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

The effect of a chronic glucose osmotic diuresis on electrolyte homeostasis was evaluated in alloxan diabetic rats with urine volumes greater than 150 ml/day and glycosuria of 4 to 10 gm/day. Results were compared with control rats for periods up to 84 days. Sodium and potassium intake and urinary losses were significantly higher in diabetic animals throughout the study periods. Negative Na balance, however, persisted for only four days, and negative K balance for only 18 days. Blood volumes were elevated probably secondary to the osmotic effect of hyperglycemia (serum glucose greater than 600 mg %). Plasma renin activity decreased progressively, in part because of an early decrease in renin substrate at a time when renin concentration was normal. Despite hyperkalemia, mean plasma aldosterone was not increased compared with that in control rats, suggesting diabetic rats had relative hypoaldosteronism. Although three diabetic rats became hypertensive, no significant difference in mean blood pressure was observed between the groups. The results suggest that diabetic rats have losses of Na and K early in their diabetes, following which mechanisms to conserve Na and K are activated preventing further electrolyte depletion despite continuation of the osmotic diuresis. Decreased renin activity with inadequate stimulation of aldosterone would contribute to K conservation. Maintenance of Na balance must be explained by increased Na intake and other renal Na conserving mechanisms.
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PMID:Renin-angiotensin-aldosterone system, electrolyte homeostasis and blood pressure in alloxan diabetes. 45 34

Treatment of streptozocin (STZ)-induced diabetic rats with sodium selenate (10-15 mumol.kg-1.day-1) for 7 wk resulted in a decrease in plasma glucose, food intake, and water intake to control or near control levels. Plasma insulin was reduced in control rats given sodium selenate to the level found in the diabetic and treated diabetic group. Treatment did not affect control rats with regard to the other measurements cited. Sodium selenate enhanced weight gain in responding diabetic rats to that seen in controls; sodium selenate's actions thus resembled those of insulin. Thus selenate, like vanadium, appears to have insulinlike effects when administered in vivo.
Diabetes 1991 Dec
PMID:Insulinlike effects of sodium selenate in streptozocin-induced diabetic rats. 175 7

Randomly chosen medical charts of 212 elderly subjects in 11 nursing homes were reviewed to determine which characteristics of the subjects were most closely associated with their diet prescriptions. The chart reviews indicated that 104 (49.0%) of the 212 subjects had some type of nutrient-modified diet prescription. Eight patients who were tube fed were not included in subsequent analyses. Sodium restriction was the most common modification (60 [29.4%] of the remaining 204 patients) and calorie-controlled diets were also common (52 [25.5%] of the patients). Of the 55 patients with hypertension, 31 (56.4%) had no sodium restriction. Only 10% of all low-sodium diets limited sodium to 2 g per day. Of the 38 patients with diabetes, 7 (18.4%) had no prescription for calorie control, and there was no indication that increased dietary fiber was encouraged for diabetic patients. Only one of the 121 subjects with a diagnosis of coronary heart disease or atherosclerosis had a prescription for a cholesterol-lowering diet. Characteristics of the subjects not specifically related to diet or diagnosis, such as age, sex, duration of stay, and level of care, had no significant relationship to diet prescription. These findings suggest that the practitioners in our sample were not convinced of the efficacy of modified diets to control disease for most nursing home residents.
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PMID:Use of modified diets in nursing homes. 191 38

Dehydration, in childhood as in adulthood, may origin from an inadequate water ingestion or an excessive water elimination. Causes may be found in fever, vomiting, scalds, pulmonary hyperventilation, diabetes. Water loss during acute diarrhea in children can be even 6-7 times higher in comparison with an healthy child. Together with water, electrolytes are lost. We differentiate dehydration in isonatremic d. (70% of cases), hyponatremic d. (10%) and hypernatremic d. (20%) basing on Sodium loss. Important dehydration causes severe clinical symptoms as shock, renal and cardiocirculatory failure, convulsion, coma. Symptoms at the central nervous system level derivate both from hyperosmolarity in brain cells and from thrombosis or hemorrhages in subdural sites. Dehydration, following acute diarrhea, is slight when weight loss is lower than 5%. The child health conditions still remain good. Dehydration become moderate if weight loss reaches 5% and the child starts suffering. When the weight loss reaches 10%, dehydration is now severe and circulatory deficiency becomes evident. When it is higher than 10%, prognosis is very severe and shock and coma may be observed. In the present work, we illustrate the different ways of rehydration after acute diarrhea. Initially, oral rehydration must be established with one of the oral solutions, differing each other for amount of electrolytes and glucose. Recently, a new solution, "supersolution", has been presented differing from the other ones for electrolytes concentration and for the presence of rice starch instead of glucose. In most cases of diarrhea, oral rehydration appears adequate but sometimes an intravenous rehydration becomes necessary, e.g. in case of vomiting, CNS depression and in any case of severe gastroenteric symptomatology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dehydrated child]. 189 82

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

Although activation of polyol pathway has been proposed as one of the etiologic factors of diabetic complications, precise mechanism of the effect of polyol accumulation is still unclear. In order to test the hypothesis that there is an association of polyol pathway with myo-inositol metabolism, we measured myo-inositol content in cultured rat glomerular mesangial cells. By exposing the cells to high concentrations of glucose, intracellular myo-inositol content was reduced from 12.39 +/- 0.64 nmol/mg protein at 0 mmol/L glucose to 6.54 +/- 0.38 nmol/mg protein at 27.5 mmol/L glucose and 4.88 +/- 0.43 nmol/mg protein at 55 mmol/L glucose. This decrease of myo-inositol content was partially prevented by co-incubation with aldose reductase inhibitor, sorbinil. To examine further the mechanism of myo-inositol depletion, myo-inositol uptake by mesangial cells was studied. Major myo-inositol uptake process was sodium-dependent, saturable, and ouabain sensitive with Vmax of 171 pmol/mg protein/20 min and Km of 33 mumol/L. Sodium-dependent myo-inositol uptake was significantly inhibited by glucose in a dose-dependent manner only when glucose was present during uptake experiment, and kinetic analysis revealed the inhibition was competitive. Aldose reductase inhibition failed to prevent inhibitory effect of glucose on myo-inositol uptake. These data suggest that myo-inositol content of glomerular mesangial cells, which is reduced by high concentrations of glucose, is maintained by two processes: a glucose-sensitive but sorbitol-insensitive process, sodium-dependent myo-inositol uptake; and a sorbitol (aldose reductase) sensitive process, myo-Inositol depletion under high glucose condition may induce dysfunction of mesangial cells seen in diabetes.
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PMID:Glucose inhibits myo-inositol uptake and reduces myo-inositol content in cultured rat glomerular mesangial cells. 210 41

Aminoglycoside nephrotoxicity in experimental animals can be reduced by calcium loading, inducing diabetes, and giving thyroid hormone, while a potassium deficient diet enhances aminoglycoside nephrotoxicity. This study investigated whether potassium loading protects against gentamicin nephrotoxicity in the rat. In part I, group GK ate a diet containing 3.5% potassium and drank 0.2 mol/L KCl. Pair-fed rats eating a standard diet, group G, ate a 1% potassium diet and drank water. After 10 days, each group received gentamicin subcutaneously, 60 mg/kg twice daily for 8 days. The control groups, K and C, received the high or normal potassium diet, respectively. To control for a protective effect from a high solute load, the effect of equimolar NaCl loading was studied in group GNa and Na. At the end of the 8 days of gentamicin, inulin clearance was significantly higher in GK compared with G(0.6 +/- 0.1 v 0.3 +/- 0.1 mL/min per 100 g body weight [BW], P less than 0.05), but group GNa (0.4 +/- 0.1 mL/min per 100 g BW) was not different from group G. Morphological studies demonstrated that potassium-loaded rats (group GK) had significantly less proximal tubular necrosis compared with rats on a standard potassium diet, group G. Sodium loading did not protect against cellular necrosis. Part II studied renal function, cortical Na,K-adenosine triphosphatase (ATPase) and gentamicin accumulation after 2 days of gentamicin to determine the early functional and biochemical effects of potassium loading before overt renal functional impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of KCl loading in gentamicin nephrotoxicity. 216 23

A survey of dietitians at renal transplant centers in the United States was conducted to identify diet modifications currently used for nondiabetic adults after kidney transplantation. The survey focused on the diet recommended for the first 21 days after successful transplantation. Questionnaires were mailed to 100 centers randomly selected from a comprehensive list obtained through the Organ Transplant Coordinating Office of the Texas Medical Center, Houston. A 66% response rate was obtained. The results of the survey showed that dietitians were most frequently recommending 1.2 to 1.5 gm protein per kg body weight, 40% to 50% of total energy as carbohydrate, a fat intake of less than 30% of total energy, and an energy level consistent with achieving or maintaining desirable body weight. Sodium intake was most commonly restricted to 2 to 4 gm, whereas potassium and phosphorus intakes were individualized according to the patient's serum values. Comments on the returned questionnaires indicated that many institutions were reviewing and updating their transplant diet to include a polyunsaturated fat to saturated fat ratio and restrictions of cholesterol and simple sugars. The findings of the survey indicated that the renal transplant diet should focus on optimal protein and energy intake as well as restriction of simple sugars, total fat, cholesterol, and saturated fat to restore nitrogen balance and minimize clinical symptoms of post-transplant diabetes and hyperlipidemia.
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PMID:Renal transplant diet recommendations: results of a survey of renal dietitians in the United States. 234 58

The effect of progressive increases in intraluminal glucose concentration on proximal tubule sodium absorption was studied in normal and streptozotocin diabetic rats by microperfusion. Each tubule was perfused twice, with and without glucose added to the perfusion fluid. Net sodium and water absorption were markedly enhanced by 300-500 mg% intraluminal glucose in both normal and diabetic rats. Substituting the transported but nonmetabolized glucose analogue, alpha-methyl D-glucoside for glucose also resulted in marked stimulation of sodium absorption, whereas substituting bicarbonate and acetate for chloride in the perfusion solution inhibited the effect of glucose. These observations suggest that the stimulation of sodium absorption by glucose was mediated by the brush border Na/glucose cotransporter. Sodium concentration and osmolality were found to fall markedly to hypotonic levels when high glucose concentrations were in the perfusion fluid. This luminal hypotonicity may be an important driving force for proximal fluid absorption. In poorly controlled diabetes, high filtered glucose concentrations may lead to enhanced proximal sodium and water absorption, which could in turn contribute to volume expansion, hypertension, and renal hypertrophy.
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PMID:Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats. 236 20

Proximal tubular reabsorption of sodium and water was investigated in long-term insulin-dependent diabetic patients with normoalbuminuria (group I, n = 19), microalbuminuria (group II, n = 39), diabetic nephropathy (group III, n = 12) and in 13 healthy age-matched subjects. Glomerular filtration rate was measured with the single injection, 51Cr-EDTA technique. The fluid flow rate out of the proximal tubules was assessed by the renal lithium clearance. Although glomerular filtration rate was significantly elevated in the diabetic patients (Group I: 122 +/- 16, Group II: 121 +/- 18, Group III: 110 +/- 17, CONTROLS: 105 +/- 13 ml/min X 1.73 m2), lithium clearance was similar in the four groups (Group I: 19 +/- 6, Group II: 22 +/- 7, Group III: 19 +/- 5, CONTROLS: 23 +/- 4 ml/min X 1.73 m2). Both absolute and fractional proximal reabsorption of sodium and water was enhanced in diabetes. Indices of distal tubular function did not differ between controls and patients with insulin-dependent diabetes. Sodium clearance was about the same in the four groups. Our study suggests that the enhanced proximal reabsorption of sodium and water in insulin-dependent diabetic patients is still observed despite the presence of incipient or overt diabetic nephropathy.
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PMID:The increased proximal tubular reabsorption of sodium and water is maintained in long-term insulin-dependent diabetics with early nephropathy. 259 38


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