SEARCH · PubMed Health

Results for “GLYCOSURIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

PubMed1985

Impaired potassium and magnesium homeostasis in acute tubulo-interstitial nephritis.

Although acute tubulo-interstitial nephritis is increasingly recognized as a cause of acute renal failure, little is known about renal tubular function in this disease. We report on two patients with acute tubulo-interstitial nephritis who demonstrated abnormalities in proximal and distal tubular function. The first patient developed hyperkalemia presumably from a potassium secretory defect in the distal nephron. The second patient developed an incomplete Fanconi's syndrome with glycosuria and aminoaciduria and two heretofore unreported complications of acute interstitial nephritis: hypokalemia and hypomagnesemia secondary to urinary losses of these cations. Careful monitoring of renal tubular function is indicated in patients with acute tubulo-interstitial nephritis.

Acute Disease↗

PubMed1995

Severe renal hypouricemia secondary to hyperbilirubinemia.

A 64-year-old man with alcoholic liver cirrhosis had a progressive decrease in the serum uric acid (UA) until it became undetectable, an increase renal UA clearance, mild glycosuria with normal serum glucose and a decrease in the tubular reabsorption of phosphate in association with cholestasis secondary to a gallbladder carcinoma. All these abnormalities returned to normal when the serum bilirubin levels decreased following surgical treatment. This clinical observation suggests that the reversible renal tubular transport defect was secondary to high levels of serum bilirubin.

Bilirubin↗

PubMed1979

Cadmium nephropathy.

Cadmium is an inessential trace metal which accumulates in human tissues from contamination of food, water or air. The kidney is the critical organ following long-term, low-level absorption either by inhalation or ingestion; accumulation occurring in tubular epithelium in the form of a cadmium-metallothionein complex, giving rise to tubular dysfunction. In a group of 12 cadmium workers some of whom were followed for up to 16 years, tubular proteinuria, renal glycosuria, aminoaciduria, hypercalciuria and defects of concentration and acidification have been observed. Two men became recurrent renal stone formers and 1 man, who had nephrocalcinosis when first seen, later developed vitamin D-resistant osteomalacia. Renal tubular dysfunction following cadmium exposure may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may eventually develop.

Aged↗

PubMed1978

The course of development of glucose intolerance in the monkey (Macaca mulatta).

Longitudinal studies of the rhesus monkey reveal a syndrome of diabetes mellitus in those that become middle-aged and obese. The sequence of events in the development of the disease progresses from normoinsulinemia with normoglycemia through stages of hyperinsulinemia followed by below normal insulin levels with hyperglycemia and glycosuria. We believe the rhesus to be an excellent nonhuman primate model for maturity-onset diabetes in humans.

Age Factors↗

PubMed1996

Effects of ofloxacin administration on the reliability of urine glucose testing.

OBJECTIVE: To study the effects of ofloxacin on the reliability of urine glucose testing. DESIGN: Open-label, nonrandomized. SETTING: A university-affiliated tertiary care hospital, ambulatory clinic. PARTICIPANTS: Ten healthy volunteers (8 men and 2 women) aged 22-39 years. MAIN OUTCOME MEASURES: Phase I (in vitro) involved the addition of selected amounts of ofloxacin to a set of standard 50-mL urine samples prepared to simulate glycosuria. Phase II (in vivo) involved the oral administration of ofloxacin 400 mg to 10 subjects. Urine was collected: (1) immediately predose, (2) pooled 0-4 hours postdose, and (3) pooled 4-8 hours postdose. Known glucose concentrations were then added to these samples. Clinitest and Diastix tests were performed on all samples. The accuracy of these tests in determining glucose concentrations was compared among urine samples taken before and after ofloxacin dosing. RESULTS: None of the ofloxacin concentrations in phase I (0, 25, 50, 100, 200, 400, and 800 micrograms/mL) influenced these testing methods at the urine glucose concentrations of 0.0%, 0.5%, 1%, and 2%. Likewise, the accuracy of these two tests was unaffected by ofloxacin administration in phase II. CONCLUSIONS: In single-dose administration, ofloxacin does not interfere with Clinitest or Diastix for determining urine glucose concentrations.

Adult↗

PubMed1978

Glipizide in the treatment of maturity-onset diabetes: a multi-centre, out-patient study.

A multi-centre clinical assessment was carried out in 592 diabetic patients to study the efficacy and tolerance of glipizide under normal out-patient conditions. Of the total group, 347 patients were maturity-onset diabetics who had received no previous treatment or only dietary control. The other 245 patients had previously received treatment with other hypoglycaemic agents, including insulin in 23 cases. Mean initial dosage was 7.5 mg glipizide per day and this increased over the 3-month period of the study to 10.1 mg in the total group (9.3 mg in new patients). Mean post-prandial blood glucose levels and glycosuria fell rapidly during the first week and then continued to decrease slowly. Changes in mean body weight were somewhat erratic during the trial and at 12 weeks there was an apparent mean increase of 1 kg. After allowing for dropouts, analysis of the results showed that 96.7% of the new patient group and 90.5% of the total group were satisfactorily controlled and maintained on glipizide. Patient tolerance was good, and only 28 (4.7%) patients complained of side-effects, almost half of which related to mild, transient hypoglycaemia.

Adult↗

PubMed1999

Longterm treatment of psoriasis using fumaric acid preparations can be associated with severe proximal tubular damage.

Fumaric acid preparations are used as longterm and effective treatment of psoriasis. Apart from gastrointestinal, dermatological and hematological side-effects, transient renal damage was observed during treatment with fumaric acid. The case of a 38 year old woman who was treated with fumaric acid (420 mg bid) for 5 years before she complained of fatigue and weakness. According to clinical laboratory she had developed severe proximal tubular damage. Hypophosphatemia, glycosuria and proteinuria persisted although medication was stopped immediately.

Adult↗

PubMed1975

Interaction of endogenous growth hormone, cortisol, and catecholamines with blood glucose in children with brittle diabetes mellitus.

Hormonal balance was studied in eight insulin-treated diabetic children who had excessive glycosuria. Glucose, growth hormone, and cortisol in plasma were determined every 0.5 hr for 48 hr. Total catecholamines and glucose were measured and tests for ketones done in 2-hourly collections of urine. Intermittent hypoglycemia as low as 20 mg/100 ml and swings of the blood sugar curve by 200-300 mg/100 ml within 2-4 hr were documented in most patients. Peaks of growth hormone concentration in plasma (8-78 ng/ml) followed almost every sharp fall in blood glucose; these peaks were usually followed by abrupt rises of glucose and prolonged hyperglycemia. Cortisol concentration was usually within the high normal range; there was no consistent relationship to the concentration of glucose. Urinary excretion of catecholamines in most patients was between 1 and 6 mug/hr; three patients excreted up to 8-23 mug/hr during short periods and up to 190 mug in 24 hr. The causes for the high excretion of catecholamines are unknown and may not have included hypoglycemia.

Blood Glucose↗

PubMed2005

A clinical and molecular genetic study of hypophosphatemic rickets in children.

X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets, hereditary hypophosphatemic rickets with hypercalciuria, and tumor-induced osteomalacia share clinical and biochemical features, and are collectively referred to as hypophosphatemic rickets (HR). Recently, the molecular bases of HR were elucidated. A review of medical records and mutational analyses of the PHEX and FGF23 genes were performed on 17 unrelated Korean children with HR. The male-to-female ratio was 3:14, and 5 patients were familial. Initial laboratory tests revealed typical features of HR. Seven different PHEX mutations were detected in 8 patients: 2 missense mutations, 2 nonsense mutations, and 3 short deletions. No functional FGF23 mutation was detected in any patient. Patients with the PHEX mutation tended to have more severe skeletal disease than those without. Of the patients with this mutation, no genotype-phenotype correlation and no gene dosage effect were noted. Treatment with vitamin D and phosphate resulted in only a partial growth improvement in most cases, and was frequently complicated by hypercalciuria, hypercalcemia, nephrocalcinosis, or hyperparathyroidism. Renal glycosuria was detected in six cases and was associated with more severe skeletal disease. We conclude that current HR treatment is not fully safe or effective, and that close monitoring of treatment effectiveness and for complications should be performed during long-term treatment. No genotype-phenotype correlation in XLH was detected in this study, but a large-scaled study on this topic is warranted. The large proportion of patients with a normal genetic study suggests the possibility of other causative gene(s).

Child, Preschool↗

PubMed1980

Effect of insulin and nutrition on serum levels of somatomedin A in the rat.

The serum levels of somatomedin A, as measured by radioreceptor assay, were significantly reduced in rats 2 days after the administration of streptozotocin. The mean decrease was 45.4 +/- 2.9% of the initial values. In rats treated with insulin, blood glucose levels and glycosuria decreased, and serum somatomedin A returned to 108.3% +/- 11.7% of the initial values by the sixth day of treatment. In untreated diabetic rats, serum somatomedin A decreased progressively to 23.4 +/- 4.4% 8 days after streptozotocin administration. The total caloric intakes in the treated and nontreated diabetic rats were similar, suggesting that the low levels of somatomedin A in diabetic rats may be due to lack of insulin. A significant correlation was observed between serum somatomedin A values and body weight (r = 0.90) or the urinary glucose (r = -0.84) or blood glucose levels (r = -0.67). When the diabetic insulin-treated rats were fed a low protein diet, there was no increase in serum somatomedin A. Inhibitory factors in serum which interfere in the bioassay for somatomedin had no effect in our radioreceptor assay.

Animals↗

PubMed1986

Total pancreatectomy increases the metabolic response to glucagon in humans.

To evaluate the impact of glucagon deficiency on the response to glucagon replacement, we infused physiological doses of glucagon (1.25 ng/kg X min) into 9 totally pancreatectomized (PX) diabetic patients (C-peptide, undetectable) 1) for 24 h during their usual diet and insulin regimen and/or 2) for 6 h in a fasted insulin-withdrawn state. During both glucagon infusions, plasma glucagon rose from 46 +/- 2 (+/- SE) pg/ml (0-10% 3500 mol wt glucagon) to 112 +/- 9 pg/ml. In the 24-h study (n = 4), glucagon significantly increased mean 24-h glucose levels (272 +/- 27 mg/dl; P less than 0.05) and glycosuria (29 +/- 5 g/day; P less than 0.01) compared to preinfusion (158 +/- 14 mg/dl and 4 +/- 4 g/day, respectively) and postinfusion (200 +/- 35 mg/dl and 3 +/- 2 g/day) control periods. Blood ketones did not change. The 24-h glucagon infusion significantly lowered the fasting levels of the glucogenic amino acids aspartate (43%; P less than 0.01), threonine (46%; P less than 0.05), serine (46%; P less than 0.02), glycine (47%; P less than 0.01), and methionine (34%; P less than 0.02). Fasting alanine levels decreased from 835 +/- 236 to 393 +/- 66 microM (P less than 0.05). The 6-h glucagon infusion caused a 101 +/- 14 mg/dl maximal plasma glucose increment in PX (n = 8) vs. 33 +/- 11 in 5 insulin-withdrawn type I diabetic patients serving as controls (P = 0.022). Furthermore, when glucagon was infused at a higher rate (3 ng/kg X min) in 12 additional type I diabetic patients, the mean maximal plasma glucose increment (54 +/- 15 mg/dl) was still less than half that in PX, despite a 3-fold higher infusion plasma glucagon level (326 +/- 37 pg/ml). The 6-h glucagon infusion caused a significant decrease in the concentrations of glucogenic amino acids in the glucagon-deficient patients, but not in the type I diabetic patients. We conclude that 1) glucagon replacement in the PX patient markedly alters blood glucose and glucogenic amino acids, but not ketone levels; and 2) the metabolic response to glucagon is considerably more pronounced in PX patients than in type I diabetic patients. These data suggest that glucagon responsiveness is enhanced in the chronic hormone-deficient state.

Adult↗

PubMed2000

Antihyperglycemic effect of T-1095 via inhibition of renal Na+-glucose cotransporters in streptozotocin-induced diabetic rats.

T-1095, a derivative of phlorizin, is an orally active inhibitor of Na+-glucose cotransporter (SGLT). We investigated the acute antihyperglycemic effect of T-1095 in streptozotocin-induced diabetic rats (STZ rats). T-1095 and its metabolite T-1095A inhibited the SGLT activity in brush border membranes prepared from kidneys of both normal and STZ rats, but the latter agent was approximately 10 times more potent than the former. Single oral administration of T-1095 (30-100 mg/kg) dose-dependently induced glycosuria in normal rats. The fed glucose levels in STZ rats were dose-dependently suppressed by single oral administration of T-1095 (3-100 mg/kg), whereas there was only marginal hypoglycemic effect in normal rats. Since there was no effect on blood glucose in nephrectomized STZ rats, inhibition of renal glucose reabsorption rather than intestinal glucose absorption mainly contributes to the antihyperglycemic effect of T-1095. In conclusion, T-1095 is the first orally active agent which has an acute antihyperglycemic action in the absence of endogenous insulin secretion with a low risk of hypoglycemia and has therapeutic potential for treatment of diabetes mellitus.

Animals↗

PubMed1975

Epidemiological evaluation of funduscopic findings in cerebrovascular diseases. II. A multivariate analysis of funduscopic findings.

The interrelationship of the funduscopic, physical and laboratory findings, the additional information of each funduscopic finding when physical and laboratory findings were considered simultaneously, and the relative importance of each retinal finding in the funduscopic pictures were investigated by a series of multivariate analysis for 68 cerebral hemorrhage, 47 cerebral thrombosis and 230 controls in two rural towns, Akabane and Asahi, in Japan and the results were as follows: 1. For the occurrence of cerebral hemorrhage, narrowing of arteriole and irregular constriction were especially important indicators, and retinal bleeding and lateral displacement were also valuable but less than narrowing and irregular constriction. On the other hand, for the occurrence of cerebral thrombosis, arteriolar reflex was considered as the most valuable indicator, and irregular constriction, lateral displacement and white plaque were also important but less than arteriolar reflex. 2. Narrowing of arteriole was most highly related with irregular constriction while the correlation between retinal bleeding and white plaque, and also the correlation between arteriolar reflex, vertical and lateral displacement and tapering were significant. 3. A significiant correlation among physical and laboratory findings was found only between systolic and diastolic blood pressure as far as analysed. Funduscopic findings by Scheie's hypertensive and Keith-Wagener's classifications were highly correlated with systolic and diastolic blood pressure. 4. Narrowing and irregular constriction were significantly correlated with systolic and diastolic blood pressure, and the relation between retinal bleeding and glycosuria was significant. 5. An analysis of the additional information of each funduscopic finding, when evaluated with the physical and laboratory findings simultaneously, revealed that irregular constriction, lateral displacement and narrowing gave prominent additional information for the occurrence of cerebral hemorrhage, while arteriolar reflex, lateral and vertical displacement and white plaque gave valuable information for the occurrence of cerebral thrombosis. 6. It is noteworthy from these multivariate analyses that narrowing and irregular constriction may arise from a similar pathophysiological mechanism which brings out vasoconstriction and the resultant organic changes due to hypertension. It is also noticed that arteriolar reflex and A/V crossing phenomenon may come from the different pathophysiological mechanism related to arteriosclerosis. It was stressed that detailed analyses of observer variability and evolution of funduscopic findings would be necessary.

Albuminuria↗

PubMed1985

A new diabetic strain of rat (WBN/Kob).

A new, spontaneously occurring diabetic syndrome has been observed in the aged males of an inbred strain of Wistar rats, WBN/Kob. The main clinical sign, glycosuria, was first detected at about 60 weeks of age, and thereafter some animals developed hyperlipidaemia and gradual emaciation. Prior to the onset of glucosuria, male rats showed impaired glucose tolerance after a glucose load at 21 weeks of age. The histopathologic lesions of the pancreas in the diabetic males consisted of multifocal fibrosis, decreased in number and size of islets and atrophy of exocrine tissue. Multifocal inflammatory foci of varying stages were the main pancreatic lesion in prediabetic male rats. This inflammatory change was detected even in 12-week-old rats and tended to occur around the islets. Therefore focal fibrosis and the decrease in the number and size of islets were considered to result from post-inflammatory scarring. The maturity-onset of this syndrome and the impaired glucose tolerance in younger animals suggested that diabetes mellitus of this rat strain is insulin-independent type II. However, the histological lesions of the pancreas were somewhat different from previous reports of both type I and II diabetes mellitus in man and animals.

Animals↗

PubMed1993

Alteration of hepatic enzyme activities in obese KK mice treated with monosodium aspartate.

Changes in body weight, concentrations of urine glucose, blood glucose, plasma insulin and FFA and hepatic enzyme activities were investigated in KK and C57BL mice treated with monosodium-L-aspartate (MSA). MSA was administered subcutaneously to neonates at a dose of 4 mg/g body weight. The MSA-treated KK and C57BL mice were remarkably obese at 10 weeks of age. The average plasma insulin concentration in the control KK mice was 73.6 microU/ml, over 4 times higher than in the control C57BL mice. In the control KK mice, hepatic glucokinase (GK) activity was quite low, and fructose-1,6-bisphosphatase (FBP) and acetyl-CoA carboxylase (CBX) activity was much higher than in the control C57BL mice. In the MSA-treated KK and C57BL mice, the plasma insulin concentration increased to 2 to 3 times higher than in the controls. The MSA-treated C57BL mice showed an increase in GK and CBX activity and acceleration of obesity. In the MSA-treated KK mice, GK activity did not change and CBX activity decreased, and only FBP activity increased significantly. Glycosuria was induced and blood glucose and plasma FFA increased remarkably in all MSA-treated KK mice.

Acetyl-CoA Carboxylase↗

PubMed2005

Effects of zinc supplementation in patients with type 1 diabetes.

The purpose of this study was to identify the effect of oral zinc supplementation in patients with type 1 diabetes (T1DM) on metabolic control and zinc blood concentrations. The sample consisted of 20 patients with T1DM and a control group (n=17). Metabolic control was evaluated by glycemia at fast, 24 h glycosuria, and HbA1c. Zinc concentrations were measured in plasma and erythrocytes. After the first collection of biological material, oral zinc supplementation was initiated and continued for 4 mo in T1MD patients (T1). Daily dosages were established based on Dietary Recommended Intakes (DRIs), considering zinc intake based on data from other studies previously performed with this population. All analyses were repeated after supplementation (T2). Metabolic control was unsatisfactory, with an HbA1c increase at T2. There was no difference in zinc concentrations in plasma and erythrocytes between patients with T1DM and control. Zinc concentrations in plasma were within the normal range in T1MD before and after supplementation and the control. Zinc concentrations in erythrocyte presented lower than normal values for all groups. A zinc increase in erythrocyte after supplementation was observed in T1DM patients, although without statistical significance. More studies are needed to confirm oral zinc supplementation as nutritional management in diabetes.

Administration, Oral↗

PubMed2006

Type 2 diabetes mellitus in obese mouse model induced by monosodium glutamate.

The number of diabetic patients is increasing every year, and new model animals are required to study the diverse aspects of this disease. An experimental obese animal model has reportedly been obtained by injecting monosodium glutamate (MSG) to a mouse. We found that ICR-MSG mice on which the same method was used developed glycosuria. Both female and male mice were observed to be obese but had no polyphagia, and were glycosuric by 29 weeks of age, with males having an especially high rate of incidence (70.0%). Their blood concentrations of glucose, insulin, total cholesterol, and triglycerides were higher than in the control mice at 29 weeks. These high concentrations appeared in younger males more often than in females, and were severe in adult males. Also, the mice at 54 weeks of age showed obvious obesity and increased concentrations of glucose, insulin, and total cholesterol in the blood. The pathological study of ICR-MSG female and male mice at 29 weeks of age showed hypertrophy of the pancreatic islet. This was also observed in most of these mice at 54 weeks. It was recognized as a continuation of the condition of diabetes mellitus. From the above results, these mice are considered to be useful as new experimental model animals developing a high rate of obese type 2 (non-insulin dependent) diabetes mellitus without polyphagia.

Animals↗

PubMed1975

Alcoholic detosis.

Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.

Acidosis↗