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PubMedDate not supplied

[Incidence of glycosuria among the population of different age groups living in Andizhan and in the Andizhan district].

A total of 10330 persons, residents of the town of Andizhan (5292 persons) and of the rural districts of the Andizhan region (5038 persons) were examined for glucosuria; it was revealed in 306 persons (2.9%), somewhat more frequently in the urban than in the rural residents (3.1 and 2.8%, respectively); glucosuria was more incident in women than in men (3.3 and 2.4%, respectively); it was more frequently encountered in persons of older age groups than in young individuals (0.6--2.8% in persons aged under 30 years, and in 5.1--6.3% in persons aged from 30 to 70 years and older). Diabetic glycemic curves were found in 122 of 306 persons with glucosuria (39.8%); these curves were suspicious for diabetes mellitus in 63 persons (20.5%). Only in one of 149 persons (0.67%) of the control group without glucosuria was a diabetic curve revealed. The incidence of diabetic glycemic curves increased in persons with glucosuria with the advance of age (13.3% at the age of 10--19 years, and 68.4% at the age of 70 years and older). The authors recommend mass examination of the population for glucosuria by means of the glucose tolerance test for a more complete and timely diagnosis of diabetes mellitus. This is particularly expedient in case of persons of older age groups.

Adolescent↗
PubMed1976

Diabetes mellitus in the guinea pig.

Spontaneous diabetes mellitus has been documented in a colony of guinea pigs. The contagious nature of the disease has been verified, but the nature of the infectious agent is not known. Animals from the original colony or animals exposed to the colony with normal glucose tolerance tests (GTT) became diabetic, as evidenced by elevated one- and four-hour GTT values, and in most cases have significant glycosuria. The severity of pathologic changes in the pancreatic islets parallel, in general, the severity of the clinical symptoms (glycosuria and abnormal GTT). Those animals with severe glycosuria and elevated FBS as well as one- and four-hour GTT values had the most pronounced degranulation and most prominent cytoplasmic inclusions in islet B cells. The severity of scarring in the islets can be correlated with the duration of the overt diabetic state. The other clinical parameters of note were elevated serum triglycerides, normal serum but elevated aortic cholesterol, and absence of ketonemia or ketonuria. The reproductive capacity of diabetic females was compromised. While the clinical manifestations are mild or variable, the presence of significant islet pathology is reminiscent of human juvenile diabetes mellitus. These findings lend support to the concept that infectious and/or immune mechanisms could be operative in the etiology and pathogenesis of human diabetes mellitus.

Animals↗
PubMed1979

Effects of dietary cadmium on rhesus monkeys.

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.

Animals↗
PubMed1977

The spontaneously diabetic Wistar rat. Metabolic and morphologic studies.

A new, spontaneously diabetic syndrome has been recognized in nonobese outbred Wistar rats of both sexes. The age at detection of first glycosuria has varied from 48 to 120 days, with a mean of 67 days. Eighteen rats have been studied, 14 untreated and four during and after cessation of insulin treatment. The affected animals have demonstrated a spectrum of severity, with hyperglycemia (252-732 mg./dl.), hypoinsulinemia (0-1 ng./ml.), and hyperketonemia. The severely ketotic rats, with total blood ketone body levels between 6 and 13 mM, showed rapid loss in weight and dehydration over one to six days. The moderately ketotic (1-5 mM) declined gradually in weight over 15 days, with marked polyuria and glycosuria. The stable rats, with ketonemia less than 1 mM, sustained their weights, polyuria, and glycosuria for longer than 40 days. A relative or absolute increase in plasma immunoreactive glucagon and elevated levels of free fatty acids and branched-chain amino acids were observed in relation to the severity of the syndrome. Intraperitoneal arginine or tolbutamide elicited no insulin response, but the glucagon response to arginine was exaggerated. Pancreatic insulin content was normal or moderately decreased. Light-microscopic examination of pancreases of ketotic animals at the end stage of the disease showed islets to be very small and rare, consisting virtually of non-beta cells. In stable and earlier ketotic rats, the islets were small, with reduction in beta-cell number and a striking inflammatory cell infiltration. Surviving beta cells showed variable degranulation. This model of spontaneous diabetes in nonobese rats displays insulin deficiency, glucagon excess, and ketosis, with a dramatic inflammatory lesion during active beta-cell destruction.

Aging↗
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↗
PubMed1979

Altered immune reactivity in encephalomyocarditis-M variant (EMC-M)-induced diabetes in mice.

Approximately 50% of DBA/2j male mice infected with EMC-M develop glycosuria with suppressed immune responsiveness to the mitogens PHA, Con A and PWM. The greatest degree of suppression was noted with Con A treated cultures. In vivo treatment with Levamisole, a known T cell stimulant, especially increased the response to Con A but exacerbated the diabetogenic state as reflected by increased occurrence of glycosuria. Virus infected mice, given anti-lymphocyte serum (ALS), showed marked amelioration of the diabetic syndrome. Indomethacin, a non-steroidal anti-inflammatory agent as well as a prostaglandin-synthetase inhibitor, partially reversed the in vitro splenic cell suppression of infected animals.

Animals↗
PubMedDate not supplied

[Renal diabetes. Apropos of 103 cases in children].

A longitudinal study of 103 cases of renal glycosuria (94 families) led to the following conclusions. 1. When the condition is genetically determined, it is probably inherited as an autosomal recessive. 2. There is no relationship with diabetes mellitus. 3. The renal glycosuria is persistent but does not get worse.

Adolescent↗
PubMed1979

Characterization of renal defects in dogs with a syndrome similar to the Fanconi syndrome in man.

Ten adult dogs with multiple spontaneous defects of renal tubular reabsorption were studied. Clinical signs included polydipsia, polyuria, and glycosuria for 2 to 12 months. Eight of the dogs were Basenjis. Urinalyses revealed hyposthenuria, glycosuria, and amino aciduria in most dogs. Renal function was normal in 5 dogs and slightly reduced in the remainder. Moderate metabolic acidosis had developed in 3 dogs. Renal clearance studies revealed reduced tubular reabsorption of glucose, phosphate, sodium, potassium, and uric acid. Abnormal glucose tubular maximal curves were found. Results of oral glucose tolerance tests were normal. Two patterns of abnormal amino aciduria were evident: generalized amino aciduria and a pattern similar to that of cystinuria in dogs. Radiography of long bones and bone densitometry did not reveal any skeletal abnormalities. Five of the dogs died within 90 days of diagnosis; death was due to acute renal failure associated with profound dehydration, acidosis, and papillary necrosis. The other dogs remained stable without treatment after 18 months. Histopathology of kidneys did not reveal uniform abnormalities; some dogs had variable and nonspecific changes and others were normal. Electron microscopy did not reveal ultrastructural abnormalities in renal tubular cells. It was concluded that the syndrome in these dogs represents a new entity of renal disease in dogs, similar to idiopathic Fanconi syndrome in man.

Animals↗
PubMed1978

Effect of oral glucose ingestion on renal phosphate reabsorption and clearance in vitamin D-resistant rickets.

The effect or oral glucose ingestion on renal phosphate reabsorption was studied in 13 patients with the inherited form of vitamin D-resistant rickets (VDRR) and 5 normal subjects. In contrast to the normal subjects, glycosuria developed in six VDRR patients after glucose ingestion and resulted in a further 43% decrease in renal phosphate reabsorption. This was accompanied by a 33% increase in phosphate clearance. This was not attended by differences in fasting glucose or phosphorus levels between groups, or in their respective values 1 h after glucose ingestion. Baseline renal phosphate reabsorption was less and baseline phosphate clearance was greater in those VDRR subjects who developed glycosuria. The accumulated data suggest that excessive glucose ingestion by some patients with VDRR may add an additional insult to the phosphaturia characteristic of this disorder. This, in turn, would further compromise the response of circulating phosphate to therapeutic attempts at oral phosphate supplementation, thereby reducing the efficacy of oral phosphate therapy on skeletal growth and development in this disorder.

Adolescent↗
PubMed1979

Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis.

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.

Adolescent↗
PubMed1979

Induction of diabetes in animals by parenteral administration of ferric nitrilotriacetate. A model of experimental hemochromatosis.

Rats and rabbits parenterally treated with a large daily dose of ferric nitrilotriacetate manifested diabetic symptoms such as hypergycemia, glycosuria, ketonemia, and ketonuria after approximately 60 days fo treatment. The blood insulin response to oral glucose loading was poor. Heavy iron deposits were found in liver parenchymal cells and in pancreatic exocrine cells, although some iron was deposited in the macrophages and reticuloendothelial cells of the organs. Faint iron staining was found in some pancreatic islet cells, with a reduction in beta granules and weak zinc staining. Cirrhotic liver changes and skin pigment deposition were not observed. Repeated blood withdrawals from ferric-nitrilotriacetate-treated animals resulted in disappearance of hypergycmia, glycosuria, ketonemia, and ketonuria; disappearance of iron from the liver and pancreas; and restoration of islet beta granules to the control level.

Acetates↗
PubMed1979

Hyperosmolar diabetes presenting as acute urinary retention: report of three cases.

Three elderly patients presented at one hospital in a 2-week period with acute urinary retention precipitated by the hyperosmolar non-ketotic diabetic state. In each case routine urine testing was reported as showing 1 per cent glycosuria. The first two patients were admitted at night and blood glucose estimations were not done. This led to a delay of 16 and 12 h respectively before the appropriate therapy was instituted. It is suggested that this clinical presentation, previously unreported, may not be a rarity and represents an avoidable cause of death in patients with acute urinary retention.

Acute Disease↗