Carbohydrate metabolism
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
Glycosuria can be defined as a concentration of urinary glucose detectable using relatively insensitive, but specific, screening tests. These tests often depend on the action of an enzyme, such as glucose oxidase, incorporated into a diagnostic strip. Usually, the proximal tubular cells reabsorb most of the glucose in the glomerular filtrate. Glycosuria, as defined above, occurs only when the plasma, and therefore glomerular filtrate, concentrations exceed the tubular reabsorptive capacity. This may be because the plasma and glomerular filtrate concentrations are more than about 10 mmol/L, and therefore the normal tubular reabsorptive capacity is significantly exceeded. Very rarely, if the glomerular filtration rate is much reduced, there may be no glycosuria despite plasma glucose concentrations more than 10 mmol/L. A diagnosis of diabetes mellitus should never be made on the basis of glycosuria.
Flexible norms?
Waltraud Ernst in Histories of the Normal and the Abnormal, 2006
The prescribed diets varied considerably, depending on practitioners’ therapeutic training and preferences. In 1909 Frederik Madison Allen (1879–1964), a doctor on a fellowship at the Harvard Medical School Department of Public Health, undertook a three-year experimental trial on animals, with the aim of developing a scientifically grounded diet for diabetics.18 He caused DM of varying degrees of severity in these animals by removing all or part of their pancreas, and tested various diets on them. He found that only a very strict low-calorie diet could reduce these animals’ glycosuria and glycaemia. Allen affirmed that patients put on what was soon known as a ‘starvation diet’ avoided certain infectious complications and ketoacidosis, felt better, and could thus live for a few months or even a few years longer.19 Unfortunately, famished patients frequently tried to break their diets, and hospital staff had to police them to find those who ‘cheated’, by searching for hidden food often brought in by relatives.20
Protecting Pancreatic β-cells from Metabolic Insults
Christophe Wiart in Medicinal Plants in Asia for Metabolic Syndrome, 2017
β-Sitosterol from the stem bark of Solanum surattense Burm.f given to streptozotocin-induced diabetic Wistar rats (glycemia > 250 mg/dL) orally at a dose of 20 mg/kg/day for 21 days lowered glycemia from 271.8 to 134 mg/dL (normal 85.1 mg/dL; glibenclamide at 0.3 mg/kg/day: 123.3 mg/dL) and increased serum insulin from 7.8 to 14.3 µU/mL (normal 17.8 µU/mL; glibenclamide at 0.3 mg/kg/day: 16.8 µU/mL.378 This regimen prevented glycosuria in diabetic animals.378 In the pancreas of treated rodents, the extract increased superoxide dismutase, catalase, glutathione, glutathione S-transferase and glutathione peroxidase and decreased lipid peroxidation.378 β-Sitosterol evoked a rejuvenation of pancreatic β-cells in diabetic rodents.378
Non-diabetic glycosuria as a diagnostic clue for acute tubulointerstitial nephritis in patients with azotemia
Published in Renal Failure, 2020
Taeyeon Lee, Won Seok Yang
To assess the utility of urine glucose test in identifying ATIN as a cause of elevated creatinine, we performed a retrospective analysis of adult patients who underwent a native kidney biopsy at Asan Medical Center (Seoul, Korea) as a diagnostic evaluation for serum creatinine higher than 1.4 mg/dL. Patients aged <18 years, having diabetes mellitus or transplanted kidney were excluded. The presence of diabetes mellitus was determined by the positive history of diabetes mellitus, a fasting plasma glucose ≥ 126 mg/dL or HbA1c ≥ 6.5% [13]. Glycosuria may also occur in a person who doesn't have diabetes if blood glucose level rises higher than 170–200 mg/dL and the filtered glucose load exceeds the capacity for tubular glucose reabsorption [14]. So, the patients with blood glucose higher than 170 mg/dL on the day when urine glucose was positive were also excluded. Patients with proteinuria in the nephrotic range (24-h urine protein > 3.5 g, urine protein/creatinine >3.5 g/g or urine albumin/creatinine >2.5 g/g [15]) were excluded because ATIN-induced proteinuria is mild and only rarely is in the nephrotic range [1,2]. In some patients with nephrotic syndrome, ATIN was combined to minimal change or focal segmental glomerulosclerosis, and those patients were also excluded because nephrotic syndrome itself was an indication of a kidney biopsy to determine the pathologic type, regardless of the presence of ATIN.
High glucose-mediated overexpression of ICAM-1 in human vaginal epithelial cells increases adhesion of Candida albicans
Published in Journal of Obstetrics and Gynaecology, 2018
Hiroshige Mikamo, Yuka Yamagishi, Hiroyuki Sugiyama, Hisato Sadakata, Shun Miyazaki, Takako Sano, Tsutomu Tomita
Vulvovaginal candidiasis (VVC) is an infection related to diabetes (Grigoriou et al. 2006; Hirji et al. 2012; Geerlings et al. 2014; Njomanang Soh et al. 2016). The risk of VVC is especially high in uncontrolled diabetes (Goswami et al. 2000; de Leon et al. 2002). This is caused by glycosuria, host immune dysfunction and enhanced virulence of infecting microorganisms that occur in diabetes (Raith et al. 1983; Sobel 1989; Geerlings et al. 2014). There is a high incidence of genital infections in patients treated with sodium glucose co-transporter type 2 (SGLT2) inhibitors (Geerlings et al. 2014; Nauck 2014; Scheen 2015). These inhibitors block the reabsorption of glucose in the kidney, which decreases the blood glucose levels by excretion into the urine. This urinary glucose generates an advantageous environment for infecting pathogenic microorganisms, thus increasing the incidence of VVC.
Diabetes mellitus and laboratory medicine in sub-Saharan Africa: challenges and perspectives
Published in Acta Clinica Belgica, 2019
Justin C. Cikomola, Antoine S. Kishabongo, Marijn M. Speeckaert, Joris R. Delanghe
The International Diabetes Federation (IDF) proposes the use of glycosuria as a diagnostic test in case of classic diabetes symptoms, where a blood glucose test is not available [4]. For many years, urine glucose testing has been the major method used for diabetes monitoring. Glycosuria tests are associated with a lower sensitivity, ranging from 21–64%. The renal threshold changes from one person to another with a higher threshold in diabetic patients than in the general population. Fluid intake and urine concentration can affect the results. The urine glucose does not reflect the glycemic level at the time of examination and does not give information about hypoglycemic episodes. In addition, some drugs can interfere with the determination of glucose in the urine [27]. Notwithstanding these disadvantages, urine-based tests present some potential benefits that could be useful. These tests are 4–8 times less expensive than single blood glucose tests. They are safe, affordable and feasible for low-income countries with a small health budget and limited human and physical resources. Furthermore, urinalysis has been used for screening of subjects with diabetes risk factors (e.g. subjects with tuberculosis) [28].
Related Knowledge Centers
- Diabetes
- Fanconi Syndrome
- Glucose
- Reabsorption
- Tubular Fluid
- Ultrafiltration
- Urine
- Circulatory System
- Kidney
- Blood Sugar Level