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

Although glycosuria is important in the control of diabetes in children, few studies clearly show its significance as compared to glycemia. The aim of the present study was therefore to determine the two parameters that control glucose presence in urine, i.e. glucose glomerular filtration rate (GFR) and tubular reabsorption (JrG). GFR was measured by using a 110 min polyfructosan perfusion in 96 diabetic children and adolescents. The results are as follows: 1) In this population there is a significant correlation (p less than 0.01) between the quantity of glucose in urine and mean glycemia during the test; 2) polyfructosan clearance that reflects GFR in diabetic children without renal complication is 2.11 +/- 0.04 ml/s 1.73 m2, or 126 +/- 2.4 ml/min 1.73 m2 (mean +/- SEM); it is higher than in the reference values already published; 3) JrG is correlated with glucose filtered load (p less than 0.01), GFR (p less than 0.01) and sodium reabsorption (p less than 0.01). The ratio JrG/GFR could be substituted for the classical concept of "renal threshold", as it can be easily measured and may help in interpreting glycosuria in some diabetic children. To conclude, in IDD children, the parameters controlling glycosuria may be studied by a simple method. The clinical value of such renal exploration has still to be determined.
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PMID:[Glomerular filtration and tubular reabsorption of glucose in insulin-dependent diabetes in children]. 370 76

Aim of the present paper is to study the modifications of some laboratory parameters most related to glycaemic metabolism during 24 hours of feed-back glycaemic control by artificial beta-cell. Twelve subjects affected by insulin dependent diabetes mellitus were submitted to GCIIS BIOSTATOR Miles evaluating, before and after 24 hours, blood tryglicerides, cholesterol, uric acid, sodium, potassium. A significant variation was found between the trygliceridemic values before and after automatic control. There was no variation in natriemic values before and after control. Variations, but not significant, were found in cholesterolemic, kaliemic and uricacidaemic values.
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PMID:[Various biohumoral parameters (blood triglycerides, blood cholesterol, blood uric acid, blood electrolytes) after automatic control by an artificial pancreas in subjects with type I diabetes mellitus]. 652 87

This is the first part of a study dealing with the predicted effect of early renal function changes on later development of diabetic nephropathy. Renal function was studied by the clearance method in 128 children with insulin dependent diabetes mellitus after 0, 2, 5 and 10 years duration of the disease. The glomerular filtration rate (GFR) and filtration fraction were significantly increased after 0-5 years, but after 10 years the GFR did not differ from that of controls, which finding might indicate an earlier onset of diabetic nephropathy in children. Renal plasma flow did not differ significantly from that of controls. Increased fractional sodium excretion in cases of recent onset might indicate inadequate adaptation of the proximal tubules to the increased filtered load or to inadequate insulin therapy. An inverse correlation was found between GFR and metabolic control as evaluated clinically and by glucosylated haemoglobin concentration, i.e., poor metabolic control corresponded with high glomerular filtration rates.
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PMID:Early renal functional changes in children with insulin-dependent diabetes mellitus--their relation to metabolic control. 671 11

For some time it has been recognized that postovulatory exacerbation of hyperglycemia contributes to the instability of diabetes in many women of reproductive age. It has been suggested that increasing plasma levels of progesterone and estrogen may induce insulin resistance and consequently lead to increased hyperglycemia during the luteal phase of the menstrual cycle. Due to the fact that menstrual cycles in a given woman may vary in length and that it takes patients several days on intermediate or long-acting insulin to achieve a steady state with regard to any dosage adjustment, it is difficult to design an insulin regimen that maintains euglycemia throughout the menstrual cycle in these labile patients. Recognition of this problem led to trying a nonsequential low estrogen contraceptive as adjunctive therapy in a 20-year old woman with insulin dependent diabetes mellitus. The patient consistently suffered an exacerbation of hyperglycemia after ovulation in each cycle, lasting until the onset of menses. On 1 occasion the patient developed frank diabetic ketoacidosis. For the first 2 cycles on Lo Ovral, the hyperglycemia was postponed from the 1st postovulatory day until day 18-19 of the cycle. It was reasoned that the serum estrogen and/or progestin level might be building cumulatively, and the oral contraceptives (OCs) were subsequently withdrawn at day 19 of the cycle rather than day 21. A maximum blood glucose level of 400 mg/dl was attained at day 19 and was treated with additional regular insulin. Levels in excess of 240 mg/dl did not recur during that cycle. The following cycle OC therapy was interrupted at day 18; no blood glucose level in excess of 240 mg/dl occurred that month. Hemoglobin A1c fell from a pre-OC treatment value of 12.4% to the current A1c of 9.7%. A modest increase in blood pressure has occurred, but this is easily managed with a 2 g sodium diet and 25 mg of hydrochlorothiazide daily. On the basis of this experience, a controlled trial is warranted of low dose estrogen nonsequential OCs in lean, nonsmoking, 18-30 year old women with insulin dependent diabetes mellitus with postovulatory hyperglycemia.
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PMID:Oral contraceptives abolish luteal phase exacerbation of hyperglycemia in type I diabetes. 676 14

The effects of acute deprivation of insulin on renal glomerular and tubular functions were studied in 10 children with juvenile diabetes mellitus. Serum glucose concentrations were similar when insulin was administered (251 +/- 112 mg/dl) and when it was withheld (306 +/- 130 mg/dl; 0.5 greater than 0.2). Acute insulin deprivation was associated with a significant reduction in glomerular filtration rate, from 151 +/- 48 ml/min/1.73 m2 to 114 +/- 41 ml/min/1.73 m2 (p less than 0.01). The fractional excretion of sodium rose from 0.45 +/- 0.43 to 0.85 +/- 0.54% (p less than 0.05) and was associated with an enhanced natriuresis; the urinary excretion of sodium increased from 1.67 +/- 1.23 to 2.43 +/- 1.72 microEq/min/kg body weight (p less than 0.05), whereas the urinary excretion of phosphate was not significantly altered from control values. During insulin deprivation a drop occurred in the serum concentration of calcium from 10.37 +/- 0.52 to 9.73 +/- 0.61 mg/dl (p less than 0.01) as well as in its urinary excretion from 0.34 +/- 0.24 to 0.24 +/- 0.20 microgram/min/kg body weight (p less than 0.01). The serum concentration of potassium rose from 4.44 +/- 0.41 to 4.96 +/- 0.51 mEq/l, but its urinary excretion was not significantly different from control values. These data suggest that in juvenile diabetes mellitus the acute deprivation of insulin, dissociated from fluctuations in serum glucose concentration, is associated with a fall in glomerular filtration rate, an increased natriuresis, and a modified calcium and potassium homeostasis.
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PMID:Renal glomerular and tubular function following acute insulin deprivation in juvenile diabetes mellitus. 705 Jul 53

Abnormalities of sodium-lithium countertransport have been extensively implicated in adult primary hypertension and a relationship between sodium-lithium countertransport and family history of hypertension in children has been previously found. More recently it has been suggested that increased sodium-lithium countertransport may play a part in the pathogenesis of nephropathy in insulin dependent diabetes mellitus (IDDM). Children and adolescents with IDDM and their family members were studied. In those with IDDM (n = 36, median age 14.6 years, range 9.5-19.2 years) there was no relationship between sodium-lithium countertransport (range 0.098-0.585 mmol/l red blood cells/hour) and age, blood pressure as expressed by systolic or diastolic SD scores, glycated haemoglobin, serum lipids, or intracellular sodium concentration. A positive relationship (rs = 0.44) was found between sodium-lithium countertransport and early morning urinary albumin to urinary creatinine ratio (UA/UC), expressed as the logarithm of the geometric mean of two consecutive samples, for each individual (range 0.4-22 mg/mmol). Sodium-lithium countertransport was increased in those with IDDM compared with their non-diabetic siblings, in a paired analysis (n = 26). There was no relationship between UA/UC in the children with diabetes and sodium-lithium countertransport in their parents. These studies in this population of diabetic children indicate that increased sodium-lithium countertransport may play a part in the early stages of the development of nephropathy in IDDM.
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PMID:Sodium-lithium countertransport in children with diabetes and their families. 770 75

In Type 1 diabetes an increased total body sodium and an impaired ability to excrete a sodium load have been described. A possible involvement of the renal dopaminergic system in this abnormal sodium handling was evaluated through measurements of the urinary output of dopamine, sodium, the dopamine/sodium correlation, and through examining the effect of a dopamine infusion on urinary sodium excretion. Twenty-four hour urinary dopamine excretion was significantly lower in Type 1 diabetic patients as compared to normal controls. A significant correlation between urinary dopamine and sodium excretion was present in normoalbuminuric Type 1 diabetic patients and in normal controls. However, no such correlation could be found in microalbuminuric patients. The increase in fractional excretion of sodium during a 1 h low-dose dopamine (3 micrograms kg-1 min-1) infusion in Type 1 diabetic patients was negatively correlated with diabetes duration. Patients with short duration of diabetes (less than 15 years) had a comparable dopamine-induced increase in fractional excretion of sodium as normal controls. However, patients with longer duration of diabetes (more than 15 years) and microalbuminuric patients displayed no significant changes in sodium output during dopamine infusion. These findings suggest that in Type 1 diabetes mellitus a deficiency of renal dopamine production could be responsible for the impaired sodium handling. Longer duration of the disease and microalbuminuria seem to be associated with an uncoupling of the urinary dopamine/sodium relationship.
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PMID:Decreased urinary dopamine excretion and disturbed dopamine/sodium relationship in type 1 diabetes mellitus. 775 59

Renal responses to low-dose infusion of angiotensin II (ANGII, 1.25 and 2.5 ng.kg-1 min-1) were examined in 15 patients with type 1 diabetes and in 10 control subjects after pretreatment with lithium carbonate (750 mg, 20 mmol). Mean arterial pressure rose during ANGII infusion in both groups. The renal haemodynamic response to angiotensin II was not abnormal in the diabetic patients. Absolute proximal reabsorption of sodium was increased at baseline in the diabetic group, and fell during ANGII. Fractional lithium excretion was reduced in the diabetic patients at baseline (P < 0.05), and the fall in fractional lithium excretion during ANGII was less than in the control group (P = 0.012). In the diabetic group correlations existed between glycated haemoglobin and baseline glomerular filtration rate (P < 0.05), baseline fractional lithium excretion (P = 0.03), and the fall in fractional lithium excretion during angiotensin II infusion (P = 0.013). There was no correlation between glycated haemoglobin and absolute lithium clearance. Some indices of sodium reabsorption by the proximal renal tubule in diabetic patients correlate with prevailing chronic glycaemic control, largely reflecting changes in glomerular filtration rate. Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms.
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PMID:Renal tubular responses to low-dose infusion of angiotensin II in type 1 diabetes mellitus; relation to chronic glycaemic control. 781 87

Insulin-dependent diabetes mellitus is a multigenic autoimmune disease, for which one of the best animal models is the nonobese diabetic (NOD) mouse strain. In both humans and NOD mice, major histocompatibility complex genes are implicated as risk factors in the disease process. Other susceptibility genes are also involved, and a number have been mapped in the mouse to specific chromosomal locations. To identify further susceptibility genes, diabetic backcross mice, produced after crossing NOD/Lt to the nondiabetic strains SJL and C57BL/6 (B6), were examined for markers not previously associated with disease susceptibility. Linkage was found to loci on chromosomes 4 and 14. Of the candidate loci on chromosome 4, the gene encoding the Na+/H+ exchanger-1, Nhe-1, was the most likely, since the NOD allele was different from that of both nondiabetic strains. NOD lymphocytes were found to have a higher level of Na+/H+ exchange activity than lymphocytes from either B6 or SJL mice. Since the chromosome 4 susceptibility gene is recessive, the B6 allele should prevent diabetes. This prediction was tested in fourth-generation backcross mice, selected for retention of the B6 allele at Nhe-1. Mice homozygous for Nhe-1 developed diabetes after cyclophosphamide treatment, but heterozygotes were largely protected from disease. These results implicate the Na+/H+ exchanger (antiporter) in the development of type 1 diabetes and may provide a screening test for at-risk individuals as well as offering prospects for disease prevention.
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PMID:Genetic and physiological association of diabetes susceptibility with raised Na+/H+ exchange activity. 801 86

The aim of this work is to evaluate whether type 2 diabetes mellitus, obesity and arterial hypertension, three conditions characterized by the presence of insulin resistance, share some common genetic markers. A potential candidate is the Na+/H+ antiporter, the increased activity of which is considered a marker of essential hypertension. This ion exchanger seems to be related to the Na+/Li+ countertransport, that is considered a marker of insulin resistance in essential hypertension and in type 1 diabetes mellitus. In this study we wished to clarify whether the activity of the Na+/H+ antiporter is increased not only in hypertensive subjects, but also in obese and type 2 diabetic patients, both in the presence and in the absence of arterial hypertension. The activity of the ion exchanger was measured in peripheral blood lymphocytes (PBL) by clamping intracellular pH (pHi) at 5.8-6.2 and then detecting the rate of the proton efflux after sodium addition. In the absence of arterial hypertension, no significant difference in this parameter was observed in obese and type 2 diabetic patients in comparison with normal subjects. In the presence of arterial hypertension, there was a significant increase in the Na(+)-induced H+ efflux at the internal pH (pHi) values of 5.8 and 6.2 both in hypertensive controls and in hypertensive obese and type 2 diabetic patients (P = 0.05-0.0001 vs. normotensive subjects and patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na+/H+ antiporter activity in peripheral blood lymphocytes of obese and type 2 diabetic patients is increased only in the presence of arterial hypertension. 803 50


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