Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human kidney responds to a meat meal with an increase in glomerular filtration rate (GFR), but the mechanisms regulating kidney hemodynamics following protein intake are poorly understood in Type I insulin-dependent diabetes. In the present study we investigated GFR response to protein intake (600 gr/1.73 m2 meat meal) in nine normal subjects and 21 Type I insulin-dependent diabetic patients with normal albumin excretion rates as well as proximal tubular sodium reabsorption rates and distal sodium delivery (PRNa and DDNa). The same study was reperformed in normal subjects and diabetic patients, with less than a 5 year diabetes duration, following one week of indomethacin treatment. Normal subjects showed a 38% increase in GFR following protein intake, whereas diabetic patients showed a significantly lower response (18%, p less than 0.01). The response of GFR to protein challenge was negatively related to diabetes duration but not to baseline glomerular filtration rate. Indomethacin treatment completely prevented the protein induced GFR increase in normal subjects but not in diabetic patients. Sodium reabsorption rate was increased following protein challenge both at the proximal and distal tubular level, as was net natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Type I insulin-dependent diabetic patients show an impaired renal hemodynamic response to protein intake. 296 53

Control of arterial blood pressure at near-normal levels is of importance for the prognosis of patients with Type 1 (insulin-dependent) diabetes mellitus. In non-diabetic populations patient compliance to antihypertensive therapy is frequently poor, especially in young people. Thirty-seven consecutive eligible patients with longstanding Type 1 diabetes and persistently uncontrolled hypertension were questioned about their preferences regarding hypertension treatment. Throughout they expressed a strong desire for more information about hypertension and for active participation in monitoring of blood pressure and therapeutic decision-making. In addition, they showed considerable reluctance to accept a pharmacological intervention. Therefore, in order to improve blood pressure control, the patients participated in a structured outpatient hypertension treatment and teaching programme for groups of about 6 patients consisting of four teaching sessions at weekly intervals. The programme comprised home-monitoring of blood pressure and involvement of the patients in treatment decision-making. In 34 patients who had a complete follow-up examination after an average of 16 months, mean sitting arterial pressure had decreased from 111 to 101 mmHg (p less than 0.001) and 53% of the patients were below 140/90 mmHg. The number and dosage of prescribed antihypertensive agents remained unchanged by the intervention. Sodium intake was not reduced during the study, but pulse rate decreased significantly in patients treated with beta-adrenergic blockers and serum uric acid rose in patients on diuretic therapy, suggesting increased adherence of the patients to prescribed antihypertensive drug therapy. In 34 comparable Type 1 diabetic patients who were not subjected to a hypertension treatment and teaching programme mean arterial blood pressure remained unchanged during a 12-month period.
 ...
PMID:Uncontrolled hypertension in type 1 diabetes: assessment of patients' desires about treatment and improvement of blood pressure control by a structured treatment and teaching programme. 297 58

Sodium-potassium-ATPase activity was measured in excised dorsal root ganglia of streptozotocin-diabetic rats, 2 months after induction of diabetes. In comparison with age-matched controls, there was a decrease in both the total and ouabain-insensitive activity, indicating an overall reduction in ouabain-sensitive activity of 46%. This decrease may explain the reduced amino-acid uptake exhibited by diabetic sensory ganglia and could be relevant to the development of diabetic neuropathy.
 ...
PMID:Sodium-potassium-ATPase activity in the dorsal root ganglia of rats with streptozotocin-induced diabetes. 298 69

Sodium plasma level was followed every three months in 70 non insulin dependent diabetic patients; 112 prescriptions were performed. Five different oral hypoglycemic drugs were used but patients were taken no more than one drug in the same time. 21% of prescription were associated with a low sodium plasma level but it was beneath 129 meq in only 8% of them; a low sodium plasma level was observed with every oral hypoglycemic agent; when the drug was interrupted a normal sodium plasma level was restored; when patients were put under another agent, hyponatremia did not recidive. 67% of patients were free of any symptom. Interference with biological parameters, age of the patients, duration of diabetes and other therapy are studied.
 ...
PMID:[Hyponatremia induced by hypoglycemic sulfonamides: a study of 70 patients]. 307 90

Adhesion of bovine endothelial cells on fibronectin and collagen before and after nonenzymatic glycation in vitro has been studied. Nonenzymatic glycation of these proteins reduced their ability to bind endothelial cells. Furthermore, nonenzymatically glycated fibronectin failed to bind to normal and nonenzymatically glycated gelatin and to fibrin. So gelatin and fibrin Sepharoses can be used to separate highly glycated fibronectins from fibronectins with a low degree of nonenzymatic glucose substitution. Sodium dodecylsulfate polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidences for the role of nonenzymatic glycation of proteins in the development of vascular complications in long-term diabetes and of atherosclerosis.
 ...
PMID:Diminished adhesion of endothelial aortic cells on fibronectin and collagen layers after nonenzymatic glycation. 340 68

Anterior ischemic optic neuropathy (A.I.O.N.) may cause optic disc edema in type-I diabetes. A.I.O.N. affects diabetic patients of all ages. Such optic neuropathy is more likely to become bilateral in diabetics than in the non-diabetic subjects. A 41-year-old diabetic insulin-dependent woman presented A.I.O.N. in RE; 5 years later, the same affection occurred in LE. The clinical course was relatively benign in both eyes, with good functional restitution. The patient was treated by high doses of Sodium Salicylate and Sulfinpyrazone. The pathogenesis of optic disc edema in type-I diabetes is, according to Hayreh (1981), ischemia of different grade in the district of the posterior ciliary arteries: microangiopathy, rheological anomalies and atherosclerotic added lesions produce a variability of clinical pictures of increasing seriousness. Our case has an intermediate position in such a continuous spectrum. The VEP supported the diagnosia of A.I.O.N.
 ...
PMID:Anterior ischemic optic neuropathy in type I diabetes. 345 16

To look for possible determinators of the pathological readings of vitreous fluorophotometry in diabetes reported by other groups, we studied 32 insulin-treated patients, 22 of whom had fluorescein angiograms without pathological changes, while 10 had background retinopathy. 14 healthy subjects matched for age and blood pressure served as controls. Sodium fluorescein, 17 mg/kg body weight, was injected intravenously and ocular fluorophotometry performed 60 and 120 minutes later. Blood drawn 5, 45 and 120 minutes after the injection was assayed for total and ultrafiltrable fluorescein and the intraocular readings corrected for average preceding free plasma fluorescein. Patients without retinopathy did not differ from controls in any intraocular measure, while patients with retinopathy showed significantly increased readings in the posterior (60 min: 12 +/- 7 vs. 6 +/- 4, p less than 0.01, 120 min: 26 +/- 35 vs. 11 +/- 5, p less than 0.05) and middle vitreous (60 min: 6 +/- 3 vs. 3 +/- 3, p less than 0.001, 120 min: 11 +/- 5 vs. 8 +/- 5, p less than 0.01 (X 10(-9) g/ml fluorescein, mean +/- SD)). No significant relations to systolic or diastolic blood pressure, blood glucose, hemoglobin Alc or serum creatinine were found in any of the diabetic groups. Re-examination of 7 patients 4-14 days later in a non-fasting state showed no significant changes.
 ...
PMID:Ocular fluorophotometry in insulin-treated diabetic patients with and without retinopathy. 638 56

In order to determine whether diabetic cardiomyopathy in rats is associated with altered contractile proteins, male and female rats were made diabetic with intravenous streptozotocin (STZ). Calcium ATPase activity of cardiac actomyosin was significantly decreased after 1 week of diabetes and was depressed by 60% by 2 weeks. Rats pretreated with 3-O-methyl glucose to prevent the hyperglycemia caused by STZ had normal Ca2+-actomyosin ATPase activities, and non-diabetic rats whose food was restricted to keep their body and heart weights similar to those found in diabetic animals had only a slight fall in actomyosin ATPase activity. Ca2+-ATPase and actin-activated ATPase activities of pure myosin were similarly depressed in preparations from hearts of diabetic animals. Sodium dodecylsulfate gel electrophoresis and isoelectric focusing failed to reveal differences in the patterns of contractile proteins or light subunits between diabetics and controls, but pyrophosphate gels showed a shift in the myosin pattern. Because of depressed circulating thyroid hormone levels in diabetic animals, cardiac contractile proteins were also studied in preparations from thyroidectomized rats. Calcium activities of actomyosin and myosin ATPase were lower than values found in hearts of diabetic rats. When diabetic animals were kept euthyroid with thyroid replacement, actomyosin ATPase activity was still depressed. Thus STZ diabetes causes a significant decrease in cardiac contractile protein ATPase activity. This may be related to altered proportions of myosin isoenzymes.
 ...
PMID:The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins. 645 19

To induce diabetes mellitus in 8 steers, they were fasted for 96 hours and given 110 mg of alloxan/kg of body weight (IV, in 1 dose) immediately before refeeding. Subsequently, 4 of the steers were treated with insulin (0.1 to 3 U/kg) to control hyperglycemia and 4 were not given insulin. Four control steers were fasted and refed. Fasting increased serum phosphorus, total protein, and bilirubin and decreased serum magnesium and potassium. Refeeding returned serum values of magnesium, potassium, total protein, and bilirubin toward base-line values, regardless of treatment group. However, serum phosphorus remained increased in steers with alloxan-induced diabetes and was not lowered by insulin injections. Sodium and chloride values were depressed in steers with alloxan-induced diabetes; these values remained significantly (P less than 0.05) lower than base-line values, even in steers given insulin. Fat infiltration was evident in the pancreas, liver, and to some extent, kidneys of steers with alloxan-induced diabetes, but was occasionally present in tissues of steers given insulin.
 ...
PMID:Metabolic responses to fasting and alloxan-induced diabetes mellitus in steers. 649 40

To study renal tubular reabsorption and tubulo-glomerular balance in diabetic children, glomerular filtration rate (GFR) and tubular reabsorption rates of sodium, glucose, ultrafilterable calcium, and phosphate were measured during fasting in 26 ambulatory type I (insulin-dependent) diabetic children without clinical signs of microangiopathy (age 7-14 yr; duration of diabetes 3-14 yr). Similar measurements were made in 28 healthy school children (age 8-14 yr). Mean GFR in the diabetic children was significantly higher than in the normal children (138 versus 109 ml/min/1.73 m2, P less than 0.01). Mean tubular reabsorption rates of sodium, glucose, and calcium were significantly increased in the diabetic subjects (P less than 0.001). In contrast, tubular reabsorption rate of phosphate in the diabetic subjects was not enhanced. The renal threshold concentration of phosphate (TmPO4/GFR) was suppressed in the diabetic compared with the healthy subjects (1.23 versus 1.73 mmol/L, P less than 0.001). TmPO4/GFR was unrelated to circulating parathyroid and growth hormone concentrations but correlated inversely with the reabsorption rate of glucose (r = -0.53, P less than 0.01). Sodium reabsorption was closely correlated to GFR in both diabetic (r = 0.99, P less than 0.0001) and healthy subjects (r = 1.00, P less than 0.0001), and both groups showed identical regression lines. The tubular glucose reabsorption rate was independent of GFR in the diabetics. Tubular calcium and phosphate reabsorptions correlated equally well with sodium reabsorption and with GFR in the diabetic and healthy subjects (P less than 0.001). The maximal reabsorption of phosphate relative to GFR was lowered in the diabetic children.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 May
PMID:Tubular reabsorption rates as related to elevated glomerular filtration in diabetic children. 660 35


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>