scholarly journals Simple and accurate determination of urinary glucose excretion with anthrone reagent

Diabetologia ◽  
1968 ◽  
Vol 4 (5) ◽  
pp. 278-280 ◽  
Author(s):  
J. Zweens ◽  
P. R. Bouman
Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 155-LB
Author(s):  
CAROLINA SOLIS-HERRERA ◽  
MARIAM ALATRACH ◽  
CHRISTINA AGYIN ◽  
HENRI HONKA ◽  
RUPAL PATEL ◽  
...  

2017 ◽  
Vol 37 (1) ◽  
pp. 9-17 ◽  
Author(s):  
So Ra Kim ◽  
Yong-ho Lee ◽  
Sang-Guk Lee ◽  
Sun Hee Lee ◽  
Eun Seok Kang ◽  
...  

1991 ◽  
Vol 80 (1) ◽  
pp. 71-76 ◽  
Author(s):  
R. C. Mühlbauer ◽  
H. Fleisch

1. The renal handling of glucose was determined in male X-linked hypophosphataemic (Hyp/Y) mice and in control littermates (+/Y) aged 4 months. Plasma glucose concentration and urinary glucose excretion were measured before and during stepwise increase in glycaemia induced by an acute infusion of glucose. The relationship between plasma glucose concentration and urinary glucose excretion was monitored per ml of glomerular filtrate in mice fed high and low phosphate diets. 2. Hyp/Y mice fed the high phosphate diet showed a significantly higher glucosuria compared with +/Y littermates. When glycaemia was increased, Hyp/Y mice developed frank glucosuria earlier than +/Y animals. In Hyp/Y mice we could not find a threshold below which virtually no glucose was excreted in the urine, whereas this was clearly visible in +/Y mice. These differences persisted in animals fed the low phosphate diet. 3. Using the acute response to the glucoregulatory hormones, glucagon and insulin, administered exogenously, we found that the regulation of plasma glucose concentration did not differ between Hyp/Y and +/Y mice. 4. The significantly lower plasma glucose concentration observed in Hyp/Y as compared with +/Y mice decreased further during fasting. 5. We conclude that the renal reabsorptive capacity for glucose is defective in Hyp/Y mice and their low plasma glucose concentration may be explained by the renal leak. Therefore the X-linked phosphataemic mouse appears not only to be characterized by a defect in renal phosphate and calcium reabsorption but also by an altered glucose reabsorption.


2002 ◽  
Vol 282 (3) ◽  
pp. E643-E649 ◽  
Author(s):  
Sara C. Rathman ◽  
Brandon Lewis ◽  
Robert J. McMahon

Previous studies have demonstrated that glucocorticoids alter biotin metabolism. To extend these studies, the effect of dexamethasone on biotin pools was analyzed in rats consuming a purified diet containing a more physiological level of dietary biotin intake (0.06 mg/kg). Acute (5 h) dexamethasone administration (0.5 mg/kg) elicited elevated urinary glucose output as well as elevated urinary biotin excretion and serum biotin. Renal and hepatic free biotin was also significantly elevated by acute dexamethasone administration. Chow-fed rats treated with an acute administration of dexamethasone demonstrated significantly elevated urinary glucose excretion, urinary biotin excretion, and serum biotin, but no change in tissue associated biotin was detected. Chronic administration of dexamethasone (0.5 mg/kg ip) over 4 days significantly elevated urinary glucose excretion 42% but had no effect on urinary biotin excretion, serum biotin, or hepatic- or renal-associated free biotin. These results demonstrate the existence of potentially novel regulatory pathways for total biotin pools and the possibility that experimental models with high initial biotin status may mask potentially important regulatory mechanisms.


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