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PubMed1995

A prospective evaluation of ifosfamide-related nephrotoxicity in children and young adults.

BACKGROUND: Ifosfamide has been associated with proximal renal tubular dysfunction resembling Fanconi-like syndrome and leading to rickets in young children. The characteristic manifestations of this nephrotoxicity include phosphaturia and hypophosphatemia, glycosuria, aminoaciduria, renal tubular acidosis, and urinary loss of low molecular weight serum proteins. However, the relationship between acute ifosfamide nephrotoxicity, which is frequently subclinical, and long term renal damage is unclear. In this prospective study, the laboratory features of ifosfamide-induced acute nephrotoxicity were characterized further and correlated with the development of chronic nephropathy. METHODS: The renal function of newly diagnosed children and young adults with high risk sarcomas was followed during therapy with a high dose ifosfamide-containing regimen. Serum and urine were collected regularly immediately before and after 5-day cycles of ifosfamide throughout treatment for determination of the fractional excretion of electrolytes (sodium, potassium, phosphate, magnesium, calcium) and glucose and urinary excretion of amino acids and beta 2-microglobulin. RESULTS: Significant changes in the renal threshold of phosphate excretion, the fractional excretion of calcium and glucose, and the urinary excretion of beta 2-microglobulin were observed when comparing pretreatment values with those at the end of a 5-day treatment cycle. The median renal threshold of phosphate excretion decreased from 1.22 to 0.82 mmol/L (P < 0.0001). The median fractional excretions of calcium and glucose increased from 1.05% to 1.68% (P < 0.0001) and 0.05% to 0.08% (P = 0.0006), respectively. Beta 2-microglobulin excretion increased by 70-fold from 0.02 to 1.42 mg/mmol (P < 0.0001). Except for glucose and beta 2-microglobulin excretion, renal parameters returned to baseline before the next ifosfamide treatment cycle. Acute aminoaciduria was observed in 21 of 23 patients. Chronic nephrotoxicity, as defined by the development of a Fanconi-like syndrome or chronic tubular electrolyte loss requiring oral supplementation, developed in the three patients with the highest urinary excretion of beta 2-microglobulin after ifosfamide therapy. CONCLUSIONS: Prospectively, high dose ifosfamide was associated with a 4% incidence of Fanconi-like syndrome; however, evidence of acute reversible subclinical nephrotoxicity was observed for all patients. Severe beta 2-microglobulinuria appeared to be a prognostic laboratory indicator for the development of chronic nephrotoxicity.

Adolescent↗

PubMed1978

Autosomal dominant Fanconi syndrome with early renal failure.

The "idiopathic" Fanconi syndrome occurs mostly sporadically, occasionally as an autosomal recessive trait. However, few instances of autosomal dominant inheritance have been reported. We described a father and son with the Fanconi syndrome, ie, with renal glycosuria, generalized aminoaciduria, phosphaturia, metabolic acidosis, and bone disease. No other causes of the Fanconi syndrome were found. Both father and son developed end stage renal disease. Aminoaciduria in excess of that seen in renal insufficiency is shown by comparison with published data for amino acid excretion in uremia. Renal transplantation in the father has improved kidney function with no evidence of Fanconi syndrome. This family is unique in that there are no other reports of autosomal dominant Fanconi syndrome with progression to early renal failure.

Adolescent↗

PubMed1994

Protection from experimental autoimmune diabetes in the non-obese diabetic mouse with soluble interleukin-1 receptor.

We have evaluated the effects of a treatment with soluble interleukin-1 receptor (sIL-1R) in the accelerated model of autoimmune diabetes induced by cyclophosphamide (CY) in the non-obese diabetic (NOD) mouse. Prior to the CY challenge (350 mgkg body weight), female euglycemic NOD mice were randomly divided into three groups (A-C). Groups B and C were treated daily from 1 day before to 13 days after the CY challenge with sIL-1R at doses of 0.2 and 2 mg/kg body weight. Group A was treated with PBS. By 2 weeks after CY administration, an acute form of autoimmune diabetes with glycosuria, hyperglycemia and severe insulitis occurred in the majority (13/20, 65%) of the control mice (group A). In contrast, repeated injections with sIL-1R protected NOD mice from insulin-dependent diabetes mellitus (IDDM) development in a dose-dependent fashion; the incidence of IDDM was 53.3% (8/15) in the mice treated with 0.2 mg/kg and only 6.7% (1/15) in those treated with 2 mg/kg. However, none of the doses of the sIL-1R reduced the extent of insulitis in NOD mice. Importantly, the anti-diabetogenic property of sIL-1R may not involve major T cell function impairment; accordingly, in parallel experiments, splenic lymphoid cells from NOD mice not challenged with CY, but treated with 2 mg/kg sIL-1R for 5 consecutive days showed a normal distribution of mononuclear cell subsets and maintained their capacity to secrete interferon-gamma and IL-2 and to proliferate in response to polyclonal mitogenic stimulation with concanavalin A.

Animals↗

PubMed1992

Spontaneously diabetic biobreeding rats and impairment of bile acid-independent bile flow and increased biliary bilirubin, calcium and lipid secretion.

Chemically induced diabetes has been reported to induce profound changes in bile formation, but possible toxic effects of the streptozotocin or alloxan used cannot be excluded totally. This study was undertaken to evaluate biliary function in spontaneously diabetic female biobreeding rats with a diabetes duration of 2 wk and compare them with nondiabetic littermates. Diabetic animals evidenced glycosuria, hyperglycemia and hypoinsulinemia. Biliary concentration and secretion of bile acids, cholesterol and phospholipids were significantly increased, with no enhancement in the lithogenic index of bile. Bile flow and the biliary secretion of sodium, potassium, chloride and bicarbonate were significantly reduced despite the increased bile acid secretion. The cholestatic condition was confirmed by an increased serum concentration of bile acids and a higher activity in serum of the alkaline phosphatase liver isoenzyme. Biliary calcium concentration increased without any change in its serum concentration. A linear relationship was observed between biliary calcium and bile acid secretion. Serum concentration of unconjugated and of conjugated bilirubin was increased 1.6-fold and 8-fold, respectively, with a 1.5-fold enhanced biliary secretion of bilirubins despite the cholestasis; this points to an enhanced bilirubin production. An increased proportion of conjugated bilirubin was found in serum together with an enhanced bilirubin diconjugate/monoconjugate ratio in bile. A higher UDP-glucuronyltransferase activity and a delayed transit of bilirubin could account for these effects. Administration of insulin to diabetic animals tended to reverse the above reported changes. The spontaneously diabetic biobreeding rat thus represents a model of bile acid-independent cholestasis with enhanced biliary bile acid and calcium secretion and with presumably an enhanced bilirubin production.

Animals↗

PubMed2007

Effects of a vitamin D3 analog on diabetes in the bio breeding (BB) rat.

Non-hypercalcemic analogs of vitamin D(3) modulate the immune response through antigen-presenting cells (APCs) and activated T-cells. A large population-base case-control showed that vitamin D(3) intake significantly decreases the risk of type 1 diabetes development. The aim of this study was, therefore, to observe the in vivo effects of a vitamin D(3) analog administered to Bio Breeding (BB) rats. 1,25-Dihydroxy-16,23Z-diene-26,27-hexafluoro-19-nor vitamin D(3) (BXL-219, formerly Ro 26-2198) (BioXell, Milan, Italy) was administered in vivo to BB rats from days 42 to 110 of life at 0.2 microg/Kg BW. Control animals received only vehicle (olive oil, 4.8 microl/100 g BW). The animals of these two groups were subjected to insulin treatment as they became diabetic. Insulin (Humulin, 28.6 UI/day) was administered irrespective of diabetes occurrence to another group of rats for comparison. Blood glucose, insulin levels, glycosuria, degree of islet infiltration, and the expression of some antigens were observed. Results showed that the vitamin D(3) analog reduced diabetes incidence, although limitedly, in BB rats while administration of oral insulin increased diabetes incidence. In addition, the vitamin D(3) analog did not stimulate an enhancement in the expression of CD4 and CD25 in BB rats as it does in NOD mice, which may explain the failure of this as well as other antidiabetic treatments in the BB animal model of type 1 diabetes.

Animals↗

PubMed1998

The role of dietary zinc in modifying the onset and severity of spontaneous diabetes in the BB Wistar rat.

The goal of this study was to determine whether zinc supplementation in the diet of diabetes-prone BB Wistar rats will delay or prevent the onset of overt diabetes. Male Wistar BB rats were fed diets containing either 1000 ppm (HZ), 50 ppm (NZ), or 1 ppm zinc (LZ) starting at 30 days of age. Non-diabetes-prone rats were fed NZ and designated as controls (NORM). Beginning at 60 days, the rats were checked for glycosuria and, if positive, were given an i.p. glucose tolerance test (IPGTT). All remaining animals underwent an IPGTT at 100 days and were sacrificed. At 90 days of age HZ rats had a lower incidence of diabetes (19%) than NZ (53%) or LZ (44%) animals (P < 0.015). By age 100 days, for the HZ group, there was a 60% reduction in the number of expected overt diabetic rats. HZ animals also had higher concentrations of both pancreatic and serum insulin and exhibited lower serum glucose and triglycerides. Immunohistochemistry of HZ rats was clearly different from NZ rats and showed evidence of nearly normal pancreatic endocrine activity. Data indicate that dietary treatment of diabetes-prone BB Wistar rats with zinc appears to be an effective approach for delaying or preventing the onset of diabetes in genetically predisposed rodents. This finding may suggest further experimental studies regarding dietary means for preservation of pancreatic function.

Adolescent↗

PubMedDate not supplied

Effects of chronic treatment with lisinopril on cardiovascular complications in streptozotocin diabetic and DOCA hypertensive rats.

The present study was undertaken to study the effects of chronic treatment with lisinopril on the cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosteroneacetate (DOCA) hypertensive rats. Injection of STZ produced severe glycosuria (> 2%), hyperglycemia, hypoinsulnaemia, polydypsia, polyphagia and loss of body weight. It also produced hypothyroidism, hypercholesterolaemia, hypertriglyceridaemia, hypertension, bradycardia and decreased left ventricular developed pressure (LVDP). Elevation in serum creatinine level and increased activity of liver enzymes were also found in STZ treated animals. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in non-diabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment of STZ-diabetic rats with DOCA did not aggravate cardiac depression or hyperglycaemia. Treatment of rats with lisinopril (1 mg kg-1, p.o. daily for six weeks), in diabetic and diabetic hypertensive animals prevented STZ induced loss of body weight and hypertension, bradycardia and hypothyroidism. It also prevented STZ induced hyperglycemia and hypoinsulinaemia in both diabetic and diabetic hypertensive animals. There was a reduction in cholesterol, triglyceride, and LDL levels; the ratio between total cholesterol to HDL and LDL to HDL and an improvement in LVDP at higher filling pressure in diabetic as well as diabetic hypertensive animals. Treatment with lisinopril also prevented hypertrophy and elevated levels of serum creatinine, SGOT and SGPT in diabetic animals. In conclusion, the present data suggests that STZ-DOCA model may not be considered as the ideal model for the study of cardiovascular complications of combined treatment hypertension and diabetes. However, the present investigation presents a number of beneficial effects of lisinopril treatment in diabetic with or without hypertensive rats and it may be considered as one of the drugs of choice in treatment of hypertension when it is associated with diabetes mellitus.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Transport of inorganic phosphate in renal cortical brush-border membrane vesicles of cadmium-intoxicated rats.

The effect of cadmium intoxication on the renal proximal tubular phosphate transport system was studied in adult male Sprague-Dawley rats. Subcutaneous injections of CdCl2 at a dose of 2 mg Cd/kg body wt per day for 2 weeks induced marked polyuria, glycosuria, proteinuria, and phosphaturia, which are characteristics of chronic cadmium intoxication. In the renal cortical brush-border membrane vesicles prepared from cadmium-intoxicated rats, the cadmium content was drastically increased and the Na(+)-dependent phosphate uptake was markedly attenuated. Similar results were obtained in normal membrane vesicles directly exposed to free cadmium. These results indicate that cadmium intoxication impairs the Na(+)-phosphate cotransport system in the proximal tubular brush-border membrane, which may lead to phosphaturia in intact animals.

Animals↗

PubMed2001

Differential regulation of mouse kidney sodium-dependent transporters mRNA by cadmium.

Chronic exposure to cadmium can result in renal glycosuria. Previously, we reported that cadmium reduced the relative abundance of the sodium-glucose cotransporter mRNA (Blumenthal et al., Toxicol. Appl. Pharmacol.149, 49-54, 1998). To investigate this phenomenon further, we isolated full-length cDNA clones encoding both high- and low-affinity sodium-dependent glucose transporters SGLT1 and SGLT2, respectively, from cultured mouse kidney cortical cells. We also amplified a fragment of another putative sodium-glucose cotransporter with homology to the known SAAT1/pSGLT2 or SGLT3 from our cultured cells and named it SGLT3. In order to examine the effect of cadmium on these transporters, primary cultures of mouse kidney cortical cells were exposed to micromolar concentrations of cadmium for 24 h and levels of SGLT1, SGLT2, and SGLT3 mRNA were determined by semiquantitative RT-PCR. Five to 10 microM of cadmium inhibited sodium-dependent uptake of the glucose analog, alpha-methyl D-glucopyranoside and progressively reduced the level of SGLT1. Cadmium also inhibited SGLT2 mRNA by 37%, but no further decline was observed at concentrations of cadmium greater than 5 microM. While cadmium inhibited SGLT1 and SGLT2, it significantly stimulated the expression of SGLT3 by fivefold. These results imply that individual sodium-glucose cotransporter mRNA species are not regulated in a similar fashion. In addition, the isolation of three separate SGLT species from these cultures suggests that, in addition to SGLT1 and SGLT2, glucose reabsorption by renal epithelial cells might involve additional glucose transporters such as SGLT3.

Amino Acid Sequence↗

PubMed1983

Experimental hypothalamic or genetic obesity in the non-insulin-dependent diabetic rat.

Non-insulin-dependent diabetes was obtained in adult rats by neonatal administration of streptozotocin (100 mg/kg). Obesity was obtained in the same animals either by a ventromedial hypothalamic lesion in adult non-insulin-dependent diabetic Wistar rats, or by using genetically obese Zucker rats. In diabetic rats, weight gain was similar to that in non-diabetic rats, whether hyperphagia was due to a ventromedial hypothalamic lesion or to a genetic factor. Glucose-induced insulin release in vivo was increased in obese diabetic rats compared with non-diabetic rats. Despite this enhanced insulin secretion, both diabetic 'fatty' Zucker rats and diabetic rats with hypothalamic obesity showed a deterioration of glucose tolerance. Moreover, about one-third developed overt diabetes with permanent or transient glycosuria. We conclude that when insulin-deficient rats are made hyperphagic, they are able to increase their insulin secretion and become obese. In some of these animals the occurrence of obesity aggravates the diabetes. The obese diabetic rat appears to be a suitable laboratory model for the study of the relationship between obesity and diabetes.

Animals↗

PubMed1981

Diabetic control in patients treated with once or twice-daily insulin injections, including a comparison of conventional beef and highly purified pork insulins.

Twenty patients were changed from a single daily injection of beef insulin (a mixture of soluble and protamine zinc insulin) to two daily injections (mixtures of soluble and isophane insulins). This was associated with a reduction, one month later, in the concentration of glycosylated haemoglobin (HbA1) and in the degree of late evening glycosuria. A reduction was shown 6 months later in antibody binding of beef and pork insulin by serum. Subsequent conversion to a twice daily regime of highly purified pork insulin was not associated with further improvement in diabetic control, but was associated after 1 month with a reduction in daily insulin dose, and after 5 months with a further reduction in antibody binding of beef and pork insulin by serum. Patients failing to show a C-peptide response to intravenous glucagon had a fall in HbA1 after conversion from a once to a twice daily insulin regime, which correlated inversely with insulin antibody binding estimated at the beginning of the study.

Adolescent↗

PubMed1980

Renal glucosyltransferase activity in highly-inbred spontaneously diabetic Chinese hamsters.

A modified glucosyltransferase assay using degraded gelatin as acceptors was found to be enzyme concentration- and time-dependent in the Chinese hamster kidney extracts. In 54 Chinese hamsters selected from 7 highly inbred sublines with or without spontaneous glycosuria, the glucosyltransferase activity (0.78-3.25 unit/g) in the kidney was found to be significantly correlated (P = 0.0002) to blood sugar concentrations (60-475 mg/dl). However, subline-dependent variation in glycosyltransferase activity was also evident and, in animals from 2 of the 5 diabetic sublines, similar activity of glucosyltransferase was found in their kidneys as in those of nondiabetic animals. It was concluded that renal glucosyltransferase activity was affected by blood sugar level as well as by genetically determined factor(s).

Animals↗

PubMed1988

Dietary prevention of diabetes in the non-obese diabetic mouse.

Diabetes prone NOD female mice were fed diets containing different proteins from just before weaning. Only mice receiving meat meal or casein as the protein source developed diabetes at the rate expected from this colony. Lactalbumin and gluten did not precipitate diabetes except in a small number. Casein hydrolysate in lieu of protein protects against overt diabetes, but only if introduced early. The animals which did not show overt diabetes nevertheless had intermittent trace glycosuria and the majority showed mild degrees of periinsular lymphocytic infiltration.

Animals↗

PubMed1985

Continuous infusion of glucose with model assessment: measurement of insulin resistance and beta-cell function in man.

Continuous infusion of glucose with model assessment (CIGMA) is a new method of assessing glucose tolerance, insulin resistance and beta-cell function. It consists of a continuous glucose infusion 5 mg glucose/kg ideal body weight per min for 60 min, with measurement of plasma glucose and insulin concentrations. These are similar to postprandial levels, change slowly, and depend on the dynamic interaction between the insulin produced and its effect on glucose turnover. The concentrations can be interpreted using a mathematical model of glucose and insulin homeostasis to assess insulin resistance and beta-cell function. In 23 subjects (12 normal and 11 with Type 2 (non-insulin-dependent diabetes) the insulin resistance measured by CIGMA correlated with that measured independently by euglycaemic clamp (Rs = 0.87, p less than 0.0001). With normal insulin resistance defined as 1, the median resistance in normal subjects was 1.35 by CIGMA and 1.39 by clamp, and in diabetic patients 4.0 by CIGMA and 3.96 by clamp. In 21 subjects (10 normal and 11 Type 2 diabetic) the beta-cell function measured by CIGMA correlated with steady-state plasma insulin levels during hyperglycaemic clamp at 10 mmol/l (Rs = 0.64, p less than 0.002). The CIGMA coefficient of variability was 21% for resistance and 19% for beta-cell function. CIGMA is a simple, non-labour-intensive method for assessing insulin resistance and beta-cell function in normal and Type 2 diabetic subjects who do not have glycosuria during the test.

Body Weight↗

PubMed1983

Electron microscopy of renal and ocular changes in virus-induced diabetes mellitus in mice.

The eyes, kidneys and pancreas of mice (SJL/J) infected with encephalomyocarditis virus were examined by light and electron microscopy. Diabetic mice with the longest duration (6 months) of diabetes showed marked renal and ocular alterations. Fasting blood glucose levels were 17.8-21.9 mmol/l and glycosuria was present. Clinically, based on ophthalmoscopy and fluorescein angiography, retinal vessels were normal. Histologically, moderately decreased numbers of pericytes were noted following trypsin digestion. The basement membrane of inner retinal vessels showed significant thickening in diabetic mice. Corneal epithelial oedema was present and surface microvillus projections were decreased compared with control mice. The kidneys of the same animals showed nodular and diffuse glomerulosclerosis and mesangial thickening. Electron microscopy showed excessive accumulation of basement membrane-like material in the mesangium and the peripheral glomerular region. Histologically, moderate to advanced kidney disease was associated with relatively early retinopathy.

Animals↗

PubMed1982

Development of diabetes in Japanese subjects with impaired glucose tolerance: a seven year follow-up study.

Five hundred and seven subjects with postprandial glycosuria underwent a 50g oral glucose tolerance test in an epidemiological survey of diabetes mellitus carried out in 1964-1965 in the town of Osaka, Japan. The oral glucose tolerance test was repeated 7 years late in 207 (40.8%) of the subjects. The results of the initial and the follow-up test were classified into three categories according to the new WHO criteria: normal, impaired glucose tolerance and diabetes. Most of the diabetic subjects (84.8%) remained unchanged between the initial and follow-up test. Of the subjects with impaired glucose tolerance at the time of the initial test, 38.5% showed diabetes in the follow-up test, while another 38.5% returned to normal. On the other hand, 13.5% of the normal subjects in the initial test developed impaired glucose tolerance or diabetes in the follow-up test. The rate of worsening to diabetes was related closely to the 2-h blood glucose value at the initial test. In addition, the rate of worsening was higher in males and obese subjects than in females and non-obese subjects. A multiple logistic analysis indicated that the fasting and 2-h glucose values were significantly predictive of worsening to diabetes.

Adolescent↗

PubMed1996

Enterotoxaemia in goats.

Enterotoxaemia of sheep and goats occurs worldwide, but the condition in goats is poorly understood. The disease in goats is mostly caused by Clostridium perfringens type D, although the role of the toxins of this microorganism in the pathogenesis of the disease is not fully understood. The disease occurs in three forms, peracute, acute and chronic, the cardinal clinical sign of the acute and chronic forms being diarrhoea. The main biochemical alterations are hyperglycaemia and glycosuria, while at necropsy the disease is often characterized by haemorrhagic colitis. The typical histological changes observed in the brain of sheep with enterotoxaemia are not considered to be a common feature of enterotoxaemia in goats. Although the pathogenesis of caprine enterotoxaemia has not yet been properly defined, it is usually accepted that the presence of C. perfringens type D in the small bowel, together with a sudden change to a diet rich in carbohydrates, is the main predisposing factor for the disease. Vaccination seems to be poorly effective in preventing caprine enterotoxaemia, which might be due to the fact that the enteric form of the disease is partially independent of circulating C. perfringens toxin. More studies are needed on caprine enterotoxaemia, especially of its pathogenesis and immunity, in order to develop more efficient control measures for this disease.

Animals↗

PubMed1977

Loss of body weight and fat during exercise in a cold chamber.

Ten men spent one week in a cold climatic facility performing a simulated arctic military exercise demanding an energy expenditure of 13-16 MJ-day-1. Although the ration pack was adequate, extensive plate wastage led to a negative energy balance of 2.2 MJ-day-1. Fluid intake was also insufficient, with a 3.25% decrease of body weight, and a 9.7% decrease in skin thickness over the cold exposure. Extensive fat mobilization was indicated by a decrease of skinfold thicknesses, an increase of body density, and associated ketonuria and glycosuria. The fat breakdown far exceeded the calculated energy deficit, and it is postulated that much of the "surplus" energy was required for synthesis of additional muscle protein. In the arctic environment, both energy and fluid balances are better maintained because there are few distraction from the simple pleasure of preparing and eating meals.

Adipose Tissue↗