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)

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 antihypertensive efficacy and metabolic effects of cyclopenthiazide 125 micrograms were compared with cyclopenthiazide 500 micrograms in patients with non-insulin dependent diabetes and hypertension in a double blind, randomized crossover study. After a 6-week placebo period 24 patients with non-insulin dependent diabetes mellitus, stabilized on diet or oral hypoglycaemic agents, who had a mean diastolic blood pressure between 90 and 120 mmHg after receiving placebo for 6 weeks were given 125 micrograms or 500 micrograms cyclopenthiazide for 12 weeks. Patients then received placebo for a further 6-week period, following which they received the alternate treatment dosage for 12 weeks. There were no differences between doses in their antihypertensive effects. While 500 micrograms significantly reduced systolic and diastolic blood pressures, only diastolic pressure was significantly reduced by 125 micrograms from pre-treatment values. The higher dose of cyclopenthiazide had greater effects on measures of diabetic control than did the 125 micrograms dose and the rise in blood glucose after 12 weeks' treatment with 500 micrograms was significantly different from pre-treatment values. Cyclopenthiazide 125 micrograms had significantly less effect on triglycerides, potassium and urate, than did 500 micrograms. Cyclopenthiazide 500 micrograms resulted in a significant fall in serum potassium from pre-treatment values. There were no intertreatment differences in the other variables measured. Cyclopenthiazide 125 micrograms is as effective as 500 micrograms in reducing diastolic blood pressure in mildly hypertensive non-insulin dependent diabetic patients. The higher dose had more pronounced adverse effects on glucose control and serum concentrations of triglycerides, potassium and urate.
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PMID:The antihypertensive and metabolic effects of low and conventional dose cyclopenthiazide in type II diabetics with hypertension. 180 32

NIDDM and hypertension are both characterized by insulin resistance and/or hyperinsulinemia. In IDDM, factors associated with nephropathy produce hypertension. To avoid exacerbation of the metabolic condition, and to prevent further deterioration in glycemic control, treatment of hypertension in the diabetic patient should include the administration of medication with the fewest adverse effects on glucose homeostasis. If diuretics are to be used, it appears that loop diuretics may be preferable to the thiazides or potassium-sparing compounds. Among the remaining classes of antihypertensive drugs, ACE inhibitors may be the agents of choice because of their potential positive effects on insulin sensitivity and renal function, and their lack of severe adverse side-effects.
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PMID:Insulin sensitivity and blood lipids during antihypertensive treatment with special reference to ACE inhibition. 197 44

The aim of this study was to analyze Na,Li countertransport in erythrocytes from adolescents with insulin dependent diabetes mellitus (IDDM) and to see if those with elevated values present distinct clinical features, in particular as regards arterial pressure and urinary albumin excretion (UAE). Twenty-nine adolescents with IDDM (17 males, 12 females, mean age 15 +/- 0.6 years, mean diabetes duration 11.4 +/- 0.7 years) and fifteen healthy age-matched control subjects (8 males, 7 females, age 14.5 +/- 1 years) were investigated. Diabetic adolescents had a RBC Na,Li countertransport activity higher than age matched normal controls; geometric mean 283 (95% limits 259-340) vs. 193 (169-252) mumol/l RBC/h; p less than 0.01. Seven out of 29 subjects had values higher than the 95th percentile of normal subjects (Counter +). Both systolic and diastolic arterial pressures were significantly higher in Counter + than in Counter - patients. No significant differences were found as regards age, body mass index, diabetes duration, HbA1c, fructosamine, serum potassium, triglycerides, creatinine clearance and UAE. The logarithm of systolic pressure was independently positively correlated with ln Na,Li countertransport (r = 0.38; p less than 0.05), ln [Nai] (r = 0.38; p less than 0.05), and ln body mass index (r = 0.5; p less than 0.01) in diabetic patients. The main finding of this study is that diabetic adolescents with a high erythrocyte Na,Li countertransport rate have an arterial pressure significantly higher than patients with normal Na,Li countertransport fluxes.
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PMID:Erythrocyte Na,Li countertransport and arterial pressure in diabetic adolescents. 208 7

Aim of this study is to evaluate whether among type I diabetic adolescents (IDDM) the erythrocyte Na-Li countertransport (CNT Na-Li) is correlated with arterial pressure and tubular sodium reabsorption. We have studied 16 IDDM adolescents (age 15 +/- 0.5 year) et 15 normal subjects (age 14.5 +/- 1 year). CNT Na-Li, creatinine and lithium clearances (as markers of glomerular filtration rate and proximal tubular sodium reabsorption) have been measured in all subjects and nocturnal urinary albumin excretion rate (UAER) was measured in IDDM adolescents. CNT Na-Li was 308 +/- 26 mumol Li/l RBC/h in IDDM adolescents and 211 +/- 74 mumol Li/l RBC/h in controls (p less than 0.01). The fractional excretion of lithium (FELi) was significantly reduced in IDDM adolescents compared to normal subjects (12 +/- 2 vs 19 +/- 2%; p less than 0.01). Among the IDDM adolescents, 5 had the CNT Na-Li higher than the 95th percentile of controls (greater than 360 mumol Li/l GR/h); their systolic arterial pressure was significantly higher than in diabetics with normal CNT Na-Li (126 +/- 2 vs 116 +/- 2; p = 0.03), while there were no differences for diabetes duration, glycemic control, serum potassium, creatinine clearance, FELi and UAER. The relationship between CNT Na-Li and arterial pressure in IDDM adolescents deserves further studies.
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PMID:[Erythrocyte sodium-lithium countertransport in diabetic adolescents]. 212 63

Eight patients with type I diabetes mellitus have been operated on to form a distal splenorenal anastomosis (DSRA). A critical period (the 6th and the 7th days) postoperation has been observed when severe metabolic acidosis develops; to prevent its development, transfusions of 4% sodium bicarbonate solution (1.5-2.01) have been administered before the critical period for 24 hrs, with the metabolic condition monitored by biochemical analyses. Studies of metabolism in these patients after surgery have revealed a complete normalization of the acid-base balance and of potassium level, as well as a reduction of the blood glucose concentration. The doses of exogenic insulin have been reduced by 30%, this being associated with a tendency to an increase of the levels of endogenic insulin, C-peptide and glucagon of the blood. This helps a better stabilization of the diabetic process after the formation of a DSRA.
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PMID:[Characteristics of the postoperative period in diabetes mellitus type 1 in patients with distal splenorenal anastomosis]. 219 74

Diabetic ketoacidosis is an all too frequent and sometimes preventable complication of Type I diabetes mellitus, responsible for significant morbidity and mortality within the diabetic population. Precipitating diseases account for the majority of deaths occurring in patients admitted in diabetic ketoacidosis, but some deaths are still attributable to ketoacidosis alone, despite recent advances in therapy and management. Recognition of the ketoacidotic state is paramount to optimal therapy, and often hinges on the diagnostic acumen of the physician. Since 20 to 30% of patients presenting in diabetic ketoacidosis do so as the initial manifestation of their previously undiagnosed disease, physicians must maintain a high level of suspicion for this condition. Understanding the pathogenetic mechanisms leading to and prevailing in diabetic ketoacidosis will allow physicians to intervene in a rational manner, approaching therapy with specific end-points in mind: (a) restoration of optimal volume status; (b) reversal of acidosis; (c) reduction of serum glucose levels; (d) replacement of specific electrolytes in a timely manner; (c) institution of appropriate therapy for any precipitating cause; and, (f) careful monitoring of the patient's biochemical, physical and mental parameters to allow adjustment in therapy as necessary. The mainstay of treatment for diabetic ketoacidosis is appropriate fluid and insulin therapy. Low-dose intravenous infusion is now the accepted mode of insulin delivery for patients with this condition. Potassium replacement is almost always necessary, often requiring massive amounts of this ion due to the total body depletion seen with the development of ketoacidosis. Controversy still surrounds routine use of phosphate in diabetic ketoacidosis but replacement may be needed if serum levels fall toward the lower limits of normal values, to avoid the potential adverse effects of phosphate depletion. Administration of bicarbonate is also controversial and should be reserved for patients whose pH is less than 7.0 to 7.1 and then it should be added to intravenous fluids, not given as an intravenous bolus. Efforts toward preventing diabetic ketoacidosis should be of prime importance to physician and patient alike. Preventive measures should include patient education about diabetes mellitus, precipitating factors of diabetic ketoacidosis, signs and symptoms of early metabolic decompensation, rational insulin therapy during minor illness and appropriate timing of physician contact to help avoid this serious and sometimes fatal complication of diabetes mellitus.
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PMID:Management of diabetic ketoacidosis. 250 77

One hundred and twenty-eight surgical operations in diabetic patients have been studied to assess the effectiveness, under routine clinical conditions, of a management regimen based on the use of glucose-insulin-potassium infusion (GIK). Forty-four non-insulin-dependent diabetic (NIDDM) and 41 insulin-dependent diabetic (IDDM) patients received GIK. Mean blood glucose on the day of operation was 9.3 +/- S.D. 2.2 mmol/l in NIDDM and 8.9 +/- 2.3 mmol/l in IDDM patients. Acceptable control on the day of operation (defined as mean blood glucose 5-12 mmol/l without hypoglycaemia) was achieved in 70 (82%) patients. Eleven of 15 failures were attributable to incorrect implementation of the protocol. Though 10 units Soluble insulin/500 ml 10% glucose (0.32 units/g glucose) was needed in 61% of patients, 26% required a higher and 13% a lower dose. Plasma potassium concentration did not change after 24 h of GIK infusion, but sodium concentration fell (136 +/- 5 to 132 +/- 5 mmol/l; p less than 0.01), with 12 of 32 patients having post-operative values less than 130 mmol/l. Forty-three NIDDM patients undergoing minor surgery were managed without insulin, and acceptable control was achieved in 40 (93%). We conclude that the regimen described is a satisfactory routine means of managing diabetes during surgery, but that optimal results depend on careful monitoring with appropriate alteration of therapy.
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PMID:Management of diabetes during surgery with glucose-insulin-potassium infusion. 295 Nov 40

Intra- and extracellular levels of magnesium and potassium were determined in 16 subjects with insulin-dependent type I diabetes mellitus (IDDM) and 30 healthy controls. Subjects with IDDM had lower levels of magnesium in muscle biopsies (p less than 0.001), plasma (p less than 0.001), and mononuclear cells (p less than 0.05), and higher urinary excretions of magnesium (p less than 0.01), and lower levels of potassium in muscle biopsies (p less than 0.001), and erythrocytes (p less than 0.05), as compared with those in controls. Magnesium hydroxide (500 mg/day) was administered orally to the diabetics. The levels of magnesium and potassium in muscle biopsies increased (p less than 0.001; p less than 0.001), while the plasma levels of magnesium and the urinary excretions of magnesium increased only temporarily, during 21 weeks of treatment. The requirements of insulin were reduced (p less than 0.001) during the course of the study, whereas the levels of glycosylated hemoglobin (HbA1c) and glucose were not changed. The findings indicate that administration of magnesium hydroxide is useful to treat muscular magnesium and potassium deficiency in diabetics.
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PMID:Oral administration of magnesium hydroxide to subjects with insulin-dependent diabetes mellitus: effects on magnesium and potassium levels and on insulin requirements. 305 47

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


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