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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythrocyte sodium-hydrogen antiport activity was measured by Orlov's method in 36 healthy volunteers (18 with negative, 18 with positive family history of hypertension) and 52 subjects with type 1 insulin-dependent diabetes mellitus: 29 patients were without known diabetic complications, 23 patients with microangiopathy (10 with diabetic retinopathy, 13 with 'incipient' diabetic nephropathy). Normotensive healthy adults had similar antiport activities independently of a positive or negative family history of hypertension (6.45 +/- 2.61 vs. 5.80 +/- 3.07 mmol/l of cells per h, respectively). Sodium-hydrogen antiport resulted 8.38 +/- 3.91 mmol/l of cells per h in the 29 uncomplicated diabetic patients, significantly higher (p < 0.05) compared to healthy subjects, both without and with family hypertension. Complicated diabetics confirmed to have an exchange rate higher than healthy controls (8.18 +/- 2.50 mmol/l of cells per h, p < 0.01): patients with retinopathy showed the highest antiport activity (8.96 +/- 2.95 mmol/l of cells per h, p < 0.01), while patients with nephropathy had milder antiport overactivity (7.58 +/- 2.02 mmol/l of cells per h), not significantly different from either uncomplicated diabetics or healthy controls. Thus, an increased sodium-hydrogen exchange rate in peripheral erythrocytes does not seem to be an early indicator of diabetic nephropathy.
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PMID:Erythrocyte sodium-hydrogen antiport activity is not a predictor of diabetic nephropathy. 888 26

The effects of dietary salt restriction on the renin-angiotensin system, glomerular filtration rate (GFR), renal size, and albuminuria were assessed in streptozotocin diabetic rats. Two series of experiments were performed: one short-term with severe salt restriction and the second long-term with moderate salt restriction. The first studied the effect of a very-low-salt diet for 4 weeks on GFR, renal size, and plasma angiotensin II concentration in diabetic and control rats. Diabetic and control male Sprague-Dawley rats received either a very-low-salt (0.005% NaCl) or a normal-salt (0.4% NaCl) diet. Diabetes was associated with a 49% increase in GFR, a 34% increase in kidney weight, and an 85% reduction in plasma angiotensin II when compared with control rats (P < 0.001). Sodium restriction in diabetic rats reduced GFR, restored plasma angiotensin II to control values, and retarded kidney growth when compared with diabetic rats receiving a normal sodium diet. GFR correlated negatively with plasma angiotensin II (r = -0.65, P < 0.001) and positively with kidney weight (r = 0.66, P < 0.001). In the second experiment, serial measurements of albuminuria and GFR were performed in control, diabetic, and salt-restricted (0.05% NaCl) control and diabetic rats over 24 weeks. Albuminuria showed a continuous rise in the diabetic rats when compared with control rats. Salt restriction attenuated the increase in albuminuria over the whole study period as well as reducing blood pressure and kidney weight in the diabetic rats. In conclusion, sodium restriction was associated with a lower GFR and kidney weight after 4 weeks and reduced levels of albuminuria, kidney weight, and blood pressure after 24 weeks in diabetic rats. Salt restriction may have an important role in the prevention and treatment of diabetic nephropathy.
Diabetes 1997 Jan
PMID:Salt restriction reduces hyperfiltration, renal enlargement, and albuminuria in experimental diabetes. 897 Oct 91

A community-based epidemiological survey of coronary heart disease and its risk factors was carried out over the period 1984-87 on a random sample of adults aged 25-64 years: 13,723 adults living in Delhi and 3375 in adjoining rural areas. ECG examination and analysis of fasting blood samples for lipids were performed on subjects with the disease and asymptomatic adults free of clinical manifestations. The overall prevalence of coronary heart disease among adults based on clinical and ECG criteria was estimated at 96.7 per 1000 and 27.1 per 1000 in the urban and rural populations, respectively. Prevalences of a family history of coronary heart disease, hypertension, obesity and diabetes mellitus were significantly higher in the urban than in the rural population, and smoking was commoner among rural men and women. Mean levels of total serum cholesterol and low density lipoprotein cholesterol were higher among urban subjects; the mean level of triglycerides was higher in rural subjects. The proportions with total cholesterol levels > 190 mg/dl were 44.1% and 23.0% in urban and rural men, respectively, and 50.1% and 23.9% among urban and rural women, respectively. High density lipoprotein cholesterol levels < 35 mg/dl were found in 2.2% of urban men and 8.0% of rural men compared with 1.6% and 3.5% among urban and rural women, respectively. An abnormal ECG pattern (Q wave or ST-T changes) in asymptomatic individuals is also considered to be a risk factor for coronary heart disease. In asymptomatic adults, 1.7% of urban men and 1.2% of urban women showed abnormal Q waves compared with 0.3% of rural men and 0.4% of rural women. A higher proportion of asymptomatic women showed ST-T changes in both populations. Rural men and women had higher total calorie and saturated fat intakes than urban subjects. Differences in dietary cholesterol intake were marginal. Sodium intake was greater in urban adults. Average daily consumption of alcohol by urban men was 12.7 ml ethanol compared with 2.4 ml in rural men.
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PMID:Urban-rural differences in the prevalence of coronary heart disease and its risk factors in Delhi. 914 48

Sodium-lithium countertransport (SLC) in erythrocytes represents one of the transmembrane sodium transport systems. SLC activity is elevated in arterial hypertension, diabetes mellitus type I (IDDM) complicated with nephropathy, hyperlipidemia, hyperuricemia and pregnancy. Increase of SLC is considered as a genetic marker of primary arterial hypertension. In present paper SLC was assessed in 12 patients with IDDM without nephropathy (group I), 12 patients with IDDM complicated with diabetic nephropathy on hemodialytic treatment (group II), 15 patients treated with haemodialysis due to non-diabetic nephropathy (group III) and 12 healthy subjects (group IV). All groups were matched in respect of age. Serum creatinine concentration and inulin clearance were similar in groups I and IV as well as in groups II and III. SLC was assessed according to method described by Canessa and coworkers (1980). SLC activity in group II (0.60 mmol/l litre of erythrocytes/h; 0.43-0.94; 0.28-1.22) (median, 25%-75%, min.-max.) was significantly higher than in other groups-group I (0.30; 0.20-0.38; 0.12-0.57), group III (0.24; 0.16-0.33; 0.11-0.38) and group IV (0.20; 0.15-0.25; 0.12-0.27). In 3 patients of group I the values were higher than in all examined of groups III and IV and approximated to mean values of group II. The results confirm a significant rise of SLC activity in patients with IDDM complicated with end-stage diabetic nephropathy. SLC activity in end-stage renal disease due to non-diabetic nephropathy does not differ from values in healthy subjects. It seems that elevated SLC activity in IDDM might be a genetic marker foretelling development of nephropathy.
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PMID:[Activity of sodium-lithium cotransport in erythrocytes of patients with diabetes mellitus type I (IDDM) complicated by diabetic nephropathy in the renal failure stage]. 944 Dec 88

Sodium-lithium countertransport activity has been proposed as a marker for hypertension and is lower in black compared to Caucasian subjects both with and without vascular disease. The question arises of what is the primary kinetic locus of the altered behaviour of the countertransporter in black subjects and whether this is also seen in normotensive subjects from other non-Caucasian ethnic groups. We studied the sodium-lithium countertransporter in four ethnic groups (black [n = 45], Caucasian [n = 45], Chinese [n = 40], and South Asian [n = 39]) of age-matched normotensive males (age range 18-35 y) with no first-degree family history of hypertension or diabetes. The clinical and laboratory characteristics of the subjects were similar in all four ethnic groups. Minor differences noted were: significantly higher mean height, weight and serum creatinine concentration (P < 0.001) and significantly lower plasma triglyceride concentration (P = 0.02) in the black compared to the other study groups. Sodium-lithium countertransport activity (mmol Li/l RBC h) was significantly lower in the black subjects (0.113 [0.013-0.265]) compared with the other groups (Caucasian, 0.247 [0.037-0.614]; Chinese, 0.210 [0.100-0.707]; South Asian, 0.211 [0.037-0.617]; P < 0.001). No differences were noted between the four study groups in respect of kNa. Mean (s.d.) Vmax values (mmol Li/l RBC h) were also reduced in the black subjects (0.152 [0.088]) compared to the other ethnic groups (Caucasian, 0.376 [0.159]; Chinese, 0.364 [0.182]; South Asian, 0.329 [0.155]; P < 0.001) and there was a strong relationship between countertransport activity and Vmax (r > 0.52; P < 0.001; for each of the study groups). The differences in mean Vmax noted between the Caucasian, South Asian and Chinese subjects were not significant. These results show that, when compared with three other selected ethnic groups, black subjects demonstrate an altered behaviour with respect to Vmax of the sodium-lithium countertransporter, which occurs in the absence of demonstrable vascular pathology.
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PMID:Kinetic characteristics of the erythrocyte sodium-lithium countertransporter in black normotensive subjects compared with three other ethnic groups. 1146 63

Sodium selenate, administered intraperitoneally (i.p.), resulted in an improvement in glucose tolerance in treated diabetic rats. Fed rat plasma glucose levels were reduced by selenate treatment in streptozotocin diabetic rats. The lowest values of blood glucose were reached within 3 weeks of beginning the treatment. Food and fluid consumption was reduced in treated compared to untreated diabetic rats. Diabetic treated rats did not release insulin in response to a glucose challenge and insulin release in response to a challenge was markedly reduced in control treated rats. Assessment of heart function using a working heart apparatus showed that treated diabetic rats with improved blood glucose levels had normal heart function at 8 weeks of diabetes in contrast to hearts from non-treated diabetics. This study extends previous observations on the in vivo insulin-like effects of sodium selenate.
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PMID:Sodium selenate corrects glucose tolerance and heart function in STZ diabetic rats. 954 46

Sodium fluorescein angiography is a widely used routine ophthalmological diagnostic procedure which enables the study of chorioretinal microcirculation and consists of the injection of sodium fluorescein into the systemic bloodstream. The aim of the present study was to evaluate whether or not fluorescein interferes with erythrocyte properties during the angiographic procedure. In a group of 37 patients, 26 with non-insulin-dependent diabetes mellitus (DM) with and without retinopathy, and 11 without diabetes mellitus (non-DM) although affected by other ophthalmological diseases, all undergoing routine angiography, blood samples were drawn before (T0) and 30 min (T30) after fluorescein injection. The erythrocyte aggregation index (EAI), membrane lipid fluidity and erythrocyte acetylcholinesterase activity were determined in both groups. After fluorescein injection there was no statistical change in EAI and erythrocyte membrane fluidity in either group. Erythrocyte acetylcholinesterase activity, a marker of membrane protein integrity, decreased significantly (p < 0.01) in the DM group. Membrane lipid fluidity did not change with fluorescein injection, however (i) in the DM group erythrocyte membranes became more rigid than in the non-DM (DPH: p < 0.01); (ii) EAI and membrane lipid fluidity became significantly correlated (r = 0.6263, p < 0.05) in non-DM patients at T30. In conclusion, fluorescein administration for angiographic procedures seems to interact with erythrocyte membrane, namely, in diabetic patients, which may interfere with the blood flow in the microcirculation.
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PMID:The effect of sodium fluorescein angiography on erythrocyte properties. 969 34

The aim of the study was to evaluate the role of urinary kallikrein in the regulation of renal hemodynamics and sodium handling in insulin-dependent diabetes mellitus (IDDM), and to test the effect of acutely induced hyperglycemia. Urinary kallikrein excretion was evaluated (1) under basal conditions and after stimulation with i.v. furosemide (0.5 mg x kg(-1)), (2) during glycemic clamp-induced eu- and hyperglycemia (5 and 12 mmol/L) and, (3) during time-controlled euglycemia in 21 short-term IDDM patients without microalbuminuria and in 18 weight-, age- and gender-matched healthy controls. Sodium excretion and renal hemodynamics using the clearances of inulin and para-amino-hippuric acid were measured during examinations in both groups. The baseline urinary kallikrein excretion during clamp-induced euglycemia was comparable in diabetic and control subjects (10.89+/-5.98 versus 10.38+/-3.73 mUE x min(-1)), whereas it was decreased in the baseline for furosemide (5.77+/-3.22 versus 10.9+/-3.7 mUE x min(-1); p < 0.01) and even after furosemide administration (12.0+/-1.6 versus 21.3+/-2.0 mUE x min(-1); p < 0.01) while the patients were hyperglycemic. During intravenous dextrose-induced hyperglycemia, the urinary kallikrein excretion significantly declined in diabetic patients (10.89+/-5.98 versus 5.45+/-0.88 mUE x min(-1); p < 0.01), whereas it did not change in controls (10.38+/-3.73 versus 12.55+/-5.47 mUE x min(-1)). A decrease in the fractional excretion of sodium and an attenuated rise in natriuresis after furosemide administration have been found in diabetic compared to control subjects. There were no significant relationships between kallikrein excretion and (1) renal hemodynamics, which was comparable in both groups, or (2) plasma renin activity, plasma and urine aldosterone and cortisol. We conclude that short-term IDDM without renal hemodynamic alterations is associated with decreased basal and furosemide-stimulated kallikrein excretion, which is directly related to the blood glucose level. The decreased activity of the renal kallikrein-kinin system might be involved in the increased tendency to sodium retention in diabetic patients.
J Diabetes Complications
PMID:Decreased urinary kallikrein with hyperglycemia in patients with short-term insulin-dependent diabetes mellitus. 974 43

Regardless of the specific antihypertensive agent used, the most important aspect of the management of the patient with coexistent hypertension and renal disease is adequate control of the blood pressure. The current JNC VI recommendation is for a reduction to a target blood pressure of 130/85 mm Hg, or to a lower value of 125/75 in patients with greater than 1 g proteinuria per day. Impaired renal sodium excretion leading to extracellular fluid volume (ECFV) expansion is the most clinically important mechanism leading to renal parenchymal hypertension. Sodium restriction and loop diuretics constitute the cornerstone of effective antihypertensive therapy. Control of blood pressure in patients with chronic renal disease may be difficult without measures that address ECFV. JNC VI recommends the use of angiotensin converting enzyme (ACE) inhibitors in patients with hypertension and chronic renal disease to control hypertension and to slow progressive renal failure. ACE inhibitors have been found by clinical trials to be useful agents in the settings of established insulin-dependent diabetes mellitus (IDDM) nephropathy, non-insulin-dependent diabetes mellitus (NIDDM) nephropathy, IDDM patients with normal blood pressures and microalbuminuria, NIDDM patients with microalbuminuria and normal renal function, and a variety of nondiabetic renal diseases, especially in the setting of significant proteinuria. Calcium antagonists are effective for treating hypertensive patients with chronic renal impairment but have not been studied as intensively as ACE inhibitors with regard to their ability to slow the progression of renal insufficiency independently of their blood-pressure-lowering effects. The initial results for calcium antagonists and for combination calcium antagonist-ACE inhibitor therapy have been promising. The angiotensin II antagonists have theoretical advantages for use in renal impairment, and seem to have similar renal hemodynamic and antiproteinuric effects to ACE inhibitors, but further clinical study is needed.
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PMID:Renoprotective effects of antihypertensive drugs. 1007 16

All experiments were performed on conscious, freely moving male Long Evans as well as Diabetes incipidus (Brattleboro) rats (300-320 g). The endothelin-A (ETA) receptor antagonist BQ-123 (Neosystem) was administered through femoral vein cannula. Arterial blood pressure was measured trough femoral artery catheter. The bladder was cannulated for urine collection via a small suprapubic incision. After a 40 min control period BQ-123 infusion (16.4 nmol/kg/min, 25 microliters/min) was started and continued for 50 min. The effect of 32.8 nmol/kg/min BQ-123 infused in conscious Brattleboro rats was also investigated. Plasma and urine concentrations of sodium, potassium and chloride as well as osmolality were determined. Glomerular filtration rate (GFR) was estimated using the clearance of endogenous creatinine. Endothelin-A receptor inhibition by 16.4 nmol/kg/min BQ-123 infusion in conscious Long-Evans rats decreased urine flow rate by 38.4% (p < 0.02) and increased urine osmolality by 30.3% (p < 0.05). Sodium, potassium, chloride excretion did not alter. Endothelin-A receptor inhibition by 16.4 nmol/kg/min and by 32.8 nmol/kg/min BQ-123 infusion in conscious Brattleboro rats did not produce any change in urine flow rate, urine osmolality or excretion of the electrolytes studied. Endothelins acting via ETA receptors may function as an inhibitor of water reabsorption in the kidneys of conscious rats.
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PMID:Renal excretory function in conscious Long Evans and vasopressin deficient (Brattleboro) rats after endothelin-A receptor inhibition. 1067 32


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