Disease relevance of Glycosuria

• AS-6, when given as a 0.025-0.2% admixture in the diet, dose-dependently ameliorated polydipsia, polyuria, and glycosuria in the genetically obese diabetic mouse, C57BL/KsJ db/db, while neither insulin nor tolbutamide showed any beneficial effects [1].
• Blood glucose was significantly increased, and glycosuria was evident at all three time points of IDDM [2].
• Supplemental vitamin A (Group 3) did not affect the hyperglycemia, hyperphagia, polydipsia or glycosuria, but increased the breaking strengths of the incisions of the diabetic rats (468 +/- 40 g, p less than 0.001), and the sponge hydroxyproline (2.38 mg/100 mg sponge, p less than 0.001) [3].
• As in the two previously described patients, this patient had a normal serum glucose level, underlying hypertension, and onset of glycosuria between 2 and 16 weeks after initiation of therapy with an angiotensin-converting enzyme inhibitor [4].
• Glycosylated hemoglobin in diabetes mellitus: correlations with fasting plasma glucose, serum lipids, and glycosuria [5].

High impact information on Glycosuria

• However, nicotinic acid therapy resulted in the deterioration of glycemic control, as evidenced by a 16% increase in mean plasma glucose concentrations, a 21% increase in glycosylated hemoglobin levels, and the induction of marked glycosuria in some patients [6].
• When splenocytes were transferred from diabetic NOD, male NOD-+/+ and NOD-+/lpr developed diabetes with the incidence of 89 and 83%, respectively, whereas NOD-lpr/lpr did not show glycosuria by 12 wk after transfer [7].
• Chronic administration of a PPAR-alpha agonist (0.5% [wt/wt] fenofibrate) or a PPAR-gamma agonist (3 mg x kg(-1) x day(-1) rosiglitazone) completely prevented the development of glycosuria [8].
• A 75-g oral glucose tolerance test (OGTT) was performed in 615 nonobese pregnant women (mean +/- SD age 29.7 +/- 4.3 yr) who were referred to the Division of Internal Medicine at our diabetes center because of glycosuria [9].
• Four of six NOD mice given nicotinamide from the day of the first occurrence of marked glycosuria displayed a disappearance of glycosuria and an improvement in glucose tolerance during the therapy; however, urine sugar became negative in only one of six mice that received nicotinamide from 1 to 2 wk after the onset of marked glycosuria [10].

Chemical compound and disease context of Glycosuria

• 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 [11].
• The inverse correlation between renal threshold and creatinine clearance limits the usefulness of measuring glycosuria in patients with nephropathy [12].
• Injection of streptozotocin in newborn rats induced a severe diabetic syndrome on day 4 after birth, with acute hyperglycaemia and glycosuria [13].
• Proximal tubular dysfunction, resembling adult Fanconi's syndrome, was suggested by an increased urinary loss of phosphate and urate and glycosuria [14].
• Those with a random blood glucose exceeding 12.5 mmol/l were considered diabetic, and all of these patients had glycosuria together with elevated total glycosylated haemoglobin and fructosamine concentrations [15].

Biological context of Glycosuria

• The injection of glucose (100 mg) into the cisterna magna of intact anesthetized cats elicited immediate glycosuria and natriuresis without significant changes in blood glucose concentration [16].
• The introduction of the glucokinase transgene in insulin receptor null mice did not prevent the development of glycosuria [17].
• These effects of captopril were not associated with detectable changes in body weight or levels of glucose, protein glycosylation, glycosuria, or renal histologic changes secondary to glycosuria [18].
• Time-dependent deviations from the control model were evident in all ANIT treated animals consisting of glycosuria, bile aciduria, an initial decrease in taurine levels followed by taurinuria and a reduction of tricarboxylic acid cycle intermediate excretion [19].
• These data indicate that the effect of glucose infusion on the renal clearances of uric acid, xanthine and oxypurinol was not related to osmotic diuresis but induced by glycosuria and/or hyperglycemia [20].

Anatomical context of Glycosuria

• 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 [21].
• A diagnostic 75 g oral glucose tolerance test was performed on patients with one or more of the following abnormalities: glycosuria, random plasma blood glucose 7.8 mmol/l to 12.5 mmol/l, glycosylated haemoglobin 8.5%, and fructosamine 2.20 mmol/l. By these criteria, the prevalence of diabetes in this community was found to be 9.8% [15].
• The LLC-PK1 cell line represents a good in vitro model for cyclosporine renal tubular toxicity, as the in vivo observation of glycosuria and proximal tubular cell vacuolation in cyclosporine nephrotoxicity can be reproduced [22].
• We conclude that in the absence of islet cell antibodies or human leukocyte antigen DR3/DR4 heterozygosity, incidental hyperglycemia or glycosuria is unlikely to be associated with progression or diabetes [23].
• These results suggest that one mechanism of the cadmium-induced glycosuria is a loss of active Na(+)-glucose cotransport carrier in the proximal tubular brush-border membrane by direct interaction with free cadmium [24].

Gene context of Glycosuria

• Fasting blood glucose and serum insulin concentrations did not change during GH administration, and no glycosuria was detected in morning urine samples [25].
• The administration of STZ caused significant increases in levels of glycosuria, proteinuria, albuminuria, glycemia, total cholesterol and AI, as well as in lipid peroxidation products in the brain, plasma and kidney, whereas it decreased the GSH content and SOD, GSH-Px and catalase activities [26].
• Earlier observations of glycosuria with normal blood glucose levels in some MODY families suggest an additional renal manifestation of the respective genetic defect [27].
• Treatment of mice with Poly [I:C] alone [50 micrograms twice weekly, an inducer of Interferon (IFN) alpha/beta] or in conjunction with rIL-2 was even more effective, completely preventing glycosuria for 20 weeks [28].
• Using non-obese diabetic mice, we have evaluated the role of the adrenergic system and eNOS on progression of the disease METHODS AND RESULTS: When glycosuria is high (20 to 500 mg/dL), there is a selective reduction in the response to alpha1 and beta2 agonists but not to dopamine or serotonin [29].

Analytical, diagnostic and therapeutic context of Glycosuria

• Serum enzyme levels and blood urea nitrogen were not elevated, nor were glycosuria or proteinuria present [30].
• They were treated at the age of two months with vehicle (control group) or alloxan (100 mg/kg s.c.). Such treatment caused hyperglycemia (greater than 250 mg/dl) and glycosuria in most of the animals [31].
• No correlation was observed between NAG/Cre ratio levels and age, duration of disease, pubertal stage, body mass index, fasting blood glucose, glycosuria, insulin requirement and blood pressure [32].
• High field (400 and 600 MHz)1H NMR urinalysis revealed increased excretion of lactic acid, acetoacetate, alanine, valine, lysine, glutamine and glutamate and a severe, time-dependent glycosuria [33].
• Effects of castration and androgen on glycosuria appearance in the diabetic KK mice induced by monosodium glutamate administration [34].

References