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PubMed1987

New establishment of hypertensive diabetic animal models: neonatally streptozotocin-treated spontaneously hypertensive rats.

Hypertensive diabetic animal models have been developed by injecting streptozotocin (STZ) in neonatal stroke-resistant spontaneously hypertensive rats (SHRSR) and stroke-prone SHR (SHRSP) at the age of two days. After the treatment, the animals showed mild insulin deficiency and mild hyperglycemia at the age of three to four months. Diabetic nephropathy was produced particularly in STZ-treated SHRSR at the age of six months. The effect of neonatal STZ injection on hyperglycemia varied among normotensive Wistar-Kyoto rats (WKY), SHRSR, and SHRSP; SHRSR showed the highest glucose levels, SHRSP showed intermediate levels, and WKY was the lowest. All STZ-treated SHRSR showed glycosuria, while glycosuria was not observed in the treated SHRSP and WKY. Histologic study indicated that these strain differences were partly ascribed to differences in islet B-cell sensitivity to toxic effects of STZ. The development of hypertension was not accelerated in these SHRSR and SHRSP compared with respective nontreated controls. Since STZ-treated SHRSR develop mild diabetic symptom with hypertension and develop mild diabetic glomerulosclerosis, they are good models for studying vascular complications or other problems relating to the synergism between hypertension and diabetes mellitus.

Animals↗
PubMed1980

Ageing, a factor aggravating chronic toxicity of cadmium.

Two groups, each of 4 rabbits, 17 and 4 months old, respectively, were given s.c. administrations of cadmium (Cd) at a dose level of 0.5 mg/kg/day 6 times per week for up to 32 weeks. In 17-month-old rabbits, low-molecular-weight proteinuria appeared in the 3rd week, proteinuria, glycosuria and anemia in the 6th week; and all animals died by the 8th week. In 4-month-old rabbits, low-molecular-weight proteinuria and anemia appeared in the 6th--9th weeks, proteinuria, glycosuria and aminoaciduria by the 12th week; and all animals died by the 32nd week. The results suggest that ageing may aggravate the chronic toxicity of cadmium.

Aging↗
PubMed1980

Nephrotic syndrome and multiple tubular defects in children: an early sign of focal segmental glomerulosclerosis.

The nephrotic syndrome is rarely associated with renal tubular defects, and the combination has been reported only in association with advanced renal insufficiency. We report here five children with nephrotic syndrome and multiple tubular defects which evolved when glomular filtration rate ranged between 56 and 90 ml/minute/1.73 m2. The tubular defects were first noted at 3, 4, 4, 7, and 22 months after the onset of the nephrotic syndrome, and renal glycosuria was the first sign in all five children. Glycosuria was intermittent in three patients, constant in two, and ceased with loss of kidney function. Four patients had hyperaminoaciduria and renal tubular acidosis (two of four tested had distal renal tubular acidosis). Three patients had decreased tubular reabsorption of phosphorus and defective maximum concentrating capacity. All five had focal segmental glomerulosclerosis proven by renal biopsy. Over a follow-up period of seven years, all of the children have developed advanced renal insufficiency, four of the five have required dialysis or transplantation within 21 to 72 months after onset, and one has stabilized renal function at 35 ml/minute/1.73 m2. The one patient receiving a kidney transplant has had recurrence of focal segmental glomerulosclerosis in the transplanted kidney and became nephrotic with three subsequent transplants. Our experience suggests that the nephrotic syndrome associated with tubular defects in children forms a subgroup of focal segmental glomerulosclerosis, with rapid progression to renal insufficiency and the potential for recurrence of the lesion in the transplanted kidney.

Acidosis, Renal Tubular↗
PubMed2001

Dietary patterns and risk factors of diabetes mellitus among urban indigenous women in Fiji.

The dietary patterns of indigenous Fijians are changing rapidly. Dietary relationships in regard to the prevalence of diabetes are poorly studied in Fiji. A survey was conducted to show the relationship of dietary patterns and other lifestyle factors for the development of diabetes among urban indigenous women in Fiji. A sample of 200 Fijian women aged 30-39 who agreed to participate were interviewed by the use of semiquantitative food frequency, 3 day-24 h recall study. Physical activity and ceremonial dietary customs were also taken into consideration. Anthropometry included measurements of height, weight, waist and hip. Total percentage bodyfat measurements and glycosuria tests were also conducted. The results showed high rates of obesity manifested in high percentage bodyfat, high body mass index (BMI) and high waist and hip ratio (WHR). The mean 24 h dietary intake exhibited a moderate intake of protein, high intake of fat and a low intake of carbohydrate. The carbohydrate reduction was a result from the decline in consumption of traditional staples. Consumption of cereals and related products favored the high intake of butter and margarine and also encouraged the use of cooking oil in frying varieties of flour products. The daily intake of anti-oxidant vitamins of beta-carotene and vitamin E were low, however there was a high intake of vitamin C. The food frequency study revealed cassava, bread and sugar were consumed daily as the main carbohydrate foods. Fish and meat were the most frequently consumed protein foods. The main beverage was sweet tea with whole-cream milk. Butter, margarine, coconut cream, cheap lamb flaps and cooking oil provided the main sources of fat. Levels of physical activity included high sedentary lifestyles with a high rate of subjects being overweight and obese. Ceremonial dietary customs showed a high consumption of meat and fish. Fruits were rarely consumed. Glycosuria existed among the age group under study. The impact of dietary transition, coupled with dietary excesses and physical inactivity, seem to be potential risk factors of diabetes among the indigenous women in the urban area.

Adult↗
PubMed2004

Autosomal recessive renal proximal tubulopathy and hypercalciuria: a new syndrome.

BACKGROUND: The best described primary inherited proximal tubulopathies include X-linked hypercalciuric nephrolithiasis (XLHN), caused by a mutation in the chloride channel gene CLCN5, and classic Fanconi's syndrome, the genetic basis of which is unknown. The aim of this study is to examine the clinical, biochemical, and genetic characteristics of a highly consanguineous Druze family with autosomal recessive proximal tubulopathy and hypercalciuria (ARPTH), a syndrome not reported previously. METHODS: Three children (2 girls, 1 boy) of the family referred for evaluation of renal glycosuria and hypercalciuria and 10 of their close relatives were evaluated clinically and biochemically. All study participants underwent genetic analysis to exclude involvement of the CLCN5 gene. RESULTS: Evaluation of the 3 affected children showed glycosuria, generalized aminoaciduria, hypouricemia, uricosuria, low molecular weight (LMW) proteinuria, and hypercalciuria in all 3 children and phosphaturia in 2 children. They had no metabolic acidosis or renal insufficiency. One affected girl had nephrocalcinosis. Two children had a history of growth retardation and radiological findings of metabolic bone disease. Parathyroid hormone and 1,25-dihydroxyvitamin D [1,25(OH)2Vit D] blood levels in affected children were normal. Unaffected family members examined had no renal tubular defects or LMW proteinuria. Genetic linkage analysis excluded cosegregation of the ARPTH phenotype with the CLCN5 locus. CONCLUSION: ARPTH is a new syndrome characterized by nonacidotic proximal tubulopathy, hypercalciuria, metabolic bone disease, and growth retardation. It can be distinguished from XLHN by its autosomal recessive mode of inheritance and normal serum levels of calciotropic hormones, as well as the absence of LMW proteinuria in obligate carriers. The gene mutated in ARPTH remains to be identified.

Bone Diseases, Metabolic↗
PubMed1980

Diabetic diets: high carbohydrate combined with high fiber.

The ideal level of carbohydrate intake for diabetics placed on high-fiber diets is unknown. Nineteen diabetics, therefore, took part in a total of twenty-four 5-day studies of fiber supplementation (guar) with carbohydrate intakes ranging from 22 to 61% of total calories. Where carbohydrate formed more than 40% of the calorie intake, there was a mean 64% reduction in glycosuria over the last 2 days on guar (P < 0.001, 14 studies, 11 patients). No significant reduction in glycosuria was seen in the 10 studies on lower carbohydrate intakes. This suggests that dietary fiber supplements in diabetes should be given against a background of higher rather than lower carbohydrate intake.

Adult↗
PubMed2003

Validation of volume kinetic analysis of glucose 2.5% solution given by intravenous infusion.

BACKGROUND: The distribution and elimination of glucose solutions can be analysed by means of a volume kinetic model, but the ability of the model to predict plasma dilution ('model linearity') has not been evaluated. METHODS: Six male volunteers received four separate infusions of glucose 2.5%: 10 ml kg(-1) and 15 ml kg(-1) over 30 min, and 15 ml kg(-1) and 25 ml kg(-1 )over 60 min. The kinetic model was fitted to measurements of plasma glucose concentration and haemodilution. RESULTS: The mean volume of distribution for the glucose was 9.2 (SEM 0.4) litres while the infused fluid expanded a central body fluid space (V(1)) of 3.1 (0.3) litres. Increasing the amount of infused fluid, but not the infusion rate, resulted in a proportional increase in the area under the curve for plasma glucose and plasma dilution, the only confounder being glycosuria. The bias of computer simulation was slightly increased by rebound hypoglycaemia, which could occur with the highest infusion rates, but the accuracy was almost identical regardless of whether the kinetic parameters from all 24 experiments or from any of the subgroups were used. CONCLUSION: The volume kinetic model for glucose 2.5% is linear and can therefore be used for computer simulation as long as marked glycosuria does not occur.

Adult↗
PubMed1991

Tubular dysfunction in nephrotic syndrome: incidence and prognostic implications.

Although some cases of tubular dysfunction (TD) associated with nephrotic syndrome have been described, the incidence and the characteristics of this complication remain unknown. We investigated the presence of TD (renal glycosuria, aminoaciduria, metabolic acidosis with normal anion gap, hypouricaemia, and throughout hypophosphataemia) in 36 patients with nephrotic syndrome. Ten patients (group 1) showed glycosuria at some time during the course of their illness, ranging from 2.5 to 11.2 g/24 h. In addition, seven of them had metabolic acidosis with normal anion gap, five aminoaciduria, and two hypouricaemia. Membranous glomerulonephritis was the most frequent aetiology in group 1 patients (7 of 10). Proteinuria and serum creatinine (SCr) were significantly higher in group 1 patients than in the 26 remaining patients without TD (group 2): 10.2 +/- 3.7 versus 6.7 +/- 2.9 g/24 h (P less than 0.01) and 3.2 +/- 1.9 versus 1.6 +/- 0.9 mg/dl (P less than 0.05) respectively. The appearance of TD coincided with a clear worsening of renal function in most of group 1 patients. In addition, at the end of follow-up, SCr had increased from 3.2 +/- 1.9 to 5.6 +/- 3.3 mg/dl (P less than 0.05) in this group. In contrast, SCr did not show significant changes in group 2 (1.6 +/- 0.9 versus 2.1 +/- 2.2 mg/dl). In conclusion, a significant proportion (27.7%) of patients with nephrotic syndrome present TD data at some moment of their course; the appearance of this complication appears to be a sign of poor prognosis.

Adolescent↗
PubMed1979

Clofibrate and diabetes control in patients treated with oral hypoglycaemic agents.

1. Twenty-two maturity-onset type diabetics treated with oral hypoglycaemic agents entered a single-blind crossover study using placebo (periods A and C, 2 months each) and clofibrate (2 g/day; period B; 2 months). 2. In thirteen patients, under reasonably good control, clofibrate did not reduce fasting or post-prandial blood glucose, nor 24 h glycosuria; no improvement was noted in the M-value, an index of diabetes control. 3. In contrast, in nine patients, with poor diabetes control, clofibrate reduced 24 h glycosuria and significantly improved the M-value. 4. In all patients, clofibrate therapy was associated with a significant 19-23% reduction in plasma fibrinogen. 5. It is suggested that addition of clofibrate may be useful in maturity-onset diabetics not adequately controlled by diet combined with oral hypoglycaemic agents.

Blood Glucose↗
PubMed1984

Renal glucose transport after kidney transplantation.

Tubular maximal transport of glucose (TmG), plasma glucose threshold ( PGT ) and fractional maximal tubular reabsorption (TmG/GFR) were measured in fourteen kidney-grafted patients. Seven patients showed decreased PGT and normal or decreased TmG/GFR (type A or B renal glycosuria (RG) ), whereas seven other patients showed normal values. No difference was found between the two groups with respect to parameters of renal function and to clinical parameters characterizing kidney transplantation. The only difference observed between the two groups was the rate of decrease of plasma creatinine levels during the 1st week after transplantation: it was faster in the group without renal glycosuria. No difference was seen between the two groups of patients with respect to the number of rejection episodes occurred over the first 12 months.

Adult↗
PubMed1997

Improving effect of carteolol on bodyweight and carbohydrate and lipid metabolic responses in the OLETF rat.

1. Carteolol, a non-selective beta-blocker with intrinsic sympathomimetic activity, admixed in a pellet diet was administered to Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of spontaneous non-insulin-dependent diabetes mellitus with mild obesity. A high dose of carteolol (0.02%) suppressed bodyweight gain without affecting food and water consumption until the appearance of glycosuria. Carteolol tended to reduce the cumulative incidence of glycosuria at 26 weeks after the beginning of administration (55, 17 and 25% in control rats, and in rats fed a low (0.002%) and high dose of carteolol, respectively). 2. At the 26th week of administration, the high dose of carteolol decreased visceral fat weight, such as that of retroperitoneal and epididymal adipose tissue, whereas the liver and the kidney were not affected. 3. Although plasma glucose and triglyceride levels in non-fasted rats were elevated with age, carteolol tended to delay the increases in those parameters. Carteolol suppressed the increase in plasma glucose levels, which indicate the diabetic pattern, in a 25th week oral glucose tolerance test. 4. These findings indicate that carteolol induces improvements in bodyweight and carbohydrate and lipid metabolism in an obese condition. Consequently, carteolol may be useful for the treatment of hypertension with obesity in order to prevent cardiovascular events.

Adipose Tissue↗
PubMed1990

Descriptive epidemiology of non-insulin dependent diabetes mellitus detected by urine glucose screening in school children in Japan.

During the period from 1974 through 1988, we annually examined approximately 225,000 to 386,400 school children residing in Tokyo for glycosuria to detect juvenile diabetes. If the first test was positive for glucose, glycosuria was confirmed by a second test. In children who gave a positive result in both the first and second tests 0-GTT were performed. All 124 patients were diagnosed as NIDDM according to the criteria of the WHO Report on Diabetes of 1985. The incidence of NIDDM in children in Japan has increased in recent years and from 1984 to 1986 was approximately 3.8 per 100,000 per year. The frequency of NIDDM increases with age up to 14 years. In about 84% of cases, the body weight at diagnosis is more than 20% above the ideal weight and the height is often above average. There is a high frequency in families with a history of diabetes. Diet and exercise therapy in newly diagnosed patients irrespective of the presence or absence of obesity may result in remission, but some cases may require insulin therapy or oral administration of a hypoglycemic drug to obtain a better glycemic control. Children with NIDDM are more likely to be complicated by incipient retinopathy within two years after diagnosis than those with IDDM. Therefore, it is important to keep strict glycemic control to prevent diabetic complications in NIDDM children just as in juvenile onset IDDM.

Adolescent↗
PubMed2006

Potential causes of weight gain in type 1 diabetes mellitus.

AIM: To investigate the potential causes of weight gain with insulin therapy and improved diabetic control in type 1 diabetes mellitus. METHODS: This was an open-label prospective study of insulin therapy of 6 months duration in an academic medical centre. Twenty-one subjects with type 1 diabetes were enrolled. The goal was to achieve an haemoglobin A1c (HbA1c) in the range of individuals without diabetes (<5.6%). At baseline, 3 and 6 months, weight, resting energy expenditure, appetite assessment, food intake, activity level, HbA1c and 24-h glycosuria and urea nitrogen were measured. Plasma leptin, ghrelin and adiponectin levels and body fat were measured at baseline and 6 months. RESULTS: At baseline, average weight was 73.7 +/- 17.4 kg and HbA1c was 10.0 +/- 2.2%. Weight increased by 2.15 kg (2.69% of baseline) by 6 months whereas the HbA1c dropped by 1.71% (16.3%) to 7.9%. Energy intake differences between 3 and 6 months had a negative correlation with weight gain, but the changes in glycosuria, appetite scores and the frequency of hypoglycaemia did not correlate with weight gain. Glycaemic control did not correlate with weight change but tended to correlate with fat mass increase (p = 0.064; r = -0.51). An increase in the activity levels between 3 and 6 months correlated with decreasing fat mass (p = 0.037; r = -0.74). The changes in the appetite scores had a negative correlation with fat mass gain (p = 0.035; r = -0.61). The changes in lean body mass correlated with protein and total energy intake (p = 0.007, r = 0.85 and p = 0.003, r = 0.73 respectively). The changes in leptin levels correlated with weight gain. CONCLUSIONS: The lipogenic effect of insulin with subsequent increase in fat mass may be the primary cause of this weight gain that can be attenuated by the increases in the activity levels. The negative correlation of energy intake and appetite scores with fat mass gain suggests that they do not play a significant role in fat mass gain whereas energy intake did correlate with lean body mass gain.

Adult↗
PubMed1997

Antidiabetic efficacy of BRL 49653, a potent orally active insulin sensitizing agent, assessed in the C57BL/KsJ db/db diabetic mouse by non-invasive 1H NMR studies of urine.

High resolution 1H nuclear magnetic resonance (NMR) spectroscopic analysis of biofluids is a recently established tool for evaluating inherited and acquired errors in metabolic control. In the present study 1H NMR analysis of urine was used to monitor efficacy of BRL 49653, a potent and selective antihyperglycaemic agent, following oral administration for up to 36 weeks to the genetically diabetic C57BL/KsJ db/db mouse. The effects of BRL 49653 on carbohydrate and fatty acid metabolism were monitored by determination of changes in concentrations of low molecular weight urinary metabolites. A qualitative comparison of the NMR spectra of urine from untreated diabetic mice with those of lean littermates and literature examples revealed several abnormalities, the majority of which could be explained in terms of the non-insulin dependent diabetes syndrome exhibited by these animals. Quantitatively the most prominent was the extreme glycosuria of both young (8-12 weeks; 0.9 g glucose kg-1 h-1) and older (42 weeks; 2 g glucose kg-1 h-1) diabetic mice. This was accompanied by the excretion of a number of unassigned sugar derivatives and by ketone bodies. Administration of BRL 49653 (3 mumol kg-1) to db/db mice for 24 days reduced blood glucose concentrations to values comparable with non-diabetic lean littermates and reduced glycosuria by > 90%. BRL 49653 significantly reduced excretion of unassigned sugars, acetate, lactate, and the ketone bodies, acetoacetate, 3-D-hydroxybutyrate and acetone. The anti-diabetic efficacy of BRL 49653, assessed from the pattern of urinary metabolites, was maintained over a 36-week treatment period. These results demonstrate the value of 1H NMR to evaluate non-invasively the efficacy of novel therapeutic agents.

Administration, Oral↗
PubMed1987

Ultrastructural study of the effect of insulin dosage on the myocardium of spontaneously diabetic BB rats.

Cardiac ultrastructure was studied in spontaneously diabetic BB rats maintained on two different regimens of insulin daily. For 3 months from the onset of overt diabetes, one diabetic group was well controlled with daily subcutaneous administration of sufficient insulin to prevent glycosuria (9.0-13.0 U/kg). Approximately half of this dose (4.5 U/kg) of insulin was given daily to a second group of diabetic rats. Normal Wistar rats and nondiabetic BB rats were used as controls. Blood glucose values were three- to four-fold higher with respect to these controls in the diabetic BB rats receiving the smaller dose of insulin but were significantly lower than controls in diabetic animals receiving the higher insulin dose. A 30% difference in body weight with respect to the Wistar controls, obvious hyperliposis, and some nerve degeneration were seen in the low dose insulin group of diabetics. Such changes did not occur in the well-controlled insulin-treated group. Electron microscopic examination of the left ventricular tissue revealed mild damage in both groups of diabetics consisting of small focal lesions and mild edema along the sarcoplasmic reticulum and sometimes adjacent to the sarcolemma. Thus, insulin treatment, which prevented glycosuria, resulted in normal tissue lipid levels and prevented nerve damage but had little effect on the other diabetes-induced ultrastructural alterations in the myocardium of these rats.

Animals↗
PubMed1992

Urine uric acid excretion in patients with insulin-dependent diabetes mellitus.

Serum uric acid has been described as being increased in the prediabetic stage of diabetes mellitus and as being decreased in overt diabetes. In this study we compared the serum uric acid levels of patients with insulin-dependent diabetes mellitus (IDDM) to those of controls matched for sex, age and ethnic origin. Also the correlation between serum uric acid levels and the fractional excretion of uric acid in IDDM patients was investigated, as well as the correlation between glycosuria and the fractional excretion of uric acid. The mean serum uric acid was lower in IDDM patients than in normal controls (4.0 +/- 1.3 vs. 4.3 +/- 1.3 mg/100 ml; p less than 0.03), mainly due to significantly lower levels in male and Ashkenazi IDDM patients, as compared to their respective controls. The fractional excretion of uric acid was found to be elevated in IDDM patients: 13.0 +/- 8.6% (mean +/- SD). A significant negative correlation was found between serum uric acid levels and the fractional excretion of uric acid in IDDM patients (p less than 0.001), although not when the males were examined separately. We found no correlation between the fractional excretion of uric acid and the degree of glycosuria in IDDM patients. In addition, the prevalence of hypouricemia (serum uric acid less than 2.5 mg%) was the same in IDDM patients and controls.

Adult↗
PubMed1969

Diabetogenic action of streptozotocin: relationship of dose to metabolic response.

The relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. Diabetogenic activity could be demonstrated between the doses of 25 and 100 mg/kg, all indices used showing some degree of correlation with the dose administered. Ketonuria was only seen with the largest dose, 100 mg/kg. The most striking and precise correlation was that between the dose and the pancreatic IRI content 24 hr after administration of the drug, and it is suggested that this represents a convenient test system either for both related and unrelated beta cytotoxic compounds or for screening for modifying agents or antidiabetic substances of a novel type. Ability to produce graded depletion of pancreatic IRI storage capacity led to an analysis of the relationship between pancreatic IRI content and deranged carbohydrate metabolism. Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached two-thirds and three-quarters, respectively. The mild yet persistent anomaly produced by the lowest effective streptozotocin dose, 25 mg/kg, exhibits characteristics resembling the state of chemical diabetes in humans and might thus warrant further study as a possible model. Finally, the loss of the diabetogenic action of streptozotocin by pretreatment with nicotinamide was confirmed and was shown to be a function of the relative doses of nicotinamide and streptozotocin and of the interval between injections.

Animals↗
PubMedDate not supplied

Effect of ten new beta-lactam antibiotics on urine glucose test methods.

The effect of ten new beta-lactam antibiotics (cefoperazone, cefotaxime and its metabolite desacetylcefotaxime, ceftazidime, ceftizoxime, ceftriaxone, aztreonam, azlocillin, mezlocillin, piperacillin, and ticarcillin) on the accuracy of Clinitest, Diastix, and Tes Tape determinations of glycosuria was investigated. Solutions of each of the antibiotics were prepared in urine over a range of clinically obtainable drug concentrations. Urine samples from a healthy subject were used to prepare simulated diabetic urine by adding dextrose to achieve concentrations of 0.5%, 1%, and 2%. With penicillin derivatives, falsely elevated Clinitest readings generally were observed at lower glucose concentrations. When no glucose was present, cephalosporins and the monobactam, aztreonam, gave a dark green-black color that could only be interpreted as 0% on the Clinitest color chart. At higher urine glucose concentrations (1% and 2%), no interaction with Clinitest could be demonstrated, with the exception of a few falsely reduced readings. All urine solutions containing beta-lactam antibiotics were estimated accurately by both Diastix and Tes Tape. The unpredictability of the Clinitest-beta-lactam antibiotics interaction should discourage the use of this urine glucose test in patients who receive these drugs. The glucose-oxidase tests, Diastix and Tes Tape, may be used as qualitative tests for glycosuria in patients treated with beta-lactam antibiotics.

Adult↗