D-Glucose

Cosmetic ingredients (Glucose) -> CIR (Cosmetic Ingredient Review)

Humectant

log Kow = -3.00

-3.3

ANTICAKING AGENT OR FREE-FLOW AGENT, COLOR OR COLORING ADJUNCT, DRYING AGENT, FLAVOR ENHANCER, FLAVORING AGENT OR ADJUVANT, HUMECTANT, LUBRICANT OR RELEASE AGENT, NUTRITIVE SWEETENER, SOLVENT OR VEHICLE, STABILIZER OR THICKENER -> FDA Substance added to food

1.2 at 68 °F (est.) (USCG, 1999) - Denser than water; will sink

1.544

Density: 1.5620 at 18 °C/4 °C /alpha-Glucose/; 1.54 at 25 °C/4 °C /alpha-Glucose, monohydrate/; 1.5620 at 18 °C/4 °C; needles from alc ohol/beta-Glucose/

Relative density (water = 1): 1.56

Soluble

In water, 5.46X10+5 mg/L at 30 °C, 4.79X10+5 mg/L at 20 °C

Very soluble in water

Slightly soluble in ethanol; insoluble in acetone, ethyl acetate; soluble in pyrine

Solubility in water: soluble

This chemical does not meet GHS hazard criteria for 97.6% (946 of 969) of all reports.

Not Classified

Aggregated GHS information provided per 969 reports by companies from 4 notifications to the ECHA C&L Inventory.

This chemical does not meet GHS hazard criteria for 100% (3 of 3) of all reports.

Not Classified

Aggregated GHS information provided per 3 reports by companies from 1 notifications to the ECHA C&L Inventory.

Chemical: D-Glucose

D-Glucose is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of D-Glucose are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

D-Glucose: Does not have an individual approval but may be used under an appropriate group standard

Unless specifically excluded, residues resulting from the use of the following substance as either an inert or an active ingredient in a pesticide chemical formulation, including antimicrobial pesticide chemicals, is exempted from the requirement of a tolerance under FFDCA section 408, if such use is in accordance with good agricultural or manufacturing practices. Dextrose is included on this list.

Fresh air, rest.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

For any fire, wear a self-contained breathing apparatus (SCBA) in pressure-demand, MHSA/NIOSH (approved or equivalent), and full protective gear. ... On fire use water spray, dry chemical, carbon dioxide, or appropriate foam.

Keep container tightly closed in a dry and well-ventilated place. Hygroscopic. Keep in a dry place.

General storage may be used. Store in a cool, dry, well-ventilated area away from strong oxidizers, strong acids.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gas; Environmental precautions: No special environmental precautions required; Methods and materials for containment and cleaning up: Sweep up and shovel. Keep in suitable, closed containers for disposal.

Provide adequate ventilation. Avoid generating dust. Vacuum or sweep up material and place into a suitable disposal container. Clean up spills immediately, using the appropriate protective equipment.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Precautions for safe handling: Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: General industrial hygiene practice.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

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.

Recent studies suggest that meat intake is associated with diabetes-related phenotypes. However, whether the associations of meat intake and glucose and insulin homeostasis are modified by genes related to glucose and insulin is unknown. We investigated the associations of meat intake and the interaction of meat with genotype on fasting glucose and insulin concentrations in Caucasians free of diabetes mellitus. Fourteen studies that are part of the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium participated in the analysis. Data were provided for up to 50,345 participants. Using linear regression within studies and a fixed-effects meta-analysis across studies, we examined 1) the associations of processed meat and unprocessed red meat intake with fasting glucose and insulin concentrations; and 2) the interactions of processed meat and unprocessed red meat with genetic risk score related to fasting glucose or insulin resistance on fasting glucose and insulin concentrations. Processed meat was associated with higher fasting glucose, and unprocessed red meat was associated with both higher fasting glucose and fasting insulin concentrations after adjustment for potential confounders [not including body mass index (BMI)]. For every additional 50-g serving of processed meat per day, fasting glucose was 0.021 mmol/L (95% CI: 0.011, 0.030 mmol/L) higher. Every additional 100-g serving of unprocessed red meat per day was associated with a 0.037-mmol/L (95% CI: 0.023, 0.051-mmol/L) higher fasting glucose concentration and a 0.049-ln-pmol/L (95% CI: 0.035, 0.063-ln-pmol/L) higher fasting insulin concentration. After additional adjustment for BMI, observed associations were attenuated and no longer statistically significant. The association of processed meat and fasting insulin did not reach statistical significance after correction for multiple comparisons. Observed associations were not modified by genetic loci known to influence fasting glucose or insulin resistance. The association of higher fasting glucose and insulin concentrations with meat consumption was not modified by an index of glucose- and insulin-related single-nucleotide polymorphisms.

Recent studies demonstrated an adverse effect of chronic exposure to air pollution (AP) on metabolic syndrome and its components. In a population-based study, we investigated the association between exposure to ambient AP and serum glucose (SG), among subjects with normal glucose, impaired fasting glucose (IFG), and diabetes mellitus (DM).We included 1,063,887 SG tests performed in 131,882 subjects (years 2001-2012). Exposure data included daily levels of SO2, NO2 and other pollutants of industrial, traffic, and nonanthropogenic sources. Demographical, clinical, and medications purchase data were assessed. Log-transformed SG levels were analyzed by linear mixed models adjusted for seasonal variables and personal characteristics.SG increases (%increase [95% CI]), among subjects with normal glucose, IFG, and DM, respectively, were associated with 6.36 ?ppb increase of NO2 measured 24 to 72? hours before the test (0.40% [0.31%; 0.50%], 0.56% [0.40%; 0.71%], and 1.08% [0.86%; 1.29%]); and with 1.17?ppb increase of SO2 measured 24 ?hours before the test (0.29% [0.22%; 0.36%], 0.20% [0.10%; 0.31%], and 0.33% [0.14%; 0.52%]). Among DM population, weakest association was observed among patients treated with Metformin (0.56% increase in SG [0.18%; 0.95%]). In conclusion, NO2 and SO2 exposure is associated with small but significantly increased levels of SG. Although DM patients were found to be more susceptible to the AP induced SG variations, Metformin treatment seem to have a protective effect. Given the chronic lifetime exposure to AP and the broad coverage of the population, even small associations such as those found in our study can be associated with detrimental health effects and may have profound public health implications.

Maternal diabetes-induced birth defects remain a significant health problem. Studying the effect of natural compounds with antioxidant properties and minimal toxicities on diabetic embryopathy may lead to the development of new and safe dietary supplements. Punicalagin is a primary polyphenol found in pomegranate juice, which possesses antioxidant, anti-inflammatory and anti-tumorigenic properties, suggesting a protective effect of punicalagin on diabetic embryopathy. Here, we examined whether punicalagin could reduce high glucose-induced neural tube defects (NTDs), and if this rescue occurs through blockage of cellular stress and caspase activation. Embryonic day 8.5 (E8.5) mouse embryos were cultured for 24 or 36 hr with normal (5 mM) glucose or high glucose (16.7 mM), in presence or absence of 10 or 20 uM punicalagin. 10 uM punicalagin slightly reduced NTD formation under high glucose conditions; however, 20 uM punicalagin significantly inhibited high glucose-induced NTD formation. Punicalagin suppressed high glucose-induced lipid peroxidation marker 4-hydroxynonenal, nitrotyrosine-modified proteins, and lipid peroxides. Moreover, punicalagin abrogated endoplasmic reticulum stress by inhibiting phosphorylated protein kinase ribonucleic acid (RNA)-like ER kinase (p-PERK), phosphorylated inositol-requiring protein-1alpha (p-IRE1alpha), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), C/EBP-homologous protein (CHOP), binding immunoglobulin protein (BiP) and x-box binding protein 1 (XBP1) mRNA splicing. Additionally, punicalagin suppressed high glucose-induced caspase 3 and caspase 8 cleavage. Punicalagin reduces high glucose-induced NTD formation by blocking cellular stress and caspase activation. These observations suggest punicalagin supplements could mitigate the teratogenic effects of hyperglycemia in the developing embryo, and possibly prevent diabetes-induced NTDs.

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.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that D(+)-glucose is expected to have very high mobility in soil(SRC). Volatilization of D(+)-glucose from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.5X10-20 atm-cu m/mole(SRC), derived from its vapor pressure, 8X10-14 mm Hg(3), and water solubility, 5.46X10+5 mg/L(4). D(+)-Glucose is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). D(+)-Gglucose absorbs at wavelengths >290 nm(5) and, therefore, may be susceptible to direct photolysis by sunlight on soil surfaces(SRC). The dominant fate process in soil is expected to be biodegradation(SRC). Various screening studies have found D(+)-glucose to be readily biodegrade(6-10). Soil half-lives on the order of 1 day are reported(7), but a range of 0.25-19 days has also been observed(11).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that D(+)-glucose is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.5X10-20 atm-cu m/mole(SRC), derived from its vapor pressure, 8X10-14 mm Hg(4), and water solubility, 5.46X10+5 mg/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of -3.00(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Various screening studies have found D(+)-glucose to be readily biodegrade(8-12). A biodegradation half-life of about one day was reported for aquifer material(9). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(3).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), D(+)-glucose, which has a vapor pressure of 8X10-14 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase D(+)-glucose may be removed from the air by wet and dry deposition(SRC). D(+)-Glucose absorbs at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The D(+)-glucose concentration in varietal grape juices from 56 Canadian cultivars pressed in the 1988-1989 season ranged from 4.91 to 9.99 g/100 mL(1). The D(+)-glucose concentration in five prunes juices obtained from markets in Davis, CA ranged from 4.35 to 11.60 g/100 mL juice(2). The D(+)-glucose concentration in fresh apple, cherry, grape, nectarine, peach, pear, plum, kiwi fruit and strawberry juices (California-grown) were 2.14, 7.50, 9.59, 0.85, 0.67, 1.68, 4.28, 6.94 and 1.80 g/100 mL juice, respectively(2).

ENVIRONMENTAL: Glucose levels in 188 quarter for milks from different cows were determined by an enzymic procedure. Mean glucose content was 0.22 mM (standard error +/- 0.009) and results ranged from 0.02-0.57 mM. Abnormal quarters had lower glucose levels (P less than 0.01) than normal quarters but variability within each classification was large. Glucose content was negatively correlated with both somatic cell count (r = 0.49) and N-acetyl-beta-D-glucosaminidase level (r = -0.61). Milk glucose was considered to be of limited value as a diagnostic test for mastitis.

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Glucose forms colorless crystals or white granular powder. It is used in confectionary, infant foods, medicine, brewing and wine making, caramel coloring, baking and canning, source of methane by anaerobic fermentation, source of certain amino acids by fermentation. A principal industrial fermentation use of glucose is for the production of fuel ethanol as an oxygenate or octane enhancer. Glucose is hydrogenated to sorbitol for use in various food and nonfood applications. Liquid glucose is an ingredient of Cocoa Syrup, It is used as a tablet binder and coating agent, and as a diluent in pilular extracts; it has replaced glycerin in many pharmaceutical preparations. It is sometimes given per rectum as a food in cases when feeding by stomach is impossible. It should not be used in the place of dextrose for intravenous injection. HUMAN EXPOSURE AND TOXICITY: Normal fasting blood-sugar values for adults are 80 to 120 mg/dL; true glucose is 65 to 100 mg/dL. When the blood-sugar values exceed 120 (hyperglycemia), diabetes mellitus should be suspected and can be confirmed by evidence of diminished carbohydrate tolerance. Hyperglycemia and decreased glucose tolerance are seen in diabetes mettilus (to 500 mg/dL) and hyperactivity of the adrenal, pituitary, and thyroid glands. Hypoglycemia, with a blood-sugar value of <60 mg/dL and increased glucose tolerance, is encountered in insulin overdose, glucagon deficiencies, and hypoactivity of various endocrine glands. Injection of 5% soln into superficial temporal artery caused edema of eyelids, protrusion of eye, inability to move eye, necrosis of soft tissues and opacification of cornea. In one of the eyes, extensive atrophy of temporal half of choroid was observed. Maternal hyperglycemia may lead to an increased fetal lactate production resulting in metabolic acidosis. Fetal glucose excess may stimulates fetal oxidative metabolism with increases in fetal glucose and lactate entry and stimulation of fetal oxygen consumption. ANIMAL STUDIES: Calves fed with a mixture of glucose and milk substitute in the ratio of 2:1 instead of the recommended 1:1 showed depression and diarrhea, with four animals dying overnight. The post-mortem findings included dehydration, sunken eyes, congested abomasal mucosa, and distended intestines. The lungs were congested and the urinary bladder distended, the urine having a glucose content of over 0.5 g/dL. It was found that hyperglycemia increases the threshold for shivering, whereas hypoglycemia lowers the threshold on rabbits. In developmental studies in mice it was found that maternal diabetes and high glucose in vitro induce DNA damage and activates DNA damage response through oxidative stress, which may contribute to the pathogenesis of diabetes-associated embryopathy.

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.

D(+)-Glucose levels in some plants(1).

d-Glucose has been identified in 37 plants. Levels in some plants are as follows(1): /d-Glucose/[Table#1353]

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of December 17, 2015: http://actor.epa.gov/dashboard/]

D(+)-Glucose as alpha- and beta-form was present in open burn smoke particulate matter at 7.9, 12.4 and 48.4 ng/mg smoke particles from open-burning of plastic shopping bags, roadside trash and landfill garbage, respectively, in Concon Chile. It was not detected in particulate matter smoke from burning new plastic shopping bags from the United States. It was not detected in any of the plastic surface extracts prior to burning(1).

Unless specifically excluded, residues resulting from the use of the following substance as either an inert or an active ingredient in a pesticide chemical formulation, including antimicrobial pesticide chemicals, is exempted from the requirement of a tolerance under FFDCA section 408, if such use is in accordance with good agricultural or manufacturing practices. Dextrose is included on this list.

V - Various

B - Blood and blood forming organs

V - Various

QV - Various

QB - Blood and blood forming organs

QV - Various

Normal fasting blood-sugar values for adults are 80 to 120 mg/dL; true glucose is 65 to 100 mg/dL. When the blood-sugar values exceed 120 (hyperglycemia), diabetes mellitus should be suspected and can be confirmed by evidence of diminished carbohydrate tolerance. ... Hyperglycemia and decreased glucose tolerance are seen in diabetes mettilus (to 500 mg/dL) and hyperactivity of the adrenal, pituitary, and thyroid glands. Hypoglycemia, with a blood-sugar value of <60 mg/dL and increased glucose tolerance, is encountered in insulin overdose, glucagon deficiencies, and hypoactivity of various endocrine glands.

A main source of energy for living organisms. Occurs naturally and in the free state in fruits and other parts of plants. Combined in glucosides, in di- and oligosaccharides, in the polysaccharides cellulose and starch, and in glycogen.

In the skeletal system glucose serves as an essential source of energy for the development, growth, and maintenance of bone and articular cartilage. It is particularly needed for skeletal morphogenesis during embryonic growth and fetal development. Glucose is vital for osteogenesis and chondrogenesis, and is used as a precursor for the synthesis of glycosaminoglycans, glycoproteins, and glycolipids. Glucose sensors are present in tissues and organs that carry out bulk glucose fluxes (i.e., intestine, kidney, and liver). The beta cells of the pancreatic islets of Langerhans respond to changes in blood glucose concentration by varying the rate of insulin synthesis and secretion. Neuronal cells in the hypothalamus are also capable of sensing extracellular glucose. Glucosensing neurons use glucose as a signaling molecule to alter their action potential frequency in response to variations in ambient glucose levels. Skeletal muscle and adipose tissue can respond to changes in circulating glucose but much less is known about glucosensing in bone and cartilage. Recent research suggests that bone cells can influence (and be influenced by) systemic glucose metabolism.

Brain. Glucose is virtually the sole fuel for the human brain, except during prolonged starvation. The brain lacks fuel stores and hence requires a continuous supply of glucose. It consumes about 120 g daily, which corresponds to an energy input of about 420 kcal (1760 kJ), accounting for some 60% of the utilization of glucose by the whole body in the resting state. Much of the energy, estimates suggest from 60% to 70%, is used to power transport mechanisms that maintain the Na+-K+ membrane potential required for the transmission of the nerve impulses. The brain must also synthesize neurotransmitters and their receptors to propagate nerve impulses. Overall, glucose metabolism remains unchanged during mental activity, although local increases are detected when a subject performs certain tasks.

Blood glucose is an obligatory energy source for humans involved in various cellular activities, and it also acts as a signaling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water, and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion.

Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into two main phases where the preparatory phase is initiated by the phosphorylation of glucose by hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for the subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where the total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. These energy-producing reactions of glucose are limited to D-glucose as L-glucose cannot be phosphorylated by hexokinase. Glucose can act as precursors to generate other biomolecules such as vitamin C. It plays a role as a signaling molecule to control glucose and energy homeostasis. Glucose can regulate gene transcription, enzyme activity, hormone secretion, and the activity of glucoregulatory neurons. The types, number, and kinetics of glucose transporters expressed depends on the tissues and fine-tunes glucose uptake, metabolism, and signal generation to preserve cellular and whole body metabolic integrity.

Vascular calcification is a hallmark of type 2 diabetes. Glucose stimulates calcification in culture of vascular smooth muscle cells (VSMCs) but the underlying mechanisms remain obscure. We observed that high glucose levels stimulated mouse and human VSMC trans-differentiation into chondrocytes, with increased levels of Sox9, type II collagen, glycosaminoglycan and Runx2 expression, and increased alkaline phosphatase activity and mineralization. These effects were associated with increased expression of IL-1beta, which stimulated alkaline phosphatase and calcification, suggesting that glucose induces chondrocyte differentiation of VSMCs, possibly through IL-1beta activation.

The approximate half-life is 14.3 minutes following intravenous infusion. Gut glucose half-life was markedly higher in females (79 ± 2 min) than in males (65 ± 3 min, P < 0.0001) and negatively related to body height (r = -0.481; P < 0.0001).

Glucose can undergo aerobic oxidation in conjunction with the synthesis of energy molecules. Glycolysis is the initial stage of glucose metabolism where one glucose molecule is degraded into two molecules of pyruvate via substrate-level phosphorylation. These products are transported to the mitochondria where they are further oxidized into oxygen and carbon dioxide.

Growth of Escherichia coli on glucose in batch culture is accompanied by the excretion of acetate, which is consumed by the cells when glucose is exhausted. This glucose-acetate transition is classically described as a diauxie (two successive growth stages). Here, we investigated the physiological and metabolic properties of cells after glucose exhaustion through the analysis of growth parameters and gene expression. We found that E. coli cells grown on glucose in batch culture produce acetate and consume it after glucose exhaustion but do not grow on acetate. Acetate is catabolized, but key anabolic genes--such as the genes encoding enzymes of the glyoxylate shunt--are not upregulated, hence preventing growth. Both the induction of the latter anabolic genes and growth were observed only after prolonged exposure to low concentrations of acetate and could be accelerated by high acetate concentrations. We postulate that such decoupling between acetate catabolism and acetate anabolism might be an advantage for the survival of E. coli in the ever-changing environment of the intestine. The glucose-acetate transition is a valuable experimental model for comprehensive investigations of metabolic adaptation and a current paradigm for developing modeling approaches in systems microbiology. Yet, the work reported in our paper demonstrates that the metabolic behavior of Escherichia coli during the glucose-acetate transition is much more complex than what has been reported so far. A decoupling between acetate catabolism and acetate anabolism was observed after glucose exhaustion, which has not been reported previously. This phenomenon could represent a strategy for optimal utilization of carbon resources during colonization and persistence of E. coli in the gut and is also of significant interest for biotechnological applications.

When V. cholerae encounters nutritional stress, it activates (p)ppGpp-mediated stringent response. The genes relA and relV are involved in the production of (p)ppGpp, whereas the spoT gene encodes an enzyme that hydrolyzes it. Herein, we show that the bacterial capability to produce (p)ppGpp plays an essential role in glucose metabolism. The V. cholerae mutants defective in (p)ppGpp production (i.e. deltarelAdeltarelV and deltarelAdeltarelVdeltaspoT mutants) lost their viability because of uncontrolled production of organic acids, when grown with extra glucose. In contrast, the deltarelAdeltaspoT mutant, a (p)ppGpp overproducer strain, exhibited better growth in the presence of the same glucose concentration. An RNA sequencing analysis demonstrated that transcriptions of genes consisting of an operon for acetoin biosynthesis were markedly elevated in N16961, a seventh pandemic O1 strain, but not in its (p)ppGpp(0) mutant during glucose-stimulated growth. Transposon insertion in acetoin biosynthesis gene cluster resulted in glucose-induced loss of viability of the deltarelAdeltaspoT mutant, further suggesting the crucial role of acetoin production in balanced growth under glucose-rich environments. Additional deletion of the aphA gene, encoding a negative regulator for acetoin production, failed to rescue the (p)ppGpp(0) mutant from the defective glucose-mediated growth, suggesting that (p)ppGpp-mediated acetoin production occurs independent of the presence of AphA. Overall, our results reveal that (p)ppGpp, in addition to its well known role as a stringent response mediator, positively regulates acetoin production that contributes to the successful glucose metabolism and consequently the proliferation of V. cholerae cells under a glucose-rich environment, a condition that may mimic the human intestine.

Heterogeneity within the same tumor type has been described to be complex and occur at multiple levels. Less is known about the heterogeneity at the level of metabolism, within a tumor set, yet metabolic pathways are highly relevant to survival signaling in tumors. In this study, we profiled the glucose metabolism of several non-small cell lung carcinoma (NSCLC) cell lines and could show that, NSCLC display distinct glycolytic metabolism. Genetic and pharmacological perturbation of glycolysis was selectively toxic to NSCLCs with high rates of glycolysis. Furthermore, high expression of hexokinase-2, localized at the mitochondria, was a feature of the NSCLCs dependent on glucose catabolism. Our study provides evidence for quantitative metabolic diversity in NSCLCs and indicates that glucose metabolism provide differential prosurvival benefits to NSCLCs.

To observe the influence of different concentrations of bisphenol A (BPA) on glucose metabolism and lactate dehydrogenase (LDH) expression in rat Sertoli cells in vitro and investigate the mechanisms of BPA inducing male infertility. Using two-step enzyme digestion, we isolated Sertoli cells from male Wistar rats and constructed a primary Sertoli cell system, followed by immunohistochemical FasL staining. We randomly divided the Sertoli cells into a control group to be cultured in the serum-free minimal essential medium (MEM) plus dimethyl sulfoxide (DMSO) and three experimental groups to be treated with 100 nmol/L, 10 umol/L, and 1 mmol/L BPA, respectively, in the MEM plus DMSO. After 48 hours of treatment, we measured the proliferation of the cells by CCK-8 assay, determined the concentrations of metabolites by NMR spectroscopy, and detected the expression of LDH in the Sertoli cells by RT-PCR and Western blot. The purity of the isolated Sertoli cells was (96.05 +/- 1.28)% (n = 10). Compared with the control group, the 100 nmol/L, 10 umol/L, and 1 mmol/L BPA groups showed no remarkable changes in the proliferation of Sertoli cells ([98 +/- 8]%, [96 +/- 3]%, and [95 +/- 3]%, P >0.05), but the 10 umol/L and 1 mmol/L of BPA groups exhibited significantly decreased concentrations of intracellular glucose ([3.89 +/- 0.07] vs [3.36 +/- 0.24] and [3.04 +/- 0.21] pmol/cell, P <0.05) and lactate ([0.43 +/- 0.06] vs [0.29 +/- 0.05] and [0.20 +/- 0.03] pmol/cell, P <0.05). The expression of LDH mRNA was decreased with the increased concentration of BPA, while that of LDH protein reduced only in the 1 mmol/L BPA group (P <0.05). High-concentration BPA decreases the expression of LDH and alters glucose metabolism in Sertoli cells, and therefore may reduce the provision of lactate for germ cells and impair spermatogenesis.

For more Metabolism/Metabolites (Complete) data for D(+)-Glucose (9 total), please visit the HSDB record page.

Polysaccharides can be broken down into smaller units by pancreatic and intestinal glycosidases or intestinal flora. Sodium-dependent glucose transporter SGLT1 and GLUT2 (SLC2A2) play predominant roles in intestinal transport of glucose into the circulation. SGLT1 is located in the apical membrane of the intestinal wall while GLUT2 is located in the basolateral membrane, but it was proposed that GLUT2 can be recruited into the apical membrane after a high luminal glucose bolus allowing bulk absorption of glucose by facilitated diffusion. Oral preparation of glucose reaches the peak concentration within 40 minutes and the intravenous infusions display 100% bioavailability.

Glucose can be renally excreted.

The mean volume of distribution after intravenous infusion is 10.6L.

The mean metabolic clearance rate of glucose (MCR) for the 10 subjects studied at the higher insulin level was 2.27 ± 0.37 ml/kg/min at euglycemia and fell to 1.51±0.21 ml/kg/ at hyperglycemia. The mean MCR for the six subjects studied at the lower insulin level was 1.91 ± 0.31 ml/kg/min at euglycemia.

Members of the IL-6 family, IL-6 and ciliary neurotrophic factor (CNTF), have been shown to increase glucose uptake and fatty acid oxidation in skeletal muscle. However, the metabolic effects of another family member, leukemia inhibitory factor (LIF), are not well characterized. Effects of LIF on skeletal muscle glucose uptake and palmitate oxidation and signaling were investigated in ex vivo incubated mouse soleus and EDL muscles from muscle-specific AMPKalpha2 kinase-dead, muscle-specific SOCS3 knockout, and lean and high-fat-fed mice. Inhibitors were used to investigate involvement of specific signaling pathways. LIF increased muscle glucose uptake in dose (50-5,000 pM/l) and time-dependent manners with maximal effects at the 30-min time point. LIF increased Akt Ser(473) phosphorylation (P) in soleus and EDL, whereas AMPK Thr(172) P was unaffected. Incubation with parthenolide abolished LIF-induced glucose uptake and STAT3 Tyr(705) P, whereas incubation with LY-294002 and wortmannin suppressed both basal and LIF-induced glucose uptake and Akt Ser(473) P, indicating that JAK and PI 3-kinase signaling is required for LIF-stimulated glucose uptake. Incubation with rapamycin and AZD8055 indicated that mammalian target of rapamycin complex (mTORC)2, but not mTORC1, also is required for LIF-stimulated glucose uptake. In contrast to CNTF, LIF stimulation did not alter palmitate oxidation. LIF-stimulated glucose uptake was maintained in EDL from obese insulin-resistant mice, whereas soleus developed LIF resistance. Lack of SOCS3 and AMPKalpha2 did not affect LIF-stimulated glucose uptake. In conclusion, LIF acutely increased muscle glucose uptake by a mechanism potentially involving the PI 3-kinase/mTORC2/Akt pathway and is not impaired in EDL muscle from obese insulin-resistant mice.

The aim of the work is to analyze the relationship between consumption of glucose solution by rats and its absorption, and to use this fact for assessment of the absorptive capacity of the small intestine in non anesthetized animals in vivo. Consumption of glucose solution (200 g/L) by fasted rats was recorded in the control, and after administration of phloridzin--inhibitor of glucose active transport- or 3 hours after the restriction stress. On the mathematical model we studied the relative role of factors that can influence the temporal dynamics of glucose consumption by rats. The rate of glucose consumption was observed being decreased in the presence of phloridzin (1 mM), and be increased after the stress. The results of modeling are consistent with the experimental data and show that the rate of consumption of glucose solutions considerably more depends on the transport activity of the small intestine than on glucose concentration in the solution, or on the substrate regulation of the stomach emptying. Analysis of dynamics of consumption of glucose solution by intact rats may be considered as one of promising approaches to assessing the absorptive capacity of the small intestine under natural conditions.

CIR ingredient: Glucose

Formed in photosynthesis; Produced commercially by hydrolysis of cornstarch with acids or enzymes; Used in foods and medicines and as a source of certain amino acids by fermentation; Also called dextrose, but glucose is the preferred term; [Hawley] Glucose is an essential carbohydrate that is used as a substrate for energy production within the body. [Olson, p. 562]

Confectionary, infant foods, medicine, brewing and wine making, intermediate, caramel coloring, baking and canning, source of methane by anaerobic fermentation, source of certain amino acids (e.g. lysine) by fermentation.

Benzylisoquinoline alkaloids (BIAs) are a diverse family of plant-specialized metabolites that include the pharmaceuticals codeine and morphine and their derivatives. Microbial synthesis of BIAs holds promise as an alternative to traditional crop-based manufacturing. Here we demonstrate the production of the key BIA intermediate (S)-reticuline from glucose in Saccharomyces cerevisiae. To aid in this effort, we developed an enzyme-coupled biosensor for the upstream intermediate L-3,4-dihydroxyphenylalanine (L-DOPA). Using this sensor, we identified an active tyrosine hydroxylase and improved its L-DOPA yields by 2.8-fold via PCR mutagenesis. Coexpression of DOPA decarboxylase enabled what is to our knowledge the first demonstration of dopamine production from glucose in yeast, with a 7.4-fold improvement in titer obtained for our best mutant enzyme. We extended this pathway to fully reconstitute the seven-enzyme pathway from L-tyrosine to (S)-reticuline. Future work to improve titers and connect these steps with downstream pathway branches, already demonstrated in S. cerevisiae, will enable low-cost production of many high-value BIAs.

Nutrient (carbohydrate) replenisher in pharmaceuticals; food component; fluid replenisher

...Instead of lactose, as a supplement to milk for infant feeding.

(1972) 2.65X10+9 grams (minus pharmaceuticals)

(1975) 2.04X10+9 grams (minus pharmaceuticals)

(1984) 1.69X10+10 g /dextrose and glucose sirup/

(1972) 2.03X10+8 GRAMS

(1975) 2.00X10+8 GRAMS

(1984) 1.10X10+10 g /dextrose and dextrose syrup combined/

2023: 400,000,000 - <550,000,000 lb

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: D-Glucose. National Production Volume: 50,000,000 - 100,000,000 lb/yr.

Approximately 100% as a nutrient and fluid replenisher

In 10+3 t, commercial basis: (1965) 467; (1970) 549; (1975) 562; (1980) 512; (1982) 481; (1983) 490; (1984) 467; (1985) 478; (1986) 510 /Crystalline glucose/

In 10+3 t, commercial basis, Bakery: (1965) 177; (1970) 172; (1975) 159; (1980) 50; (1982) 50; (1983) 54; (1984) 54; (1985) 57; (1986) 73 /Crystalline glucose/

In 10+3 t, commercial basis, Beverage: (1965) 9; (1970) 9; (1975) 18; (1980) 68; (1982) 77; (1983) 82; (1984) 86; (1985) 82; (1986) 79 /Crystalline glucose/

For more Consumption Patterns (Complete) data for D(+)-Glucose (7 total), please visit the HSDB record page.

Dextrose is manufactured almost exclusively from corn (maize) starch in the United States. In other countries, starch from sorghum (milo), wheat, rice, potato, tapioca (yucca, cassava), arrowroot, and sago are used to varying degrees along with corn starch. Prior to the 1960s, commercial dextrose was produced using acid and acid-enzyme hydrolysis processes that yielded only about 86 and 92-94% dextrose, respectively. The development of thermostable bacterial a-amylase enzymes led to total enzyme processes that eliminated acid degradation products and increased dextrose yield to about 95-97%. In an enzymatic process, starch is hydrolyzed (thinned or liquefied) with a bacterial a-amylase. The resulting substrate is then hydrolyzed to dextrose (saccharified) using glucoamylase, a fungal enzyme that preferentially cleaves dextrose from the partially degraded starch. The initial extent of liquefaction is generally in the range of 10-20 dextrose equivalent (DE). DE is a measure of the reducing-sugar content calculated as dextrose and expressed as a percentage of the total dry substance. Several industrial enzyme liquefaction processes are used commercially. These processes are referred to as (1) enzyme-heat-enzyme, (2) low temperature, (3) dual enzyme/dual heating, (4) dual enzyme/single heating, and (5) thermal liquefaction.

Hydrolysis of cornstarch with acids or enzymes, hydrolysis of cellulosic wastes.

Grade: Technical, USP, anhydrous, hydrated.

Commercial dextrose products are produced in both dry and syrup forms. Dry products are prepared by crystallization to either an anhydrous, C6H12O6, or hydrated, C6H12O6.H2O, form. These include dextrose hydrate, anhydrous alpha-D-glucose, and anhydrous beta-D-glucose. Syrup products are produced that contain from 95 to over 99% dextrose.

(1) solid-high-glucose syrups (total sugar) and (2) high purity crystals grown in and then separated from glucose-bearing syrups /Crystalline glucose/

EPA Safer Chemical Functional Use Classes -> Processing Aids and Additives

Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Fragrance Ingredients

Cosmetics -> Humectant

Pesticide, Fertilizer, and Other Agricultural Chemical Manufacturing

D-Glucose: ACTIVE

Dextrose (D-glucose) is by far the most abundant sugar in nature. It occurs either in the monosaccharide form (free state) or in a polymeric form of anhydrodextrose units. As a monosaccharide, dextrose is present in substantial quantities in honey, fruits, and berries. As a polymer, dextrose occurs in starch, cellulose, and glycogen.