Relevant bibliographies by topics / Effect of glucose on

Academic literature on the topic 'Effect of glucose on'

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Published: 10 December 2022
Last updated: 30 January 2023

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Journal articles on the topic "Effect of glucose on"

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Aldoretta, Peter W., and William W. Hay. "Effect of glucose supply on ovine uteroplacental glucose metabolism." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 4 (October 1, 1999): R947—R958. http://dx.doi.org/10.1152/ajpregu.1999.277.4.r947.

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To test the hypothesis that glucose supply to the uteroplacenta (UP) regulates UP glucose metabolism into oxidative and nonoxidative pathways, we studied eight late-gestation pregnant sheep at low (LG) and high (HG) maternal glucose concentrations (GM), using Fick principle and tracer glucose methodology. UP glucose consumption (UPGC) correlated directly with GM( r = 0.75, P = 0.0006), and UP glucose decarboxylation ( r = 0.80, P = 0.0001), and lactate production ( r = 0.90, P = 0.0001) rates were directly correlated with UPGC. The combined fractional production rate for lactate, fructose, and CO2 from UPGC was the same in LG and HG periods. The fraction of UP oxygen consumption used for glucose oxidation increased by about 50% from LG to HG conditions; however, there was no change in UP oxygen consumption. Nearly half of UPGC was not accounted for by lactate, fructose, and CO2 production, and about two-thirds of UP oxygen consumption was not accounted for by immediate oxidation of glucose carbon just taken up by the UP. These results indicate that glucose supply directly regulates UP glucose oxidative metabolism and that there is a reciprocal relationship between UP glucose oxidation and the oxidation of other substrates.
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BERKUS, M., and O. LANGER. "Glucose tolerance test periodicity: The effect of glucose loading." Obstetrics & Gynecology 85, no. 3 (March 1995): 423–27. http://dx.doi.org/10.1016/0029-7844(94)00410-f.

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Lamb, E., R. Mainwaring-Burton, and A. Dawnay. "Effect of protein concentration on the formation of glycated albumin and fructosamine." Clinical Chemistry 37, no. 12 (December 1, 1991): 2138–39. http://dx.doi.org/10.1093/clinchem/37.12.2138a.

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Abstract Considerable debate surrounds the question of whether fructosamine concentration should be corrected for serum protein concentration (see 1 for review). Staley (2) has argued against such correction, given that, theoretically, glucose concentration is the rate-limiting step in the glycation reaction; i.e., available lysine residues willalways be in excess of reactive open-chain (carbonyl) glucose molecules, which are only 0.001% of the total (3). However, because the open-chain and cyclic forms of glucose exist in freely exchangeable equilibrium, we conjectured that, as carbonyl glucoses were removed by glycation, more glucose molecules would rapidly isomerize to the open-chainform to maintain the equilibrium, if so, then protein concentration would also be an important factor in determining the glycation rate.
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Digiacomo, Jane E., William W. Hay, and Frederick C. Battaglia. "EFFECT OF INCREASING GLUCOSE CONCENTRATION ALONE ON FETAL GLUCOSE UTILIZATION." Pediatric Research 21, no. 4 (April 1987): 340A. http://dx.doi.org/10.1203/00006450-198704010-01040.

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Schaffer, Stephen W., Cherry Ballard Croft, and Viktoriya Solodushko. "Cardioprotective effect of chronic hyperglycemia: effect on hypoxia-induced apoptosis and necrosis." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H1948—H1954. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1948.

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It is generally accepted that mild forms of diabetes render the heart resistant to an ischemic insult. Because myocytes incubated chronically in medium containing high concentrations of glucose (25 mM) develop into a diabetes-like phenotype, we tested the hypothesis that high-glucose treatment diminishes hypoxia-induced injury. In support of this hypothesis, we found that cardiomyocytes incubated for 3 days with medium containing 25 mM glucose showed less hypoxia-induced apoptosis and necrosis than cells exposed to medium containing 5 mM glucose (control). Indeed, whereas 27% of control cells became necrotic after 1 h of chemical hypoxia with 10 mM deoxyglucose and 5 mM amobarbital (Amytal), only 11% of the glucose-treated cells became necrotic. Similarly, glucose treatment reduced the extent of apoptosis from 32% to 12%. This beneficial effect of glucose treatment was associated with a 40% reduction in the Ca2+ content of the hypoxic cell. Glucose treatment also mediated an upregulation of the cardioprotective factor Bcl-2 but did not affect the cellular content of the proapoptotic factors Bax and Bad. Nonetheless, the phosphorylation state of Bad was shifted in favor of its inactive, phosphorylated form after high-glucose treatment. These data suggest that glucose treatment renders the cardiomyocyte resistant to hypoxia-induced apoptosis and necrosis by preventing the accumulation of Ca2+ during hypoxia, promoting the upregulation of Bcl-2, and enhancing the inactivation of Bad.
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Balon, T. W., and G. J. Welk. "Effects of prior exercise on the thermic effect of glucose and fructose." Journal of Applied Physiology 70, no. 4 (April 1, 1991): 1463–68. http://dx.doi.org/10.1152/jappl.1991.70.4.1463.

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It has been previously observed that the thermic effect of a glucose load is potentiated by prior exercise. To determine whether this phenomenon is observed when different carbohydrates are used and to ascertain the role of insulin, the thermic effects of fructose and glucose were compared during control (rest) and postexercise trials. Six male subjects ingested 100 g fructose or glucose at rest or after recovery from 45 min of treadmill exercise at 70% of maximal O2 consumption. Measurements of O2 consumption, respiratory exchange ratio, and plasma concentrations of glucose, insulin, glycerol, and lactate were measured for 3 h postingestion. Although glucose and fructose increased net energy expenditure by 44 and 51 kcal, respectively, over baseline during control trials, exercise increased the thermic effect of both carbohydrate challenges an additional 20-25 kcal (P less than 0.05). Glucose ingestion was associated with large (P less than 0.05) increases in plasma insulin concentration during control and exercise trials, in contrast to fructose ingestion. Because fructose, which is primarily metabolized by liver, and glucose elicited a similar postexercise potentiation of thermogenesis, the results indicate that the thermogenic phenomenon is not limited to skeletal muscle. These results also demonstrate that carbohydrate-induced postexercise thermogenesis is not related to an incremental increase in plasma insulin concentration.
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Howlett, Kirsten, Damien Angus, Joseph Proietto, and Mark Hargreaves. "Effect of increased blood glucose availability on glucose kinetics during exercise." Journal of Applied Physiology 84, no. 4 (April 1, 1998): 1413–17. http://dx.doi.org/10.1152/jappl.1998.84.4.1413.

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This study examined the effect of increased blood glucose availability on glucose kinetics during exercise. Five trained men cycled for 40 min at 77 ± 1% peak oxygen uptake on two occasions. During the second trial (Glu), glucose was infused at a rate equal to the average hepatic glucose production (HGP) measured during exercise in the control trial (Con). Glucose kinetics were measured by a primed continuous infusion ofd-[3-3H]glucose. Plasma glucose increased during exercise in both trials and was significantly higher in Glu. HGP was similar at rest (Con, 11.4 ± 1.2; Glu, 10.6 ± 0.6 μmol ⋅ kg−1 ⋅ min−1). After 40 min of exercise, HGP reached a peak of 40.2 ± 5.5 μmol ⋅ kg−1 ⋅ min−1in Con; however, in Glu, there was complete inhibition of the increase in HGP during exercise that never rose above the preexercise level. The rate of glucose disappearance was greater ( P < 0.05) during the last 15 min of exercise in Glu. These results indicate that an increase in glucose availability inhibits the rise in HGP during exercise, suggesting that metabolic feedback signals can override feed-forward activation of HGP during strenuous exercise.
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Staricha, Kelly, Nicholas Meyers, Jodi Garvin, Qiuli Liu, Kevin Rarick, David Harder, and Susan Cohen. "Effect of high glucose condition on glucose metabolism in primary astrocytes." Brain Research 1732 (April 2020): 146702. http://dx.doi.org/10.1016/j.brainres.2020.146702.

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Forbes, Johnathon L. I., Daniel J. Kostyniuk, Jan A. Mennigen, and Jean-Michel Weber. "Unexpected effect of insulin on glucose disposal explains glucose intolerance of rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 4 (April 1, 2019): R387—R394. http://dx.doi.org/10.1152/ajpregu.00344.2018.

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The physiological reasons why salmonids show glucose intolerance are unclear. In mammals, rapid clearance of a glucose load is mainly achieved through insulin-mediated inhibition of hepatic glucose production ( Ra) and stimulation of glucose disposal ( Rd), but the effects of insulin on Ra and Rd glucose have never been measured in fish. The goal of this study was to characterize the impact of insulin on the glucose kinetics of rainbow trout in vivo. Glucose fluxes were measured by continuous infusion of [6-3H]glucose before and during 4 h of insulin administration. The phosphorylated form of the key signaling proteins Akt and S6 in the insulin cascade were also examined, confirming activation of this pathway in muscle but not liver. Results show that insulin inhibits trout Rd glucose from 8.6 ± 0.6 to 5.4 ± 0.5 µmol kg−1 min−1: the opposite effect than classically seen in mammals. Such a different response may be explained by the contrasting effects of insulin on gluco/hexokinases of trout versus mammals. Insulin also reduced trout Ra from 8.5 ± 0.7 to 4.8 ± 0.6 µmol·kg−1·min−1, whereas it can almost completely suppresses Ra in mammals. The partial inhibition of Ra glucose may be because insulin only affects gluconeogenesis but not glycogen breakdown in trout. The small mismatch between the responses to insulin for Rd (−37%) and Ra glucose (−43%) gives trout a very limited capacity to decrease glycemia. We conclude that the glucose intolerance of rainbow trout can be explained by the inhibiting effect of insulin on glucose disposal.
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AGIUS, Loranne, and Mark STUBBS. "Investigation of the mechanism by which glucose analogues cause translocation of glucokinase in hepatocytes: evidence for two glucose binding sites." Biochemical Journal 346, no. 2 (February 22, 2000): 413–21. http://dx.doi.org/10.1042/bj3460413.

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Glucokinase translocates between the cytoplasm and nucleus of hepatocytes where it is bound to a 68 kDa protein. The mechanism by which glucose induces translocation of glucokinase from the nucleus was investigated using glucose analogues that are not phosphorylated by glucokinase. There was strong synergism on glucokinase translocation between effects of glucose analogues (glucosamine, 5-thioglucose, mannoheptulose) and sorbitol, a precursor of fructose 1-phosphate. In the absence of glucose or glucose analogues, sorbitol had a smaller effect than glucose on translocation. However, sorbitol potentiated the effects of glucose analogues. In the absence of sorbitol the effect of glucose on glucokinase translocation is sigmoidal with a Hill coefficient of 1.9 suggesting involvement of two glucose-binding sites. The effects of glucosamine and 5-thioglucose were also sigmoidal but with lower Hill Coefficients. In the presence of sorbitol, the effects of glucose, glucosamine and 5-thioglucose were hyperbolic. Mannoheptulose, unlike the other glucose analogues, had a hyperbolic effect on glucokinase translocation in the absence of sorbitol suggesting interaction with one site and was synergistic rather than competitive with glucose. The results favour a two-site model for glucokinase translocation involving either two glucose-binding sites or one binding-site for glucose and one for fructose 1-phosphate. The glucose analogues differed in their effects on the kinetics of purified glucokinase. Mannoheptulose caused the greatest decrease in co-operativity of glucokinase for glucose whereas N-acetylglucosamine had the smallest effect. The anomalous effects of mannoheptulose on glucokinase translocation and on the kinetics of purified glucokinase could be explained by a second glucose-binding site on glucokinase.
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Dissertations / Theses on the topic "Effect of glucose on"

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Owen, Lauren. "The effect of glucose on cognition." Thesis, Lancaster University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538621.

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Puthanveetil, Prasanth Nair. "Glucocorticoid and its effect on cardiac glucose utilization." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5038.

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Glycogen is an immediate source of glucose for cardiac tissue to maintain its metabolic homeostasis. However, its excess brings about cardiac structural and physiological impairments. Previously, we have demonstrated that in hearts from dexamethasone (DEX) treated animals, glycogen accumulation was enhanced. We examined the influence of DEX on glucose entry and glycogen synthase as a means of regulating the accumulation of this stored polysaccharide. Following DEX, cardiac tissue had limited contribution towards the development of whole body insulin resistance. Measurement of GLUT4 at the plasma membrane revealed an excess presence of this transporter protein at this location. Interestingly, this was accompanied by an increase in GLUT4 in the intracellular membrane fraction, an effect that was well correlated to an increased GLUT4 mR.NA. Both total and phosphorylated AMPK increased following DEX. Immunoprecipitation of AS 160 followed by Western blotting demonstrated no change in Akt phosphorylation at Ser473 and Thr308 in DEX treated hearts. However, there was a significant increase in AMPK phosphorylation at Thr172, which correlated well with AS 160 phosphorylation. In DEX hearts, there was a considerable reduction in the phosphorylation of glycogen synthase, whereas GSK-3-β phosphorylation was augmented. Our data suggest that AMPK mediated glucose entry, combined with activation of glycogen synthase and reduction in glucose oxidation (Qi, D., et al. Diabetes 53:1790, 2004), act together to promote glycogen storage. Our data suggest that in the presence of intact insulin signaling, AMPK mediated glucose entry, combined with activation of glycogen synthase and the previously reported reduction in glucose oxidation, act together to promote glycogen storage. Should these effects persist chronically, they may explain the increased morbidity and mortality observed with long term excesses in endogenous or exogenous glucocorticoids.
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Chen, Mimi Zhu. "The effect of bariatric surgery on glucose homeostasis." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.665171.

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Bariatric surgery is very effective at inducing weight loss and diabetes resolution in morbidly obese patients. Whether WL or increased incretin response is the crucial factor in normalising diabetes is still debatable. This thesis work prospectively investigated how bariatric surgery affected insulin action and beta-cell function in patients with morbid obesity and type 2 diabetes. Understanding these can help us to optimise diabetes treatments in patients with morbid obesity. I first discussed how obesity affects insulin sensitivity and beta-cell function, evidences that bariatric surgery is superior to conventional medical therapy at inducing weight loss and euglycaemia, and its associated mechanisms. I concluded that more robust data are needed to understand the effects of LAGB and RYGB surgery on glucose homeostasis, as this will have clinical implications for patients undergoing bariatric surgery (Chapter 1). I then described and justified the methods used for investigating insulin sensitivity and insulin secretion in the two studies (GLIPO and ISP) that make up this thesis (Chapter 2). I demonstrated that at 1 week post-op, improvements in glycaemia, insulin sensitivity and weight were the same in all patients, despite unilateral increase in incretin responses in the RYGB group. At 18 months I found that RYGB (n=32) had induced greater weight loss than LAGB (n=17). This resulted in better glycaemic control, further insulin sensitivity enhancement and marked improvements in insulin secretion and pancreatic secretory reserve in this group (Chapter 3&4). Finally, I demonstrated that marked weight loss after RYGB normalised insulin signalling (PI3K-Akt), but not glucose uptake in muscle. This suggested that major defects in the insulin signalling pathway still exist and may explain why not all patients can achieve diabetes remission after RYGB (Chapter 5). In conclusion, the degree of weight loss, not enhanced incretin response, is the major determinant of glycaemic improvement after bariatric surgery. This improvement is first brought about by improvements in insulin sensitivity followed by improvements in insulin secretion.
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Vo, Annie Phuong. "Glucose Metabolism in Cancer-Associated Fibroblasts." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11025.

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Under normal conditions, non-transformed cells rely on glycolysis followed by oxidative phosphorylation to generate ATPs. When oxygen is scarce or when cells are actively proliferating, cellular ATPs come mainly from glycolysis. Pyruvate is converted into lactate to allow glycolysis to continue. Interestingly, cancer cells have adapted to favor lactate production even at normal oxygen tensions, exhibiting a metabolic shift known as the Warburg effect. However, the metabolic state of other cellular constituents within the tumor remains mostly unknown. Cancer-associated fibroblasts (CAFs) are the most abundant stromal cells. They aid tumor growth and metastasis by providing growth factors, cytokine, ECM remodeling proteins and interacting with other tumor stromal cells. Here I show that the Warburg effect also operates in stromal fibroblasts of the tumor microenvironment. Using mass spectrometry, genetic mouse models, gene expression and methylation studies, I demonstrate that CAFs from human and mouse mammary tumors exhibit hyperactive glycolysis and a metabolic shift towards lactate production. Furthermore, this phenotype may be sustained through epigenetic modifications of endogenous hypoxia-inducible factor 1α, key regulatory enzymes fructose-bisphosphatase 1 and pyruvate kinase M2. Depletion of stromal fibroblasts or suppression of lactate production specifically in these cells alters the metabolic profile of not only the tumors but also the cancer cells and results in impeded tumor growth. These results collectively suggest that tumor growth is dependent on metabolic state and metabolic support of stromal fibroblasts, highlighting these cells as attractive therapeutic targets in controlling cancer progression.
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Messier, Claude. "Effect of glucose on memory : examination of possible mechanisms." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74362.

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Previous research has shown that ingestion of sucrose or injection of glucose following a learning experience can improve an animal's memory for that experience. The present work was directed towards elucidating the mechanisms by which sucrose and glucose produce this effect. Memory was tested by determining the effects of post-training injections of various substances on a conditioned emotional response. Glucose itself exerted a dose-dependent bidirectional action on retention. This action was shown not to depend on particular blood glucose levels. Insulin did not improve retention at any of the doses tested. Fructose, a sugar that does not cross the blood-brain barrier produced a dose-response effect on retention similar to that of glucose suggesting that fructose and glucose may act through a common peripheral mechanism. The observation of a memory improvement following injections of either 2-deoxyglucose or 3-O-methylgucose, two non-metabolized glucose analogs, suggested that the effect of glucose on retention may be due to an action on glucose transport and not to any metabolic effects of glucose. Two peripheral organs were examined for their possible involvement in the memory-improving action of glucose. This action was shown not to be dependent on the adrenal medulla which has been implicated in the action of other mnemoactive treatments. Partial denervation of the liver produced a partial attenuation of the effect of glucose on retention. The results are discussed in terms of the action of reinforcers on endogenous physiological mechanisms that modulate memory consolidation.
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Quinn, C. E. "Vascular function in impaired glucose tolerance : Effect of pioglitazone." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501394.

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Inteeworn, Natalie. "The Effect of Hypothyroidism on Glucose Tolerance in Dogs." Thesis, Virginia Tech, 2008. http://hdl.handle.net/10919/32030.

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Background: Canine hypothyroidism is thought to cause abnormalities in glucose homeostasis, but the effect on glucose tolerance and insulin sensitivity has not been determined to date. Hypothesis/Objectives: The purpose of the study was to investigate whether hypothyroidism has an effect on glucose tolerance and insulin sensitivity in dogs. We hypothesized that hypothyroidism causes insulin resistance. Animals: Sixteen euthyroid bitches were randomly selected and allocated into two groups. In 8 dogs, hypothyroidism was induced by administration of 1 mCi/kg I-131. Experiments were performed on non-anesthetized, fasted dogs in anestrous approximately 12 months after hypothyroidism was induced. Methods: The insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT) and minimal model analysis were used to determine basal insulin and glucose concentrations, acute insulin response to glucose (AIRg), insulin sensitivity (SI), glucose effectiveness (SG) and the disposition index (DI). Results: In the hypothyroid group, basal glucose concentrations were mildly decreased (P = 0.0079), whereas basal insulin was increased (P = 0.019). Insulin sensitivity was reduced in the hypothyroid group (P<0.001), whereas AIRg was higher (P=0.01). Other parameters were not different between groups. Conclusions/Clinical Importance: Hypothyroidism negatively affects glucose homeostasis by inducing insulin resistance. In hypothyroid dogs, the disposition index (insulin sensitivity x insulin secretion) remained unchanged due to a compensatory increase in insulin secretion, thereby maintaining glucose tolerance. In cases with impaired insulin secretion, such as canine diabetes mellitus, concurrent hypothyroidism can have important clinical implications in the successful management of the disease.
Master of Science
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Martino, Paul F. "The effects of dantrolene on post exercise glucose uptake." Virtual Press, 1996. http://liblink.bsu.edu/uhtbin/catkey/1020145.

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The purpose of this investigation was to determine the relationship between calcium and glucose uptake following muscle contraction with the use of the calcium channel blocker dantrolene. In previous studies an exercise model has been used to investigate the role of calcium during post-exercise glucose uptake. This study utilized electrical stimulation. It has been shown that exercise-induced glucose uptake is calciummediated, but to date no one has shown that glucose transport induced by electrical stimulation is calcium-mediated. Twenty four male Sprague Dawley rats weighing 140 g were sacrificed and their epitrochlearis muscles were removed. Four treatment groups were established: control, muscle incubated in glucose (4mM); insulin, muscles incubated in glucose (4mM) and insulin (1000uU/ml); electrical stimulation, at 50 Hz for two five minute intervals separated by one minute rest periods; insulin (1000uU/ml) and electrical stimulation at 50 Hz for two five minute intervals separated by one minute intervals. Each group consisted of contain 8-10 muscle preparations. Glucose uptake was measured through the use of a double label of radioactive mannitol and 3-O-methylglucose and analyzed using liquid scintillation. This project followed a randomized group design. Treatments were measured with a one way ANOVA.
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Winnick, Jason Joseph. "Effect of aerobic exercise on peripheral glucose uptake and endogenous glucose production in type 2 diabetes mellitus." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1157551296.

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Winnick, Jason J. "Effect of aerobic exercise on peripheral glucose uptake and endogenous glucose production in type 2 diabetes mellitus." The Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=osu1157551296.

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Books on the topic "Effect of glucose on"

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Lee, Brenda Minfei. Effects of glucose, fructose and sucrose on postprandial glucose and insulin responses. Ottawa]: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Dorrestijn, Jannette. Signal transduction related to the metabolic action of insulin. [Leiden: University of Leiden, 1998.

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Stephen, Colagiuri, and Brand Miller Janette 1952-, eds. The pocket guide to the glucose revolution and losing weight. London: Coronet, 2000.

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Goh, Tracy T. The chronic effect of free fatty acids on glucose-stimulated insulin secretion in rats. Ottawa: National Library of Canada, 1999.

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Delparte, Jude J. The effects of complex magnetic fields on the comsumption [sic] of glucose and glucose-morphine solutions. Sudbury, Ont: Laurentian University, 2003.

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Rogerson, Parker. The effect of diauxic growth on the induction of quinoprotein glucose dehydrogenase in Agrobacterium tumefaciens. Sudbury, Ont: Laurentian University, 1998.

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Wong, Evelyn Yin-Yue. Effect of viscosity modification by fiber dose and heat treatment on postprandial blood glucose response. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Lu, Bing. The effect of oxidative stress on vandate and insulin stimulation of glucose uptake in rat adipocytes. Ottawa: National Library of Canada, 1996.

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Mason, Timothy Mckim. The effect of insulin delivery route on hepatic lipid and glucose metabolism in streptozotocin-diabetic rats. Ottawa: National Library of Canada, 1998.

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Polakof, Sergio. Brain glucosensing: Physiological implications. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Book chapters on the topic "Effect of glucose on"

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Spellacy, William N. "Oral Contraceptives Effect on Glucose Metabolism." In Clinical Perspectives in Obstetrics and Gynecology, 25–33. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4612-2730-4_3.

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Chatham, John C. "The Effect of Diabetes on Glucose Metabolism." In The Heart in Diabetes, 189–214. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1269-7_9.

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Lee, Tanya, and Jean-Jacques Dugoua. "Nutritional Supplements and Their Effect on Glucose Control." In Advances in Experimental Medicine and Biology, 381–95. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5441-0_27.

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Yamasaki, Kazuo. "Effect of Some Saponins on Glucose Transport System." In Advances in Experimental Medicine and Biology, 195–206. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1367-8_18.

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Mak, R. H. K., and C. Chantler. "Glucose Metabolism in Uremia: Effect of Hemodialysis and CAPD." In CAPD in Children, 58–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70213-6_8.

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Galione, A., V. Hopps, F. Vaccaro, and F. Biondi. "Cyclosporine A + Glybenclamide. Effect on Glucose Metabolism: Preliminary Results." In Current Therapy in Nephrology, 535–37. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0865-2_140.

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Bose, Sminu, Cissy Zhang, and Anne Le. "Glucose Metabolism in Cancer: The Warburg Effect and Beyond." In The Heterogeneity of Cancer Metabolism, 3–15. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_1.

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AbstractOtto Warburg observed a peculiar phenomenon in 1924, unknowingly laying the foundation for the field of cancer metabolism. While his contemporaries hypothesized that tumor cells derived the energy required for uncontrolled replication from proteolysis and lipolysis, Warburg instead found them to rapidly consume glucose, converting it to lactate even in the presence of oxygen. The significance of this finding, later termed the Warburg effect, went unnoticed by the broader scientific community at that time. The field of cancer metabolism lay dormant for almost a century awaiting advances in molecular biology and genetics, which would later open the doors to new cancer therapies [2, 3].
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Delva, P., M. Degan, C. Pastori, and A. Lechi. "In Vitro Effect of Glucose on Intralymphocyte Free Magnesium." In Magnesium: Current Status and New Developments, 115–17. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-009-0057-8_26.

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Sasson, Shlomo, Yaqoub Ashhab, Danielle Melloul, and Erol Cerasi. "Autoregulation of Glucose Transport: Effects of Glucose on Glucose Transporter Expression and Cellular Location in Muscle." In Advances in Experimental Medicine and Biology, 113–27. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2910-1_9.

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Faure, P., S. Bouvard, A. Favier, and S. Halimi. "Zinc Protects Hela Cells Against the Glucose Induced Cytotoxic Effect." In Trace Elements in Man and Animals 10, 532–33. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_168.

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Conference papers on the topic "Effect of glucose on"

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Ziemys, Arturas, Alessandro Grattoni, Jaskaran Gill, and Mauro Ferrari. "Silica Nanochannel Surface Effect on Monosaccharide Transport." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13216.

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The interface of silica nanochannel of 10 nm was studied by molecular modeling and experimental methods. Molecular Dynamics study on glucose solution revealed that 2–3 nm of interface solution to silica walls has reduced glucose diffusivity. That reduction affects the effective diffusivity of glucose in silica nanochannel. Experimental results show Fickian-like release of glucose through 13 nm nanochannel. Molecular modeling and experimental results suggest that glucose is not sufficiently confined to possess non-Fickian behavior.
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Wang, Yunjie, and Katherine Yanhang Zhang. "The Biomechanical Properties of Arterial Elastin With Glucose Effect." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14200.

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Elastin, as one of the major extracellular matrix (ECM) components, is essential to accommodate physiological deformation and provide elastic support for blood vessels. Elastin is a long-lived ECM protein and it can suffer from cumulative effects of exposure to chemical damage, which can greatly compromise its biomechanical properties. The mechanical properties of elastin are related to its microstructure and the chemical environment. Glucose is an important carbohydrate in human body. The effect of glucose on the mechanical properties of blood vessels is especially magnified in diabetic patients [1]. Glucose can directly condense with amino groups of proteins by nonenzymatic glycation, which is one of the main mechanisms of aging [2].
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Sabah, Al-ithawi. "Measurement of blood glucose level by Faraday effect." In 4TH ELECTRONIC AND GREEN MATERIALS INTERNATIONAL CONFERENCE 2018 (EGM 2018). Author(s), 2018. http://dx.doi.org/10.1063/1.5080822.

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Ke, H., T. Yang, and G. Li. "Effect of Blood Glucose Tolerance on Pulmonary Function." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3247.

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Daniel Szöllosi, Zoltan Kovács, Evelin Várvölgyi, and Andras Fekete. "The Effect of Glucose on Electronic Taste Analyzer." In 2013 Kansas City, Missouri, July 21 - July 24, 2013. St. Joseph, MI: American Society of Agricultural and Biological Engineers, 2013. http://dx.doi.org/10.13031/aim.20131619422.

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Khalikova, Daria Alexandrovna, Sergey Vladimirovich Ankov, and Tatiana Genrikhovna Tolstikova. "EFFECT OF RHAPONTICUM CARTHAMOIDES AND CRANBERRY MEAL EXTRACTS COMPOSITION ON GLUCOSE LEVEL." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.26.

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It has been found that Rhaponticum carthamoides and cranberry meal extracts composition at an effective dose of 35:250 mg/kg after 14 days of oral administration to mice promotes a significant glucose level reduction on the background of physical and glucose challenge compared to intact control.
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Rahman, Md Sazedur, Faisal Badal, Md Shahinur Alam, Mahib Tanvir, Sazzed Mahamud Khan, and Sajal Das. "Effect of PID Controller on Blood Glucose Concentration for Varying Plasma Insulin, Independent Glucose Flux, Renal Glucose Clearance and Gut Absorption Rate." In 2021 International Conference on Automation, Control and Mechatronics for Industry 4.0 (ACMI). IEEE, 2021. http://dx.doi.org/10.1109/acmi53878.2021.9528121.

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King, Timothy W., and Gerard L. Cote. "Closed loop polarimetric glucose sensing using the pockels effect." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5760906.

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King and Cote. "Closed Loop Polarimetric Glucose Sensing Using The Pockels Effect." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.589588.

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Al-Jabiry, Ali Jasim Mohammed, and M. A. M. Hassan. "Effect of glucose(C6H12O6) addition on piezoelectricproperties for sensor application." In 2012 IEEE Sensors Applications Symposium (SAS). IEEE, 2012. http://dx.doi.org/10.1109/sas.2012.6166297.

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Reports on the topic "Effect of glucose on"

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Lahti, Janet. The effect of glucose on the food intake of goldthioglucose injected mice. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1571.

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Donahue, Katrina, Laura Young, John Buse, Mark Weaver, Maihan Vu, C. Madeline Mitchell, Tamara Blakeney, Kimberlea Grimm, Jennifer Rees, and Franklin Niblock. Effect of Glucose Monitoring on Patient and Provider Outcomes in Non-Insulin Treated Diabetes. Patient-Centered Outcomes Research Institute (PCORI), March 2018. http://dx.doi.org/10.25302/3.2018.ce.12114980.

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Araoye, Erinola, and Karina Ckless. Effects of High Fructose/Glucose on Nlrp3/Il1β Inflammatory Pathway. Journal of Young Investigators, November 2016. http://dx.doi.org/10.22186/jyi.31.5.25-30.

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Han, Yiran, Zeyuan Lu, Meng Meng, Heran Wang, Pan Ting, Gao Tianjiao, and Mingjun Liu. Effect of Acupuncture on Glucose and Lipid Metabolism in Obese Type 2 Diabetes: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0087.

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Han, Yiran, Zeyuan Lu, Meng Meng, Heran Wang, Pan Ting, Tianjiao Gao, and Mingjun Liu. Effect of Electroacupuncture on Glucose and Lipid Metabolism in Type 2 Diabetes: A protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0008.

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Bennett, Alan B., Arthur Schaffer, and David Granot. Genetic and Biochemical Characterization of Fructose Accumulation: A Strategy to Improve Fruit Quality. United States Department of Agriculture, June 2000. http://dx.doi.org/10.32747/2000.7571353.bard.

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The goal of the research project was to evaluate the potential to genetically modify or engineer carbohydrate metabolism in tomato fruit to enhance levels of fructose, a sugar with nearly twice the sweetness value of other sugars. The specific research objectives to achieve that goal were to: 1. Establish the inheritance of a fructose-accumulating trait identified in F1 hybrids of an inferspecific cross between L. hirsutum XL. esculentum and identify linked molecular markers to facilitate its introgression into tomato cultivars. This objective was completed with the genetic data indicating a single major gene, termed Fgr (Fructose glucose ratio), that controlled the partitioning of hexose in the mature fruit. Molecular markers for the gene, were developed to aid introgression of this gene into cultivated tomato. In addition, a second major gene encoding fructokinase 2 (FK2) was found to be a determinant of the fructose to glucose ratio in fruit. The relationship between FK2 and Fgr is epistatic with a combined synergistic effect of the two hirsutum-derived genes on fructose/glucose ratios. 2. Characterize the metabolic and transport properties responsible for high fructose/glucose ratios in fructose-accumulating genotypes. The effect of both the Fgr and FK2 genes on the developmental accumulation of hexoses was studied in a wide range of genetic backgrounds. In all backgrounds the trait is a developmental one and that the increase in fructose to glucose ratio occurs at the breaker stage of fruit development. The following enzymes were assayed, none of which showed differences between genotypes, at either the breaker or ripe stage: invertase, sucrose synthase, FK1, FK2, hexokinase, PGI and PGM. The lack of effect of the FK2 gene on fructokinase activity is surprising and at present we have no explanation for the phenomenon. However, the hirsutum derived Fgr allele was associated with significantly lower levels of phosphorylated glucose, G1c-1-P and G1c-6-P and concomitantly higher levels of the phosphorylated fructose, Fru-6-P, in both the breaker and ripe stage. This suggests a significant role for the isomerase reaction. 3. Develop and implement molecular genetic strategies for the production of transgenic plants with altered levels of enzymes that potentially control fructose/glucose ratios in fruit. This objective focused on manipulating hexokinase and fructokinase expression in transgenic plants. Two highly divergent cDNA clones (Frk1 and Frk2), encoding fructokinase (EC 2.7.1.4), were isolated from tomato (Lycopersicon esculentum) and a potato fructokinase cDNA clone was obtained from Dr. Howard Davies. Following expression in yeast, each fructokinase was identified to code for one of the tomato or potato fructokinase isoforms Transgenic tomato plants were generated with the fructokinase cDNA clone in both sense and antisense orientations and the effect of the gene on tomato plants is currently being studied.
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Wang, Yudong, Guifen Fu, Xiang Li, Jiaxia Han, Jingfeng Chen, and Xiaohui Wei. Effect of different continuous glucose monitoring durations on glycemic control in Diabetes：A Systematic Review With Meta-analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0080.

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Ren, Bangjiaxin, and Ming Chen. Effect of Sodium‐glucose cotransport‐2 inhibitors on lowering blood pressure in patients with pre-hypertension and early hypertension: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.2.0004.

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Mei, Manxue, Min Jiang, Zunjiang Li, Wei Zhu, and Jianping Song. Meditation Programs for Adults with Type 2 Diabetes Mellitus: Protocol for a Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0008.

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Review question / Objective: Would meditation programs affect fasting blood glucose levels and HbA(1c) of patients with type 2 diabetes mellitus? Would meditation programs intervention be of benefit for remission of depression and anxiety level? Would meditation programs improve quality of life of individuals with type 2 diabetes？ Do meditation programs affect body mass index (BMI), serum lipid levels and level of blood pressure? Which type of meditation programs is better for type 2 diabetes patients? Are there any differences of efficacy among different meditation programs? To provide valid evidence for the effect of meditation programs for type 2 diabetes by synthesizing and comparing outcomes from clinical trials. Main outcome(s): The outcomes include fasting blood glucose levels and HbA(1c).
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Craan, Andre-Gerard. Effects of insulin, sodium and D-glucose on amino acid absorption in the intestine of rats. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1448.

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