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Diabetes and Antidiabetic Therapy: Control of Glucose
Published in Richard J. Sundberg, The Chemical Century, 2017
The standard test for diabetes is the fasting glucose level, with >7.0 mmol/l indicative of diabetes and 5.6–6.9 considered prediabetic. This is supplemented by checking glucose levels 2 h after ingestion of a standard dose of glucose, called the oral glucose tolerance test. The value indicating diabetes is ≥11.1 mmol/l. with 7.8–11.0 mmol/l. considered prediabetic. One problem with the oral glucose tolerance analysis is that it is very time-sensitive with respect to glucose ingestion. Various meters are available for patient self-measurement of glucose levels. An annual test for albuminuria is recommended for both type-1 and type-2 diabetes in adults. Levels >30 mg/g are indicative of increased risk for cardiovascular disease. There is no method available for routine measurement of insulin levels.
Occupational toxicology of the kidney
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
Kidney damage is identified by evaluating indicators of kidney function in blood and urine. Since the kidney is able to compensate extremely well for loss of renal functional mass, changes in renal function may not be identified until there is significant (more than 70%) nephron damage or loss. Decreased GRF can cause azotemia characterised by elevation of the blood urea nitrogen (BUN) and creatinine. Changes in electrolytes and acid–base balance may also be present in the blood of patients with renal disease. Urine volume can be determined and urine can be examined (urinalysis) for the presence of cells, proteins, casts, and crystals which are not normally present (Kosnett 1990). The terminology for reporting this includes the cell or protein of interest, for example, albumin, and its presence in urine, albuminuria.
Role of marine polysaccharides in treatment of metabolic disorders
Published in Antonio Trincone, Enzymatic Technologies for Marine Polysaccharides, 2019
Manigandan Venkatesan, Velusamy Arumugam, Rathinam Ayyasamy, Karthik Ramachadran, Subhapradha Namasivayam, Umamaheswari Sundaresan, Archunan Govindaraju, Ramachandran Saravanan
Glycosaminoglycans (GAGs) are heteropolysaccharides with repeating units of disaccharide and consist mainly of an amino sugar (N-acetylgalactosamine or N-acetylglucosamine) and uronic acid. It is present on the surface of the extracellular matrix of almost all animal cells, through which it binds and regulates different kinds of proteins, growth factors, and cytokines for normal metabolic activity. GAGs are generally generated from mammalian tissues mainly from slaughterhouse [e.g., rooster combs, cartilage (tracheas and nasal from bovine and swine) and umbilical cords]. However, the prevalence of bovine spongiform encephalopathy and other food chain crises will eventually lead to the exploration of other sources such as microbes and marine organisms. Among the marine diversity, mollusks, squid, sea cucumbers, sponges, cartilaginous material from shark, salmon, and ray fish are potential source of GAGs (Seno and Mayer 1963; Kinoshita-Toyoda et al. 2004). The effects of GAGs have been analyzed on the type 2 diabetic mice model by administering chitosan with intraperitoneal injection of streptozotocin and maintaining the mice on a high-sugar, high-lipid diet. Treatment with GAGs from the marine worm Urechis unicinctus reversed the damage on islet of β cell and restored its function. GAGs from U. unicinctus has potent hypoglycemic activity and has the ability to improve the antioxidant mechanism of diabetic mice; improves glucose tolerance, liver glycogen content, and insulin sensitivity index; and also repairs liver and pancreatic tissue (Yuan et al. 2015). Albuminuria in type 1 and type 2 diabetic patients is significantly improved when treated with GAGs and with sulodexide (Abaterusso and Gambaro 2006). Administration with GAGs, such as low molecular weight heparin and dermatan sulfate in diabetic rats, prevents both glomerular basement membrane thickening and anionic charge density reduction in the glomerular basement membrane and sustains urinary excretion of albumin at normal levels without affecting the metabolic control of the disease (Gambaro et al. 1992). Administration with insulin prevents renal lesions in diabetic rats and controls glycemia (Rasch 1979), even in the absence of insulin treatment; animals administered with GAGs showed good results (Gambaro et al. 1992). Administration of GAGs can prevent some of the morphological and physiological alterations that occur in experimental diabetic nephropathy. In 1994, Gambaro and coworkers proved that the long-term administration of GAGs prevents morphological and functional alterations of renal tissue in diabetic rats and reversed the condition of established diabetic renal lesions. GAG administration modified renal matrix composition by the normalization of collagen gene expression and increasing glomerular 35S-sulfate incorporation.
Potential protective roles of curcumin against cadmium-induced toxicity and oxidative stress
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Jae Hyeon Park, Byung Mu Lee, Hyung Sik Kim
The major features of Cd-induced nephrotoxicity are proteinuria, aminoaciduria, glucosuria, and phosphaturia. Initial urinary biomarkers of Cd-induced renal damage include low-molecular-weight proteins such as β2-microglobulin, retinol binding protein (RBP), and enzymes such as N-acetyl-β-D-glucosaminidase. RBP is the most specific marker of proximal tubular dysfunction (Vaidya, Ferguson, and Bonventre 2008). Long-term exposure to Cd produces glomerular damage and albuminuria, resulting in the development of end-stage renal failure (García and Arceo 2018; Ginsberg 2012; Schnaper 2014). Notably, patients with diabetes are more likely to experience renal tubular damage following Cd toxicity than those without (Satarug, Vesey, and Gobe 2017). Fanconi syndrome is a rare medical condition involving impairment in protein, amino acid, glucose, bicarbonate, and phosphate reabsorption following Cd-induced oxidative stress, resulting in the apoptosis of tubular cells (Haque, Ariceta, and Batlle 2012).