets, after exclusion of sucrose and also after addition of guar in an attempt to enhance the therapeutic effect. Replacement of dietary sucrose by starch abolished significant hydrogen evolution in the morning after low doses of acarbose but did not reduce its effectiveness in decreasing the mean three-meal blood glucose area by 41% (P less than 0.002). Addition of hydrated guar to this diet reduced the mean three-meal glucose area after acarbose further by 72% (P less than 0.001) but increased hydrogen evolution. The results suggest that acarbose will be both effective and acceptable given at low dose when the dietary carbohydrate is starch.
Diabetes Care
PMID:Effect of acarbose on the 24-hour blood glucose profile and pattern of carbohydrate absorption. 692 27

The possible participation of superoxide anions, hydrogen peroxide, and hydroxyl radicals in the action of alloxan was investigated using isolated rat pancreatic islets. Exposure of islets for 5 min to alloxan (0.15 or 0.2 mg/ml) inhibited subsequent glucose-stimulated insulin release. The presence of superoxide dismutase (1000 U/ml), catalase (50 microgram/ml), or a metal chelator diethylenetriaminepentacetic acid (1 mM) markedly attenuated this effect of alloxan. Use of these agents afforded complete protection from the lower concentration of alloxan and partial protection from the higher concentration of the toxic compound. Inactivation of the enzymes or addition of excess iron to the chelating agent before its use with alloxan eliminated the protective action of these agents. The results are consistent with the proposal that hydroxyl radicals, generated via reactions that involve superoxide anions, hydrogen peroxide, and iron, mediate the deleterious effect of alloxan in pancreatic islets.
Diabetes 1980 Mar
PMID:Inhibition of alloxan action in isolated pancreatic islets by superoxide dismutase, catalase, and a metal chelator. 699 24

Fifty-gram carbohydrate tolerance tests were performed on healthy volunteers to test the activity and specificity of an alpha-glucoside hydrolase inhibitor, acarbose (BAY g 5421). Two hundred milligrams acarbose reduced the area under the blood glucose response curve by 89% (P less than 0.001) after sucrose by 80% (P less than 0.002) after starch, by 19% (N.S.) after maltose, with no effect on glucose. Breath hydrogen measurements indicated an almost complete malabsorption of the sucrose. At 50 mg acarbose, some reduction in blood glucose and insulin response to sucrose was still seen, but no significant hydrogen production. It is suggested that at lower doses, acarbose may prolong the time course over which carbohydrate is absorbed as does dietary fiber; as with fiber, it may be a useful adjunct to diabetic therapy.
Diabetes 1981 Nov
PMID:Scope and specificity of acarbose in slowing carbohydrate absorption in man. 702 48

Insulin stimulates the production of superoxide and hydrogen peroxide in various tissues. Hydrogen peroxide has been proposed to be an intracellular second messenger for insulin and a moderator of cellular proliferation and differentiation. We previously found that cell proliferation is increased in small intestinal mucosa of streptozotocin-diabetic rats. The current study was undertaken to determine if superoxide dismutase (SOD), the enzyme that converts superoxide to hydrogen peroxide, is altered in the mucosa of the alimentary tract and renal cortex of the diabetic rat, and if so, whether SOD responds to insulin treatment. Total SOD and cyanide-insensitive [manganese-containing SOD (Mn SOD)] SOD were measured by the nitroblue tetrazolium inhibition assay. We studied ad libitum fed animals, where diabetics are hyperphagic and pair-fed animals, where hyperphagia is not present. Since cyclic nucleotides appear to control cell proliferation in some tissues, we also measured cAMP and cGMP in mucosa of the small intestine. In ad libitum fed animals, total SOD was depressed in the mucosa of duodenum, jejunum, and ileum, but not in the cecum or colon of the streptozotocin-diabetic rats. The level of Mn-SOD was not affected by diabetes or insulin treatment, but the cyanide-sensitive [copper- and zinc containing SOD (Cu-Zn SOD] SOD was depressed in the small intestine and colon of diabetic rats. Insulin treatment restored total and Cu-Zn SOD activity in the small intestine to normal and increased Cu-Zn SOD activity in the colon to normal. Pair-fed animals showed the same changes in the SOD activity of jejunal mucosa that were found in ad libitum fed animals. In renal cortex, diabetes did not alter total SOD, but increased Mn SOD and decreased Cu-Zn SOD. Both responses were reversed by insulin treatment. Cyclic nucleotide concentrations were not affected by diabetes. We conclude that SOD enzymes re altered in diabetes, at least in proliferating tissues. Responses are tissue specific. The mucosa of the small intestine and colon show decreased Cu-Zn SOD, the SOD of the cecum is unaffected, and the kidney shows increased Mn SOD and decreased Cu-Zn SOD. The SOD responses of diabetics are reversed by insulin treatment.
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PMID:Superoxide dismutase activity in the intestine of the streptozotocin-diabetic rat. 704 72

The advent of electrochemical sensors for intermittent sampling of blood gases and hydrogen ions in the clinic, intensive care, and surgical units has revolutionized diagnostic and critical care medical technics. The use of electrochemical sensors for continuous transcutaneous monitoring of blood gases is further enhancing the medical surveillance of patients. The more recent introduction of glucose and other electroenzymatic sensors has stimulated broad research in the development of metabolic monitoring. For the present research, the glucose sensor widely used for the rapid specific micro-analysis of whole blood and plasma is explored for possible use as an in vivo intravascular or tissue-implanted sensor. This sensor is based on the polarographic measurement of hydrogen peroxide generated by glucose oxidase (EC 1.1.3.4) held between two membranes. The first membrane allows the diffusion of glucose, ions, and many other small molecules, while the second membrane allows the diffusion of the glucose-generated hydrogen peroxide to the platinum surface, but excludes ascorbic acid, bilirubin, and uric acid. Such sensors respond rapidly and specifically when acutely implanted subcutaneously in cats and dogs. They function well as glucose-sensor-tipped venous catheters. One sensor was repeatedly used for in vitro polarograms, subcutaneous and blood glucose monitoring, over a period of ten months, with storage in the cold between uses, with the complete retention of its response characteristics.
Diabetes Care
PMID:Implanted electroenzymatic glucose sensors. 717 79

Diabetes mellitus is a multi-component syndrome that is often complicated by angiopathy which is partly due to enhanced platelet functions. Using fluorescent dyes 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and Fura-2 AM, changes was evaluated in the concentration of baseline and thrombin-stimulated increases in intracellular ionized calcium (Ca2+i) relative to hydrogen ions in the platelets from control, insulin-treated, and non-treated diabetic rats. The cytosol of platelets from the diabetic rats were more acidic compared to the insulin-treated and normal control rats. The increased intracellular hydrogen ion concentration [H+] or decreased pH (pH) in the diabetic rat platelets is associated with an increased baseline [Ca2+]i. Upon stimulation with thrombin, the mean peak [Ca2+]i for the insulin-treated (309 +/- 97 nmol/L) and untreated (339 +/- 135 nmol/L) diabetic rats was significantly higher than the concentration for the normal rats (213 +/- 101 nmol/L). Treatment with insulin attempts to correct the diabetes-induced elevation in the baseline of [Ca2+]i and intracellular H+. These results suggest that the relationships between Ca2+ and H+ relative to binding sites are similar in the intra- and extracellular compartments. It is our conclusion that the enhanced platelet activity and associated development of vascular diseases in diabetes may be due to an increased intracellular H+ that caused an increased baseline [Ca2+]i in diabetes mellitus.
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PMID:Intracellular calcium and hydrogen ions in diabetes mellitus. 748 14


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