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

Tests were carried out on the influence of alloxan-induced diabetes mellitus on the metabolism and the ultrastructure of ovaries of juvenile rats. The diabetes mellitus caused the following changes in the metabolism: reduction in the concentration of ATP and NADPH, increase in the lactate/pyruvate quotient to above 40, reduction in the ATP/ADP quotient to below 1, reduction in the level of activity of the hydrogen-conveying enzymes G-6-P-dehydrogenase, isocitrate dehydrogenase and malate dehydrogenase, increase in the level of activity of the alkaline phosphatase, reduction of the protein content. Ultrastructure: almost complete disappearance of the rough endoplasmic reticulum, shrinkage of the mitochondria, reduction of the cristae and condensation of the matrix. The smooth endoplasmic reticulum remains unchanged, the extent of the Golgi-complex is reduced. Easy removal of the lipid deposits.
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PMID:Metabolism and ultrastructure in ovaries of alloxan-diabetic juvenile rats. 0 67

Studies of the thermal stability of rat liver glucose-6-phosphatase (EC 3.1.3.9) were carried out to further elevate the proposal that the enzymic activity is the result of the coupling of a glucose-6-P-specific translocase and a nonspecific phosphohydrolase-phosphotransferase. Inactivation was observed when micorsomes were incubated at mild temperatures between pH 6.2 and 5.6. The rate of inactivation increased either with increasing hydrogen ion concentration or temperature. However, no inactivation was seen below 15 degrees in media as low as pH 5 or at neutral pH up to 37 degrees. The thermal stability of the enzyme may be controlled by the physical state of the membrane lipids and the degree of protonation of specific residues in the enzyme protein. Microsomes were exposed to inactivating conditions, and kinetic analyses were made of the glucose-6-P phosphohydrolase activities before and after supplementation to 0.4% sodium taurocholate. The results support the postulate and the kinetic characteristics of a given preparation of intact microsomes are determined by the relative capacities of the transport and catalytic components. Before detergent treatment, inactivation (i.e. a decrease in Vmax) was accompanied by a decrease in Km and a reduction in the fraction of latent activity, whereas only Vmax was depressed in disrupted preparations. The possibility that the inactivating treatments caused concurrent disruption of the microsomal membrane was ruled out. It is concluded that exposures to mild heat in acidic media selectively inactivate the catalytic component of the glucose-6-phosphatase system while preserving an intact permeability barrier and a functional glucose-6-P transport system. Analyses of kinetic data obtained in the present and earlier studies revealed several fundamental mathematical relationships among the kinetic constants describing the glucose-6-P phosphohydrolase activities of intact (i.e. the "system") and disrupted microsomes (i.e. the catalytic component). The quantitative relationships appear to provide a means to calculate a velocity constant (VT) and a half-saturation constant (KT) for glucose-6-P influx. The well documented, differential responses of the rat liver glucose-6-phosphatase system induced by starvation, experimental diabetes, or cortisol administration were analyzed in terms of these relationships. The possible influences of cisternal inorganic phosphate on the apparent kinetic constants of the intact system are discussed.
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PMID:Quantitative aspects of relationship between glucose 6-phosphate transport and hydrolysis for liver microsomal glucose-6-phosphatase system. Selective thermal inactivation of catalytic component in situ at acid pH. 1 Mar 5

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
Diabetes Care
PMID:Mixed acid-base abnormalities in diabetes. 10 96

Two groups of patients were selected according to their plasma levels of alpha-1-antitrypsin deficiency from among 58 patients with a chronic bronchopathy. Group I had normal plasma levels of alpha-1-antytrypsin; group II had plasma values lower than normal. The pathologic conditions associated with chronic bronchopathies were studied in both groups and so were the gasometric characteristics of the same. Chronic bronchopathies in subjects belonging to group II showed a clear tendency to present normal levels of pCO2 and hydrogen ions possibly related to a greater bronchial impairment in these patients. Independently of the genetic characteristics of plasma alpha-1-antitrypsin deficiency, its general levels are the real indication of its possible etiopathogenic action. Patients with recurrent plasma alpha-1-antitrypsin deficiency, its general levels are the real indication of its possible etiopathogenic action. Patients with recurrent plasma alpha-1-antitrypsin deficiency are more susceptible to bacterial infections, liver cirrhosis, diabetes, and allergic states. All this would be related to the protective effect of this protein fraction, and its reduction according to the most recognized theories would decrease the resistance of hepatic and pancreatic cells.
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PMID:[Diseases associated with chronic bronchopathies and plasma alpha-1-antitrypsin deficiency (author's transl)]. 31 92

A 21-year old woman with poorly controlled diabetes mellitus was examined for persistent hyperchloremic metabolic acidosis. There was no evidence of ingestion of hydrochloric acid or its equivalent. Gastrointestinal loss of bicarbonate was absent. Proximal tubular bicarbonate reabsorption and distal nephron hydrogen-ion secretion were normal. Ammonia and net acid excretions were high, and thus there was no obvious cause for this acidosis. Further study revealed a very large loss of beta-hydroxybutyrate in the urine that closely approximated net acid excretion. This loss of potential bicarbonate was the principal cause for the hyperchloremic metabolic acidosis. Phosphate, urate, and beta-hydroxybutyrate fractional excretions were all abnormally high. Generalized aminoaciduria was also present, but the renal handling of glucose and bicarbonate was normal. With improved control of her diabetes, the generalized aminoaciduria disappeared, the urine beta-hydroxybutyrate loss ceased, the fractional excretions of phosphate and urate approached normal, and the acidosis was rapidly corrected.
Diabetes 1978 Jan
PMID:Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of pathophysiologic mechanisms. 41 58

The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.
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PMID:Diabetic ketoalkalosis. 45 54

Miles Laboratories has developed a Glucose Controlled Insulin Infusion System (GCIIS) designated by the Trademark (BIOSTATOR) as a tool to investigate the physiologic control parameters of carbohydrate metabolism and regulatory deficiencies in diabetes. It consists, in principle, of a rapid on-line glucose analyzer, a computer/controller for the calculation and control of insulin or dextrose infusion, and a multichannel infusion system. A silent printer records, on a minute-by-minute basis, the glucose value measured, the insulin and/or dextrose infusion rates, and the cumulative total of the insulin infused. The on-line glucose analyzer employs an electrochemical sensor with immobilized glucose oxidase and measures the hydrogen peroxide produced. Its linearity extends beyond 700 mg/dl glucose; it permits a rapid two-point calibration of the sensor and the overall calibration of the on-line analyzer without disconnecting the catheter from the patient. The system's response time, including blood sample transport from the patient, is less than 90 seconds with a blood loss of approximately 50 ml per 24 h. The insulin and dextrose infusions are governed by control algorithms; various mathematical models have been developed and employed toward improved feedback control dynamics. The rapid glucose analyzer eliminates the need for the calculation of a "predicted" glucose value and permits, instead, the use of a derivative function for dynamic control. A multichannel infusion system combines the principles of a peristaltic pump with the advantages of a precision pump performance and individual computer control for each of the pump channels.
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PMID:Feedback control dynamics for glucose controlled insulin infusion system. 48 65

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

Localized proton magnetic resonance (MR) spectroscopy was used to define biochemical changes in gray and white matter of the cerebral cortex in 22 patients with diabetes mellitus (DM), including 10 episodes of diabetic ketoacidosis (DKA), compared with MR spectra in 30 healthy subjects. Five distinct metabolic abnormalities were identified: Concentrations of glucose (Glc) (P greater than or equal to .002), ketone body or bodies, myo-inositol (P greater than or equal to .003) (with or without glycine), and choline (Cho) metabolites were increased in both white and gray matter, whereas a significant reduction of N-acetyl metabolites was found in the parietal cortex (P greater than or equal to .003). Diurnal variations in the intracerebral concentration of Glc were demonstrated in a patient with DM whose condition was stable. Elevated concentrations of ketones were detected in three episodes and excess Cho in two episodes of DKA. Evidence obtained with hydrogen-1 MR spectroscopy favors acetone rather than acetoacetate as the ketone present in the brain, which is a major target of biochemical change in DM.
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PMID:Cerebral metabolic disturbances in patients with subacute and chronic diabetes mellitus: detection with proton MR spectroscopy. 131 74

When either rat or human erythrocytes were incubated for 90-180 min in bicarbonate-buffered media prepared in 2H2O rather than 1H2O, the generation of 3HOH from D-[5-3H]glucose, the production of either 14CO2 or 14C-labelled acidic metabolites from D-[U-14C]glucose and the production of L-lactic acid from unlabelled D-glucose were decreased, to a variable extent but, in no case, by more than 30%. Hence, total substitution of 1H2O by 2H2O provides a suitable tool to study by NMR the generation of 2H-enriched L-lactic acid generated from exogenous D-[1-13C]glucose or D-[6-13C]glucose and, hence, to further explore the diabetes-induced alteration of hydrogen isotopes intermolecular transfer in the reaction catalyzed by phosphoglucoisomerase.
Diabetes Res 1992 Jan
PMID:Effect of 2H2O upon D-glucose metabolism in rat and human erythrocytes. 133 14


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