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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported a decrease in gluconeogenesis from alanine in normal pregnant women at term gestation as compared with nonpregnant women. In the present study, the effect of diabetes on alanine metabolism was examined in five gestationally diabetic (GDM) women and seven women with type I (insulin-dependent) diabetes (IDDM) during the third trimester of pregnancy. The hemoglobin A1c (HbA1c) concentrations in all subjects were within normal range, indicating good metabolic control. After an overnight fast, each subject was infused simultaneously with L-[2,3, 13C2]alanine and D-[6,6,2H2]glucose tracers as prime constant rate infusion. Plasma alanine and glucose isotopic enrichments were measured by gas chromatography-mass spectrometry. Alanine and glucose turnover rates were quantified by tracer dilution. In five subjects, the contribution of alanine carbon to CO2 was quantified by respiratory calorimetry and by measurement of 13C enrichment of expired CO2. Data from 15 previously reported normal pregnant subjects were used for comparison. The rate of alanine turnover was similar in the GDM and IDDM subjects and was not different from the normal subjects (GDM, 4.6 +/- 1.9; IDDM, 5.4 +/- 2.5; normals, 4.4 +/- 0.8 mumol/kg.min, mean +/- SD). The rate of glucose turnover was significantly reduced (P less than .05) in IDDM as compared with GDM and normal subjects (IDDM, 8.1 +/- 0.8; GDM, 11.5 +/- 3.5; normals, 12.2 +/- 2.2 mumol/kg.min). The contribution of alanine C to glucose C and expired CO2 was similar in the three groups. These data demonstrate that rigorous metabolic control results in normal glucose and alanine metabolism in diabetic pregnancy during fasting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose-alanine relationship in diabetes in human pregnancy. 190 12

[U-11-C]-glucose and positron emission tomography was used to evaluate transport and oxidative metabolism of glucose in the brain of non-diabetic and insulin dependent diabetic (IDDM) subjects. These results were compared with results obtained by the Fick principle. Blood glucose was regulated by a Biostator controlled glucose infusion during a constant insulin infusion. [U-11-C]-glucose was injected during normoglycemia as well as during moderate hypoglycemia. The tracer data were analysed using a three compartment model with a fixed correction for [11-C]-CO2 egress. During normoglycemia the influx rate constant (k1) and blood brain glucose flux of the two groups were similar. During hypoglycemia k1 increased significantly and to the same extent in both groups. During normoglycemia the tracer calculated metabolism of glucose was higher in the brain of non-diabetic than of diabetic subjects. When measured by the Fick principle the net uptake of glucose was broadly the same for the groups. During normoglycemia the molar ratio of O2 to glucose uptake was, however, lower in IDDM than in non-diabetic subjects (4.67 vs 5.50, P less than 0.05, Wilcoxon test). A significant release of lactate and pyruvate was seen in IDDM but not in non-diabetic subjects. The results imply that a larger fraction of glucose is non-oxidatively metabolized in IDDM than in non-diabetic subjects.
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PMID:A comparison of brain glucose metabolism in diabetes as measured by positron emission tomography or by arteriovenous techniques. 239 52

It is known that dehydroascorbic acid (DHAA) produces a diabetogenic effect and its content in the blood increases in diabetes mellitus. It was previously established that the generation of reducing equivalents (RE) in the course of hexosemonophosphate shunt, CO2 production and SH-glutathione regeneration in erythrocytes with and without moderate and maximum oxidation load in vitro were not disturbed in diabetes. The authors have proposed a procedure to study blood and erythrocyte DHAA reductase activity in suspension in health and in insulin-dependent diabetes mellitus by means of redoxstatometry using a device of original design. A significant acceleration of RE transfer through the erythrocyte membrane was detected in diabetes. A lowered participation in this process of the AA in equilibrium DHAA "shuttle" system was recorded in the blood of patients with diabetes mellitus what was mostly expressed under the conditions of acidosis in vitro. Probably "shuttle" function in diabetes was provided by some other redox system which might be located in the plasma. The predominant functioning of this redox system and a decrease of DHAA reductase activity in diabetes resulted in the accumulation of DHAA in the blood of patients with type I diabetes mellitus.
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PMID:[Cause of dehydroascorbic acid accumulation in the blood of patients with insulin-dependent diabetes mellitus]. 398 93

A 38-year-old man with brittle, juvenile onset diabetes mellitus and bilateral severe dry eyes with recurrent corneal ulcers developed atypical band-shaped calcifications of both corneas during a 24-hour period. Serum calcium, phosphate, and carbon dioxide levels all were within normal limits. The patient was mildly uremic but was not in renal failure. When EDTA chelation failed to clear the deposits, partial keratectomies were performed in both eyes and the specimens were examined by light and electron microscopy, including energy dispersive x-ray analysis. Microscopic studies revealed an atypical calcific keratopathy which involved neither Bowman's layer nor the most superficial stromal lamellae. The deposits were confined to deeper lamellae in the anterior stroma and by electron microscopy were composed of extracellular crystalline aggregates. Energy dispersive x-ray analysis of these aggregates confirmed the presence of calcium and phosphate. Corneal dessication appeared to be a major contributing factor in the rapid formation of these deposits.
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PMID:Bilateral acute corneal calcification. 400 Jun 45

Arginine metabolism via nitric oxide (NO) synthase and other pathways was studied in coronary endothelial cells (EC) from the spontaneously diabetic BB rat, an animal model of human type I diabetes mellitus (IDDM). EC were prepared from insulin-treated diabetic BB (BBd) and non-diabetes-prone BB (BBn) rats. Basal NO synthesis was studied in EC cultured for 48 h in medium containing 0.4 mM L-arginine. At the end of the culture period, the medium was analyzed for nitrite and nitrate (two major end stable oxidation products of NO), and the cells were used to determine arginine uptake and metabolism and the activities of some arginine-degrading enzymes. For studies of arginine metabolism, cells were incubated at 37 degrees C for 1 h in Krebs-Henseleit bicarbonate buffer (pH 7.4) containing 1 mM L(-)[1-14C]arginine or L(-)[1-14C]ornithine. The rates of production of nitrite plus nitrate by BBd EC were only 15% of those of BBn cells. This impaired NO synthesis in BBd EC was not due to alterations in arginine uptake, NO synthase activity, or intracellular arginine concentrations but might have resulted from a limited intracellular availability of cofactors of NO synthase. In addition to the arginine-NO pathway, arginine was found to be metabolized to urea, ornithine, and, to a much lesser extent, CO2 via arginase and ornithine aminotransferase. The activities of arginase and the formation of ornithine and urea from arginine were decreased by 90% in BBd compared with BBn cells. These results, coupled with the reduced NO synthesis, indicate metabolic defects in arginine metabolism in BBd EC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired arginine metabolism and NO synthesis in coronary endothelial cells of the spontaneously diabetic BB rat. 748 63

Most textbooks advise that newly diagnosed insulin dependent mellitus be admitted to the hospital for starting carefully insulin treatment. We report a pilot study for starting an outpatient insulin using continuous subcutaneous insulin infusion. In 40 newly IDDM (glycaemia over 16.5 mM/l, CO2 over 15 mM/l), intensive therapy was done by CSII = basal rate 1 unit/hour, bolus 5 units per meal. After a long explanatory talk (4 hours) with the physician and the nurse on hypo, hyperglycaemia, on blood glucose sensor and pump, 21 patients agreed to start insulin at home and 19 remained in hospital for 2 or 7 days. At days 3, 30 and 365, clinical and biological evaluation was done and at D30 patient education program for 5 days was undergone. Never emergency even was reported in any patient, and no difference appeared between the in and out patient in D1, D3 and D365 normalisation of blood glucose (3 days) or level cetone body (2 days) and total insulin dose. Our results suggest that outpatient is a safe and cost effective IDDM onset therapy.
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PMID:[Standardized ambulatory insulin therapy of initial moderate ketoacidosis in type 1 diabetes. A pilot project]. 820 90

Prospective registry of newly diagnosed cases of insulin-dependent diabetes mellitus in subjects under 20 years began in 1988 in Aquitaine, Lorraine, Basse- and Haute-Normandie (population base = 2,288,018 inhabitants under 20). The registry gave a complete coverage of the population as the capture-recapture method gave a 98% yield. The mean annual incidence was 7.6/100,000 for the period 1988-1990. A specific survey aimed at describing clinical and biological presentation at diagnosis. The main symptom was polyuria in 98% of the cases, fatigue in 58% and weight loss in 44%. Abdominal pain was reported in 34% of the cases. Diagnosis was ascertained by measurement of plasma glucose, which was > or = 11 mmol/l in 95% of the cases and associated with ketonuria in 84% of the children. Coma in 13% of the children and acidosis (total CO2 < or = 18 mmol/l) in 48% showed the severity at diagnosis. Ketonuria and acidosis were significantly more frequent in the younger age group (0-4 yr). Diagnosis was made by a general practitioner in the majority of the cases; conversely insulinotherapy was initiated at the hospital in 95% of the cases. Initial insulin treatment was 2 daily injections. Following the French experience the collaborative network EURODIAB ACE has undertaken the same survey among the European Registries. Important geographical variations in incidence rates of IDDM in children has been reported across Europe but it is not known whether this interferes with presentation at diagnosis of the disease.
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PMID:[Diagnosis of insulin-dependent diabetes in children: data from the incidence registry]. 893 70

Hepatic glucose cycling, whereby glucose is taken up by the liver, partially metabolized, then recycled to glucose, makes a substantial contribution to the development of hyperglycemia in IDDM. This stimulation of glucose cycling appears to be associated with elevated rates of fatty acid oxidation. Whether hepatic glucose cycling also contributes to the development of hyperglycemia in NIDDM is unclear. Using a model of NIDDM, the Zucker diabetic fatty (ZDF) rat, we determined whether glucose cycling was enhanced. Hepatocytes from ZDF rats exhibited higher rates of glucose phosphorylation and glycolysis, but there was no increase in the rate of cycling between glucose and glucose-6-phosphate or between glycolytically derived pyruvate and glucose. Despite the increased rates of glycolysis, the production of CO2 in liver cells from ZDF rats was no different from rates measured in cells from control animals. Instead, there was a large increase in the accumulation of lactate and pyruvate in the ZDF liver cells. The addition of 2-bromopalmitate, an inhibitor of fatty acid oxidation that inhibited glucose cycling in hepatocytes from IDDM rats, had no effect on glucose cycling in cells from ZDF rats. We therefore conclude that, unlike in IDDM, hepatic glucose cycling does not contribute to the development of hyperglycemia in the NIDDM Zucker rat.
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PMID:Hepatic glucose cycling does not contribute to the development of hyperglycemia in Zucker diabetic fatty rats. 1033 11

Pancreatic islets transplanted to treat autoimmune type 1 diabetes often fail to function (primary nonfunction), likely because of islet beta-cell apoptosis. We show that carbon monoxide (CO), a product of heme oxygenase activity, protects beta-cells from apoptosis. Protection is mediated through guanylate cyclase activation, generation of cyclic GMP (cGMP), and activation of cGMP-dependent protein kinases. This antiapoptotic effect is still observed when beta-cells are exposed to CO for 1 h before the apoptotic stimulus. In a similar manner, mouse islets exposed to CO for just 2 h function significantly better after transplantation than islets not exposed to CO. These findings suggest a potential therapeutic application for CO in improving islet function/survival after transplantation in humans.
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PMID:Carbon monoxide protects pancreatic beta-cells from apoptosis and improves islet function/survival after transplantation. 1191 17

In order to appreciate the repercussion of diabetes on the respiratory function, we measured the pulmonary volumes, the ventilatory flows, the airways resistances (Raw) and the diffusing capacity for the carbon monoxide (DLCO) of 49 diabetes distributed into 27 IDDM and 22 NIDDM aged from 15 to 56 years, compared to 31 control subjects. We found a significant decrease in the total pulmonary capacity (TCL), the vital capacity (VC), the inspiratory capacity (IC), the ventilatory flows and the DLCO. The decrease of the VC and the FEV1 will be more marked in the IDDM. The decrease of the DLCO will be more pronounced within masculine sex, it seems to be correlated with the duration of diabetes and more impaired if a diabetic nephropathy is associated especially in IDDM. Our results suggest that in the diabetes evolution, the lung is among the target organs in the degenerative complications. The respiratory tests reflect the pulmonary reach in the diabetes and provides important perspectives in the following.
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PMID:[Ventilatory mechanics and alveolo-capillary diffusion in diabetes]. 1263 65


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