Glucose

In Clinical Veterinarian Advisor: Birds and Exotic Pets, 2013

Physiology

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Glucose in the claret is derived from iii main sources:

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Intestinal absorption

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Glucose is the end-product of carbohydrate digestion, captivated by enterocytes.

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Increased blood glucose concentrations occur 2 to 4 hours after a meal in simple-stomached animals.

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Hepatic production

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Gluconeogenesis and glycogenolysis within hepatic cells produce glucose when metabolically necessary.

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Gluconeogenesis converts noncarbohydrate sources, primarily amino acids (from protein) and glycerol (from fat), in unproblematic-stomached animals.

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Glycogenolysis converts glycogen (poly-glucose) stored in hepatocytes to glucose through hydrolysis.

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Kidney production

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Gluconeogenesis and glycogenolysis inside renal epithelial cells can result in the formation of glucose when metabolically necessary.

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The plasma concentration of glucose is controlled by a number of hormones, in particular, insulin and glucagon. The physiology of glucose homeostasis is controlled primarily by insulin release in response to elevated glucose levels (postprandial), although in birds, glucagon appears to serve every bit the primary regulator. Significant species variations in glucose levels take been noted. In general, levels are lowest in reptiles (60 to 100 mg/dL) and highest in birds (200 to 500 mg/dL), with mammals in betwixt (100 to 200 mg/dL).

Glucose that is not needed for energy is stored in the form of glycogen as a source of potential energy, readily available when needed. Nearly glycogen is stored in the liver and in muscle cells. When these and other body cells are saturated with glycogen, backlog glucose is converted to fat and is stored as adipose tissue.

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Glucose

Martin Kohlmeier , in Nutrient Metabolism, 2003

Regulation

Glc concentrations in tissues and trunk fluids are stabilized by many various mechanisms, many of which involve the action of specific hormones. Overall homeostasis is maintained through directing the flux of Glc to or from glycogen stores, balancing glycolysis versus gluconeogenesis, and promoting protein catabolism in times of need.

Hormonal regulation: Among the many hormones with some result on particular tissues or metabolic sequences a few stand out considering of their dominant and overriding actions on Glc disposition. Insulin promotes uptake and oxidation of Glc by tissues and favors storage, especially in the postprandial phase. Glucagon in response to low blood Glc concentration increases Glc release from storage and synthesis from precursors. Adrenaline (epinephrine) mobilizes stores and accelerates utilization.

Insulin is produced in the beta cells of pancreatic islet cells and released in a zinc-dependent process together with its companion amylin. The rate of production and release into circulation is related to Glc-sensing mechanisms in the beta cell. ATP generation from Glc and cytosolic calcium concentration are thought to exist critical for Glc sensing. A zinc-containing enzyme, insulysin (EC3.4.24.56), inactivates insulin irreversibly in many tissues (Ding et al., 1992). Insulysin activity is inhibited by loftier concentrations of both amylin and insulin (Mukherjee et al., 2000). Insulin binds to specific insulin receptors in muscles, adipocytes, and some other insulin-sensitive tissues and triggers with the receptor kinase activity a signaling pour. The chromium-containing peptide chromodulin binds to the insulin-activated insulin receptor and optimizes its receptor kinase activeness (Vincent, 2000 ). In response to the insulin-initiated signaling cascade, GLUT4 (SLC2A4) moves to the plasma membrane and increases Glc uptake into insulin-stimulated cells several-fold. Another of import insulin effect is increased transcription of hepatic hexokinase 4 (glucokinase), which increases the availability of glucose 6-phosphate, the precursor for glycolysis and glycogen synthesis. Glycolysis is farther promoted by increased concentrations of the regulatory metabolite fructose two,6-bisphosphate (due to induction of half dozen-phosphofructo-2-kinase, EC2.7.1.105, and lower expression of fructose-2,half dozen-bisphosphate-2-phosphatase, EC3.one.three.46). At the aforementioned time, gluconeogenesis is blocked by the inhibiting outcome of insulin on phosphoenolpyruvate carboxykinase (EC4.ane.1.32) and of fructose 2,6-bisphosphate on fructose 1,6-bisphosphatase (EC3.i.3.xi). Insulin promotes glycogenesis through increasing the availability of the glucose 6-phosphate forerunner and decreasing the phosphorylation of enzymes of glycogen metabolism.

The metabolic functions of the insulin companion amylin, which tend to be in opposition to insulin action, are only beginning to be understood. They include promotion of glycogen breakdown and inhibition of glycogen synthesis. Years of excessive amylin secretion may be responsible for the beta cell decline in obesity and insulin resistance. Amylin may promote the deposition of amyloid plaques (Hayden and Tyagi, 2001) and induce beta jail cell apoptosis (Saafi et al., 2001).

Glucagon is produced and secreted by the alpha cells of the pancreas in response to low Glc concentration. Glucagon promotes the release of glucose one-phosphate from glycogen. Adrenaline and the less potently acting noradrenaline stimulate the breakdown of glycogen. These catecholamines also annul the inhibitory effects of non-glucose fuels on glycolysis.

Appetite and satiety: Low blood Glc concentration induces the feeling of hunger. According to the long-held glucostatic theory, the brain, specific areas such every bit paraventricular and supraoptic portions of the hypothalamus, integrate input from peripheral and fundamental Glc-responsive sensors and generate appetite sensation (Briski, 2000).

Amylin, on the other mitt, is secreted in response to feeding and increased blood Glc concentration and acts on histamine H1 receptors with a significant satiety-inducing and anorectic effect (Mollet et al., 2001). A satiety-inducing effect of insulin has also been reported, but may be weak or mediated through other effectors (such as amylin).

Postprandial metabolism: The influx of newly absorbed Glc and other nutrients alters the balance of hormonal and metabolic activities. As outlined higher up, the rate of insulin (and amylin) secretion increases and the rate of glucagon decreases in response to the higher blood Glc concentration. Gluconeogenesis is effectively turned off and glycolysis is turned on. Glc utilization occurs in preference to fat oxidation. When high carbohydrate intake is coupled with excessive full energy intake, fat (both from nutrition and from adipose tissue turnover) is preferentially deposited, and the sugar is used as the near-sectional energy fuel. In fact, the release of fat from adipose tissue is slowed by the increased action of insulin. This is a reminder that both timing and quantity of carbohydrate ingestion matter.

The degradation of glycogen in liver and muscles increases, though with a considerable time lag. Reconstitution of depleted glycogen stores is likely to take 1–2 days (Shearer et al., 2000). Saccharide loading for one or more days can increment glycogen stores by a 3rd or more (Tarnopolsky et al., 2001). Repleting glycogen stores by carbohydrate feeding on the evening before elective surgery instead of fasting appears to improve outcome and reduce hospital stays (Nygren et al., 2001).

Exercise: A burst of exertion, as in a short sprint, taxes the capacity of musculus to generate ATP for wrinkle. Glycolytic breakdown of Glc to lactate is an inefficient mode of fuel utilization, considering it generates only ii ATP per glucose molecule. The advantages are that glycolysis is fast, because only eleven reactions are needed, and that it operates anaerobically (i.east. does not require oxygen). The resulting lactate moves from the muscle prison cell into circulation via the monocarboxylate transporter 1 (MCT1, SLC16A1). Due to the cotransport of protons, increasing acidification of the muscle cells will promote lactate export. Lactate is used in the liver for gluconeogenesis and the resulting Glc returned to muscle for another potential circular through this lactate–glucose (Cori) cycle.

Some other of the many adaptations to musculus exertion is the increased action of GLUT4, which promotes Glc influx from apportionment.

Fasting and starvation: When tissue levels of Glc decline and new supplies from nutrient are not forthcoming, the liver and kidneys brainstorm to release Glc into circulation. This Glc comes initially from glycogen stores and from the use of Glc metabolites (lactate, pyruvate, and others) for gluconeogenesis, later from tissue protein.

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Applied science of Main Ingredients—Sweeteners and Lipids

Karl F. Tiefenbacher , in Wafer and Waffle, 2017

The Dextrose Equivalent

Dextrose equivalent (DE) is the reducing power of a starch hydrolysate expressed every bit a percentage of the reducing ability of the same weight of d -glucose. The DE provides a measure of the degree of hydrolysis of starch into maltodextrins and glucose syrups. The college the DE, the larger the corporeality of glucose and the smaller the amount of dextrins present.

For nonhydrolyzed starch the DE is nothing, whereas pure glucose (dextrose) has a DE of 100 per definition. At a depression caste of starch cleavage, from DE 3 to nineteen, maltodextrins result, which are sold in powder course. If the DE is above 20 it is called glucose syrup (corn syrup, starch syrup, maltose syrup). Depending on the process conditions with increasing starch cleavage the content of glucose (dextrose), maltose and the following oligosaccharides increases at the expense of the higher saccharides. With higher DE values, the viscosity of syrup solutions decreases and they are easier to pump. Then cost efficient syrups with high solids may be manufactured.

The DE value of a starch hydrolysate is inversely related to the average degree of polymerization (DP) of the starch hydrolysate. Equally a rule of thumb, DE   ×   DP (average) is about 120. The process is chosen conversion (Table iii.20).

Table iii.20. Conversion Groups in Starch Saccharification

Conversion Group DE-Value
Maltodextrins Below 20
Low conversion 20–38
Intermediate 39–58
High 59–73
Very high conversion Over 73

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Carbohydrate and Noncarbohydrate Sweeteners

James Northward. BeMiller , in Carbohydrate Chemistry for Food Scientists (Third Edition), 2019

Glucose syrups (Chapter seven)

Glucose syrups provide adhesiveness, body, cohesiveness, and gloss to a multifariousness of products. Glucose syrups are solutions of glucose plus other saccharides derived from starch via acrid- and/or enzyme-catalyzed hydrolysis. The dextrose equivalence (DE) values ( Chapter 7) of different syrups range from DE twenty to DE 95. Those with the lower DE values provide the best foam stabilization, prevention of sugar crystallization, and the highest viscosity. Those with the higher DE values provide the nearly sugariness and the greatest freezing bespeak depression, boiling bespeak elevation (both colligative properties), browning reaction, hygroscopicity, and season enhancement. All glucose syrups are purified products containing upwards to 85% dissolved solids. Corn syrup solids (Chapter vii) are basically stale glucose syrups of lower DE values, as merely syrups with very depression DE values can be converted to a powdered form.

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Nutrient Sensing: Carbohydrates

B.E. Levin , in Encyclopedia of Neuroscience, 2009

Glucose-Sensing Neurons as Metabolic Sensors

GE and GI neurons have differing properties with regard to their sensitivity to glucose and to other hormones and metabolic substrates. GE neurons are more sensitive to glucose than are GI neurons, only the range over which both respond to glucose is likewise a part of their anatomic location. For example, GE neurons in the VMN are maximally activated over a range of 0.1–2.5  mM glucose, while ARC GE neurons go on to increase their activity upward to five   mM glucose. These differences in sensitivity may reverberate inputs from surrounding astrocytes or neurons but might also exist due to the fact that the ThousandATP aqueduct has different proportions of sulfonylurea-binding subunits, which could alter their sensitivity to glucose. Also, because the ThouATP aqueduct is bailiwick to modulatory effects of G-protein-coupled receptors, phosphoinositol 3-kinase (as modulated by both leptin and insulin), and levels of intracellular long-chain CoA molecules derived from fatty acids, the milieu in which a given neuron finds itself combines with its intrinsic metabolic and physiological characteristics to determine how it will respond to glucose. Thus, glucose-sensing neurons are actually metabolic sensors in which the combined input of metabolites, peptides, transmitters, and hormones tin affect both their short-term and long-term ability to sense and reply to glucose.

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Corn Sweeteners

Scott Helstad , in Corn (3rd Edition), 2019

Dextrose

Dextrose is approved as GRAS in 21 CFR 184.1857. As a solid, it may exist in either the anhydrous or monohydrate form. Farther requirements for dextrose are listed under 21 CFR 168.110 (anhydrous) and 21 CFR 168.111 (monohydrate). Dextrose monohydrate may also be referred to as corn carbohydrate.

In the dextrose production process, the goal is to convert starch into every bit high a level of dextrose possible (Fig 20.12). The slurry is liquefied in the presence of α-amylase and pumped to a saccharification tank. During saccharification, an amyloglucosidase enzyme breaks down the starch hydrolyzate to dextrose consisting of levels greater than 95%. Following conversion of the hydrolyzate, the slurry is filtered and carbon-refined before demineralization. At this point, the product can be evaporated to a 71% solids solution containing 95% dextrose. Production of syrups having greater than 98.five% dextrose purity can be accomplished using an absorption-separation cavalcade to produce a 99% dextrose liquid or by dissolving pure dextrose monohydrate crystals in a solution of hot water. Pure dextrose monohydrate is made by crystallization procedure. In this process, a dextrose-rich solution is evaporated to about 75%–78% solids and cooled to about 46°C. Seed crystals from the prior batch are mixed with the mass at this bespeak to speed crystallization. A coproduct from dextrose crystallization is chosen dextrose "greens." Another minor dextrose production that can also exist produced from dextrose monohydrate is anhydrous dextrose (Hobbs, 2003).

Fig. 20.12

Fig. 20.12. Generic process for manufacturing dextrose.

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Canine Diabetes Mellitus

Richard W. Nelson , in Canine and Feline Endocrinology (4th Edition), 2015

Continuous Glucose Monitoring Systems

CGM systems are frequently used to monitor glucose concentrations in diabetic humans and are beginning to be used in diabetic dogs and cats ( Wiedmeyer et al, 2008; Affenzeller et al, 2011). CGM systems mensurate interstitial fluid glucose concentrations rather than claret glucose concentrations. The correlation between interstitial and claret glucose concentrations is practiced in diabetic dogs and cats (Davison et al, 2003b; Moretti et al, 2010). A commonly used CGM organization (Guardian Real-time) measures interstitial glucose with a small-scale, flexible sensor inserted through the peel into the subcutaneous space and secured to the pare (Fig. 6-23). Interstitial glucose is detected via the glucose oxidase reaction, and detection occurs entirely at the electrode within the sensor component. Glucose results are transmitted past a wireless transmitter to a pager-sized monitor. The interstitial fluid glucose concentration is recorded and stored every 5 minutes, and the data can be downloaded to a computer for analysis (Fig. 6-24). Calibration of the CGM system is required at initiation of and periodically during glucose monitoring. The working glucose range for the CGM system is twoscore to 400 mg/dL (2.2 to 22 mmol/50). Studies to date advise that the primary advantage of continuous glucose monitoring is detection of hypoglycemic periods that are not detected with series blood glucose curves and a PBGM device (Dietiker-Moretti et al, 2011). See Chapter 7 for more than information on continuous glucose monitoring.

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SWEETENERS

Thousand.C. Yebra-Biurrun , in Encyclopedia of Analytical Science (Second Edition), 2005

Starch-Derived Sweeteners

Glucose

Glucose, commercial name dextrose, in the aldohexose form α-d-glucose (CviH12Ohalf-dozen), is the major production from starch hydrolyzed by acid and/or enzymes. The major starch source in the Us and Japan is corn (Zea mays) and in Europe, wheat and irish potato. There is some starch and starch hydrolyzate production from cassava in the torrid zone. Glucose is sold equally anhydrous dextrose; more unremarkably as dextrose monohydrate, every bit glucose syrup or corn syrup.

Fructose

Fructose, in the ketohexose class β-d-fructose (Chalf dozenH12Ohalf dozen ), is produced from glucose by an isomerase enzyme (glucose–fructose isomerase), which converts glucose to fructose, and subsequent enrichment of the fructose fraction (equilibrium conversion is ∼50%), or isolation of fructose and crystallization. Products are high-fructose corn syrup, the nearly widely used monosaccharide sweetener, at 42, 55, and 90% fructose (with glucose, the other major component) and crystalline fructose.

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Reduced-calorie sweeteners and caloric alternatives

G.-W. von Rymon Lipinski , in Optimising Sweet Taste in Foods, 2006

Physiology

Glucose is the near of import substrate of cell metabolism. It is the sugar fulfilling the task of being the free energy transport system of the body. Several parts of the body like the nervous organisation or claret cells are completely dependent on glucose as the supplier of energy. Glucose is readily absorbed from the intestine. Any glucose not immediately needed for energy is stored equally glycogen in the liver. The healthy organism tries to maintain a constant level of glucose in blood and serum past secretion of insulin to reduce likewise loftier a level and mobilises glucose from glycogen of the liver if levels autumn below normal. Every bit metabolism of glucose is insulin-dependent and type I diabetics lack insulin and type II diabetics have insufficient insulin release, they should avoid consumption of large amounts of glucose, at least without adequate medication ( Lang 1979a; Szepesi 1996).

Glucose is fully caloric. It tin be metabolised to lactic acid past the leaner of the oral cavity. Glucose is also an excellent substrate for about all types of fermentation.

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Glucose transporters and their cellular form, role and role

Archana Navale , in Molecular Nutrition: Carbohydrates, 2019

Introduction

Glucose is a vital source of free energy to all species including humans. Every cell needs and utilizes glucose. However, due to its polar nature and relatively large size, information technology cannot cross the cell membrane past passive diffusion. Information technology requires specific transporter proteins that comport glucose across the membrane. Every bit various tissues differ in their glucose needs, there are different types of glucose transporters. This whole family of glucose transporters is divided in 2 primary types, namely, sodium-glucose linked transporters (SGLTs) and facilitated diffusion glucose transporters (GLUTs).

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