Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
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PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

Intravenous glucose tolerance tests (30 g, 5 min, constant rate) were performed in 8 IDDM patients and in 8 controls. The consequences of the osmotic pressure, induced by glucose, were investigated. Serum choline esterase was used as an endogenous marker of serum dilution. Five minutes after the end of infusion plasma glucose was raised by 182 +/- 12 mg.dl-1 in patients and by 189 +/- 6 mg.dl-1 in controls. Choline esterase values decreased by 6.6 +/- 0.8% and 6.3 +/- 1.0% respectively, P less than 0.01 each. Calculated water shifts into the extracellular space were 924 +/- 112 ml and 882 +/- 140 ml respectively. Fifteen minutes after the end of infusion glucose decreased by 32 +/- 1 mg.dl-1 in IDDM patients and by 57 +/- 2 mg-1 in controls. Serum choline esterase recovered by 2.6 +/- 0.2% and 2.7 +/- 0.2% respectively, P less than 0.01 each, indicating comparable water correction in spite of the slower fall of glucose in IDDM patients. Water correction was more rapid than glucose fall. Diuresis (46 +/- 4 ml versus 42 +/- 3 ml) or cellular uptake of serum solutes (electrolytes, amino acids, urea, creatinine) could not explain this. It is hypothesized that accumulation of free intracellular glucose reduces the osmotic gradient and facilitates cellular water re-uptake.
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PMID:Osmotic stress due to changes in plasma glucose and its regulation in IDDM patients. 152 25

A 71-year-old man with type I diabetes mellitus was admitted to the hospital for the treatment of osteomyelitis of the left great toe secondary to methicillin-resistant Staphylococcus aureus. The patient was enrolled in an investigational protocol and was treated with teicoplanin 1200 mg/day. Following 40 days of treatment, the patient developed both markedly elevated serum creatinine and blood urea nitrogen. Urine analysis also showed the presence of protein. The eosinophils were markedly elevated in the blood. The patient was subsequently diagnosed with a probable drug-induced acute interstitial nephritis. Treatment with furosemide and hemodialysis over the next two weeks failed to produce improvement in renal function. The patient was referred for long-term dialysis. The data presented in this report suggest the possible relationship of teicoplanin and the development of renal failure in this patient. Periodic monitoring of renal function and follow-up are probably warranted in patients receiving long-term teicoplanin therapy.
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PMID:Teicoplanin nephrotoxicity: first case report. 153 25

Insulin-dependent diabetes mellitus is known to be associated with impaired ability of insulin to enhance tissue glucose uptake. However, no information is available whether or not this insulin resistance extends to insulin-mediated potassium (K+) uptake. Insulin-mediated decrease in serum potassium (K+) and in blood urea nitrogen (BUN) concentration was evaluated in 20 adolescents with IDDM and 10 matched controls during a 3-h hyperinsulinemic (1.7 mU/kg/min)-euglycemic clamp study. Insulin-mediated glucose disposal rate was lower in IDDM compared with controls (37.4 +/- 3.2 vs 63.8 +/- 5.4 mumol/kg/min, P less than 0.001). The decline in serum K+ concentration following hyperinsulinemia was significantly smaller in adolescents with IDDM than controls (0.29 +/- 0.06 vs 0.67 +/- 0.08 meq/liter, P = 0.002). Similarly the decline in BUN concentration was smaller in IDDM compared with control subjects (2.10 +/- 0.40 vs 3.70 +/- 0.56 mg/dl, P = 0.03), suggestive of decreased suppressibility of proteolysis. The changes in serum K+ and BUN concentrations were correlated (r = 0.64, P = 0.02) in controls but not in diabetics. Similarly, the decrement in serum K+ concentration showed a positive correlation with the rate of insulin-mediated glucose disposal (r = 0.68, P = 0.02) in controls but not in diabetics. The correlation of glucose disposal rate with the decline in BUN concentration did not reach a level of significance (r = 0.43, P = 0.1). These results indicate that adolescents with IDDM are resistant to the ability of insulin to stimulate in vivo K+ uptake and to suppress proteolysis.
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PMID:Impaired insulin mediated potassium uptake in adolescents with IDDM. 179 13

The objective of the work was to evaluate the basic parameters of zinc metabolism, i.e. serum levels and urinary excretion of zinc (Zn) in insulin dependent diabetes. The authors investigated a group of diabetics with normal renal function (DM) and with chronic renal insufficiency as a result of diabetic nephropathy (RIDM). Two control groups were formed by healthy volunteers (C) and non-diabetic subjects with chronic renal insufficiency (RI). In diabetics without impaired renal functions (DM) the Zn serum levels did not differ significantly from controls, urinary excretion was significantly raised. The authors did not reveal a correlation of serum Zn levels with parameters of compensation of diabetes nor with the insulin dose. Urinary Zn output correlated positively with proteinuria and the average blood sugar level during the collection of urine. The authors did not find a correlation with diuresis, fractional water excretion, glycosuria or urea excretion. The fractional Zn clearance in diabetic subjects was significantly raised and correlated with the mean blood sugar level. This finding suggests a decline of the tubular Zn absorption in hyperglycaemia. In diabetics with renal failure (RIDM) the results did not differ from non-diabetics with the same degree of renal insufficiency: serum Zn levels were, as compared with healthy controls, in both groups significantly reduced, the urinary excretion being normal. Thus insulin dependent diabetes nor its metabolic compensation do not influence in a marked way serum Zn levels but lead to higher urinary Zn losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum levels and urinary excretion of zinc in patients with insulin-dependent diabetes]. 220 24

Insulin antibodies, as measured by plasma radiolabeled insulin-binding capacity, were determined in 124 newly diagnosed insulin-dependent diabetic (IDDM) children before and after 1, 3, and 5 days of insulin therapy. Controls were 35 nondiabetic children with plasma insulin binding capacity of 1.0 +/- 0.7%. The patients were divided into three groups according to their plasma insulin-binding capacity. Group 1 (N = 79) had binding within two standard deviations (SD) of the control mean, group 2 (N = 20) had insulin binding 2-6 SD above controls, and group 3 (N = 25) showed insulin-binding capacity of more than 6 SD above the control mean. After exogenous insulin therapy, plasma 125I-insulin-binding capacity dropped significantly in both groups 2 and 3, concurrent with significant increases in plasma insulin levels. The three groups differed from each other in that patients in group 3 were significantly younger than in the other groups and clinically seemed to be more severely dehydrated, as reflected in their higher levels of serum urea nitrogen, plasma glucose, potassium, and elevated pulse rate. The three groups did not differ in respect to sex, HLA-DR antigens, Coxsackie-B antibody titers, islet cell cytoplasmic antibodies, immunoglobulin level, and C-peptide levels. Only two of 446 siblings of IDDM children showed elevated insulin binding, one of whom developed IDDM 6 wk later. The presence of an insulin-binding substance probably representing insulin antibodies in some cases of newly diagnosed IDDM suggests that autoimmunity in this disorder is not limited to the B-cell membrane and cytoplasm and lends further support to the heterogeneity of IDDM.
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PMID:Correlates of insulin antibodies in newly diagnosed children with insulin-dependent diabetes before insulin therapy. 389 1

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

Mutations in the mitochondrial gene were recently identified in a large pedigree of diabetes mellitus and deafness. As the mitochondrial gene is materially inherited, Japanese diabetic patients whose mothers were also diabetic were screened, using peripheral leucocytes, for an A to G transition at nucleotide pair 3243 of the mitochondrial gene, a tRNA(Leu(UUR)) mutation. This mutation was identified in four pedigrees from among 300 unrelated patients who were screened. Diabetes co-segregated with the mutation, except in one young subject, and was maternally inherited. The apparent onset of disease occurred between 11 and 68 years of age. Some of the affected members developed hearing impairment and congestive heart failure due to cardiomyopathy, though generally long after the onset of diabetes, and these patients had therefore not been diagnosed as having a specific form of diabetes. The duration of sulphonyl-urea treatment was not more than 8 years in these pedigrees and affected members were prone to progression to insulin-requiring diabetes. Thus, these patients were secondary sulphonylurea failures. Long-term follow-up revealed that the underlying disorder in affected members is a progressive impairment of insulin secretion. Some were initially diagnosed as having IDDM based on an apparent acute onset in youth and the clinical severity of their diabetes. Others were regarded as having MODY with an aggressive course. The mitochondrial gene mutation or diabetes is not transmitted to all offspring of the affected mothers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial diabetes mellitus: prevalence and clinical characterization of diabetes due to mitochondrial tRNA(Leu(UUR)) gene mutation in Japanese patients. 805 89

The effect of diabetes in pregnancy on leucine turnover and oxidation was examined in 12 insulin-dependent diabetic (IDDM) subjects and 12 gestationally diabetic (GDM) subjects during the third trimester of pregnancy. The data were compared with those in normal pregnant women studied during the same time period and reported previously. Eight of the IDDM subjects were on continuous subcutaneous insulin infusion (insulin pump), and four were on conventional twice-daily insulin treatment. Of the GDM group, seven were on insulin therapy and five were on dietary management. Leucine kinetics were quantified using [1-13C]leucine tracer in combination with respiratory calorimetry and measurement of lean body mass using the H2[18O] dilution method. In addition, glucose kinetics were measured in insulin-treated subjects using [6,6(2)H2]glucose tracer. Despite rigorous metabolic control, fasting plasma glucose (IDDM 5.5 +/- 1.9 mmol/L [P < .05], GDM 4.7 +/- 1.3 [P < .01], controls 3.6 +/- .6, mean +/- SD) and hemoglobin A1 ([HbA1] IDDM 7.9 +/- 1.9%, GDM 7.5% +/- 2.1%) levels were higher in diabetic subjects. Although total insulin levels were higher in insulin-treated diabetic subjects, free-insulin concentrations were similar in all groups. Rates of excretion of urinary urea nitrogen and respiratory quotients were also similar. The rate of glucose turnover was lower in insulin-treated subjects compared with normals. Leucine flux, a measure of the rate of protein breakdown, and leucine oxidation were higher in IDDM and insulin-treated GDM subjects. The rate of leucine oxidation was increased in conventionally managed IDDM and insulin-treated GDM subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Leucine kinetics during a brief fast in diabetes in pregnancy. 813 88

In IDDM, the gluconeogenic turnover of amino acids is increased even if glycemia is well controlled and may be restored to normal by means of prehepatic insulin substitution. Therefore, the present study was designed 1) to investigate the influence of route of insulin administration (portal versus peripheral) on the urea production rate, which is considered to measure amino acid catabolism, and 2) to elucidate the impact of different food-protein intake. Paired studies were conducted in chronic insulin-dependent diabetic dogs maintained normoglycemic. Diabetic animals and nondiabetic controls were fed either a high-protein diet (46% of energy intake provided by proteins; study 1) or a low-protein carbohydrate-supplemented diet (20% of energy intake provided by protein; study 2) for 2 days, and flux rates of glucose and urea were measured using isotope dilution techniques. In both studies, the diabetic animals were maintained normoglycemic by glucose-controlled insulin infusion delivered either systemically or portally. In study 1 versus study 2, the animals showed lower alpha-amino nitrogen levels and concentrations of gluconeogenic amino acids, predominantly alanine. There were no significant differences in plasma glucose and glucose turnover between the experimental groups on either systemic or portal insulin infusion versus controls; however, peripheral insulin levels were higher for diabetic animals maintained with systemic versus portal insulin delivery (P < 0.05). No significant differences in glucagon, lactate, pyruvate, nonesterified fatty acids, or beta-hydroxybutyrate were observed. Urea production was significantly higher in study 1 compared with study 2: 7.48 +/- 0.83 vs. 5.97 +/- 0.59 micromol / kg / min (normal dogs); 12.97 +/- 1.86 vs. 5.54 +/- 0.60 micromol / kg / min (diabetic dogs on portal insulin); 16.11 +/- 2.59 vs. 6.82 +/- 0.70 micromol / kg / min (diabetic dogs on systemic insulin infusion); P < 0.05 for all. The diabetic dogs maintained normoglycemic with systemic insulin infusions had significantly higher rates of urea synthesis than those with portal insulin infusion (P < 0.05). It is concluded that in IDDM, even if normoglycemia is managed, there is significantly increased amino acid catabolism with posthepatic systemic insulin treatment. This increased catabolic rate is more pronounced during high-protein nourishment.
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PMID:Increased urea synthesis in insulin-dependent diabetic dogs maintained normoglycemic: effect of portal insulin administration and food protein content. 862 Oct 20


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