4410 D-Glucose Glucose is a monosaccharide containing six carbon atoms and an aldehyde group and is therefore referred to as an aldohexose. The glucose molecule can exist in an open-chain (acyclic) and ring (cyclic) form, the latter being the result of an intramolecular reaction between the aldehyde C atom and the C-5 hydroxyl group to form an intramolecular hemiacetal. In water solution both forms are in equilibrium and at pH 7 the cyclic one is the predominant. Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. In animals glucose arises from the breakdown of glycogen in a process known as glycogenolysis. Glucose is synthesized in the liver and kidneys from non-carbohydrate intermediates, such as pyruvate and glycerol, by a process known as gluconeogenesis. 50-99-7 5793 C6H12O6 White powder. 146 - 150°C 1200.0 mg/mL Very high serum levels of glucose are found in untreated diabetic (type I or type II) patients. Glucose in chronic excess causes toxic effects on the structure and function of many cells and organs, including the pancreas and pancreatic islet cells. Multiple biochemical pathways and mechanisms of action for glucose toxicity have been suggested. These include glyceraldehyde auto-oxidation, protein kinase C activation, methylglyoxal formation and glycation, hexosamine metabolism, sorbitol formation, and oxidative phosphorylation. All these pathways have in common the formation of reactive oxygen species that, in excess and over time, cause chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. Exposure of endothelial cells to high glucose causes GAPDH inhibition through reactive oxygen species-activated poly(ADP-ribosyl)ation of GAPDH by poly(ADP-ribose) polymerase. Three products from glucose metabolism (glyoxal, methylglyoxal, and 3-deoxyglucosone) form advanced glycation end products (AGEs) by reacting with amino groups on intracellular and extracellular proteins. AGEs play important roles in the pathogenesis of secondary complications of diabetes, especially with regard to microvascular disease in the retina, nerves, and kidney and likely islets. Glycated hemoglobin is a particularly important AGE. A 1% increase in absolute concentrations of glycated hemoglobin is associated with about 10-20% increase in cardiovascular disease risk. No indication of carcinogenicity to humans (not listed by IARC). High blood glucose (>7 mM) produces the symptoms of frequent urination, increased thirst, and increased hunger. Chronic exposure to high blood glucose (i.e. untreated diabetes) can cause many complications. Acute complications include diabetic ketoacidosis (characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath) and nonketotic hyperosmolar coma. Serious long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in diabetics are due to coronary artery disease. Other "macrovascular" diseases are stroke, and peripheral vascular disease. The primary microvascular complications of diabetes include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and potentially blindness. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplant. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. Treatment involves a healthy diet, physical exercise, not using tobacco, and being a normal body weight. Blood pressure control and proper foot care are also important for people with the disease. Type 1 diabetes must be managed with insulin injections. Type 2 diabetes may be treated with medications with or without insulin. 2014-08-29T06:33:43Z 2026-05-14T17:20:36Z Dextrose C00031 4167 GLC DB02379 BGC true OC[C@H]1OC(O)[C@H](O)[C@@H](O)[C@@H]1O C6H12O6 InChI=1S/C6H12O6/c7-1-2-3(8)4(9)5(10)6(11)12-2/h2-11H,1H2/t2-,3-,4+,5-,6?/m1/s1 WQZGKKKJIJFFOK-GASJEMHNSA-N 180.1559 180.063388116 Endogenous Solid -3.24 HMDB00122 CHEMBL1222250 5589 <p>Chen Gong, &#8220;Method for preparation of 2&#8217;-deoxy-2&#8217;, 2&#8217;-difluoro-beta-cytidine or pharmaceutically acceptable salts thereof by using 1,6-anhydro-beta-D-glucose as raw material.&#8221; U.S. Patent US20060003963, issued January 05, 2006.</p> CHEM003316 DTXSID7022910 NS00007629 (2R,3S,4R,5R)-2,3,4,5,6-pentahydroxyhexanal 110.38000000000001 35.923399999999994 16.37078313987151 1 6 5 11.298101552080594 -2.9810792051782764 0 1 -2.57 0.64 7.82e+02 g/l