Glucose toxicity

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

The molecular pathology of the (3-cell destruction in the course of insulin resistance is largely unknown. It has been suggested that the constant hyperstimulation of the (3-cell by glucose ( glucose toxicity ) or elevated fatty acids ( lipotoxicity ) may lead to cell damage. 

Monotherapy with sulfonylureas generally produce a 1.5% to 2% decline in HbAlc concentrations and a 60 to 70 mg/dL (3.33-3.89 mmol/L) reduction in FBG levels. Secondary failure with these drugs occurs at a rate of 5% to 7% per year as a result of continued pancreatic p-cell destruction. One limitation of sulfonylurea therapy is the inability of these products to stimulate insulin release from (1-cells at extremely high glucose levels, a phenomenon called glucose toxicity. 

Symptomatic patients may initially require insulin or combination oral therapy to reduce glucose toxicity (which may reduce /1-cell insulin secretion and worsen insulin resistance). 

Harris CS, Lambert J, Saleem A, et al (2008) Antidiabetic activity of extracts from needle, bark, and cone of Picea glauca organ-specific protection from glucose toxicity and glucose deprivation. Pharm Biol 46 126-134... 

Genetics Glucose toxicity Free fatty acid toxicity... 

Robertson, R.P., J. Harmon, P.O. Tran, Y. Tanaka, and H. Takahashi. 2003. Glucose toxicity in beta-cells Type 2 diabetes, good radicals gone bad, and the glutathione connection. Diabetes. 52 581-7. 

Robertson RP, Harmon J, Tran PO, and Poitout V (2004) Beta-cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. Diabetes 53(Suppl 1) S119-S124. 

Chronic hyperglycemia is postulated to be a major metabolic initiator or inducer of diabetic microvascular disease, including those renal glomerular changes that often lead to end-stage renal disease ( glucose toxicity ). 

Uchiyama, K. et al., Astaxanthin protects beta-ceUs against glucose toxicity in diabetic db/db... 

Tanaka, Y, Gleason, C.E., Tran, P.O. et al. Prevention of glucose toxicity in HIT-T15 cells and Zucker diabetic fatty rats by antioxidants. Proc. Natl. Acad. Sci. USA 1999 96(19) 10857-62. 

Prolonged exposure of body proteins to high concentrations of glucose results in glycatlon which damages the proteins. This is known as glucose toxicity and is responsible for many of the complications of diabetes... 

Constituent of Hdleborua vmdua and H, niger. M.p. above 250°. Sol. CHCls. Spar. sol. EtjO. Insol. H80, EtOH. Hyd. — > hellBbotesm (m.p. 140-50°) and glucose. Toxic. 

Marchetti V, Menghini R, Rizza S, Vivanti A, Feccia T, Lauro D, Fukamizu A, Lauro R, and Federici M. Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via AkVFoxO signahng. Diabetes, 55 2231-2237 (2006). 

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