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Published: 10 December 2022

Last updated: 30 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Harmayetty, Harmayetty, Ilya Krisnana, and Faida Anisa. "String Bean Juice Decreases Blood Glucose Level Patients with Diabetes Mellitus." Jurnal Ners 4, no. 2 (July 23, 2017): 116–21. http://dx.doi.org/10.20473/jn.v4i2.5022.

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Introduction: Type 2 diabetes mellitus is deficiency of insulin and caused by decreases of insulin receptor or bad quality of insulin. As a result, insulin hormone does not work effectively in blood glucose regulation. String bean juice contains thiamin and fiber may regulate blood glucose level. The aim of this study was to analyze the effect of string bean juice to decrease blood glucose level of patients with type 2 diabetes mellitus. Method: This study employed a quasy-experimental pre-post test control group design and purposive sampling. The population were all type 2 diabetes mellitus patients in Puskesmas Pacar Keling Surabaya. Sample were 12 patients who met inclusion criteria. The independent variable was string bean juice and dependent variable was blood glucose level. Data were analyzed by using Paired T-test with significance level of α≤ 0.05 and Independent T-test with significant level of α≤0.05. Result: The results showed that string bean juice has an effect on decreasing blood glucose between pre test and post test for blood glucose with independent T-test is p=0.003.In conclusion, string bean juice has an effect on blood glucose level in patients with type 2 diabetes mellitus.Discussion: The possible explanation for this findings is string bean juice contains two ingredients: thiamine and fiber. Thiamine helps support insulin receptors and glucose transporter in cells hence GLUT-4 could translocated to the cell membrane brought glucouse enter to the intracellular compartment, that leads to blood glucouse level well regulated. Dietary fiber reduces food transit time so slowing the glucose absorption. Therefore blood glucose level will be decreased.

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12

Bennal, Amruta, and Sudha Kerure. "Effect of PCOS on glucose metabolism." National Journal of Physiology, Pharmacy and Pharmacology 3, no. 2 (2013): 167. http://dx.doi.org/10.5455/njppp.2013.3.220420132.

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13

Kim, So Hun. "Effect of Exercise on Glucose Metabolism." Journal of Korean Diabetes 12, no. 1 (2011): 21. http://dx.doi.org/10.4093/jkd.2011.12.1.21.

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14

Shelton, S. D., K. A. Boggess, T. Smith, and W. N. P. Herbert. "Effect of betamethasone on maternal glucose." Journal of Maternal-Fetal & Neonatal Medicine 12, no. 3 (January 2002): 191–95. http://dx.doi.org/10.1080/jmf.12.3.191.195.

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15

Stumpf, Janice L., and Shu-Wen Lin. "Effect of Glucosamine on Glucose Control." Annals of Pharmacotherapy 40, no. 4 (April 2006): 694–98. http://dx.doi.org/10.1345/aph.1e658.

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16

Gaafar, Khadiga, Mona Khedr, Samir Bashandy, Olaa Sharaf, and Salwa El-Zayat. "Effect of Chloroquine on Glucose Metabolism." Arzneimittelforschung 52, no. 05 (December 26, 2011): 400–406. http://dx.doi.org/10.1055/s-0031-1299905.

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17

Mahoney, John J., and Christine G. Lim. "Effect of Disinfectants on Glucose Monitors." Journal of Diabetes Science and Technology 6, no. 1 (January 2012): 81–85. http://dx.doi.org/10.1177/193229681200600111.

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18

Boss, S., S. Dewar, C. Jacklyn, M. Moss, and W. Nickerson. "Haematocrit effect on two glucose monitors." Clinical Biochemistry 26, no. 2 (April 1993): 148. http://dx.doi.org/10.1016/0009-9120(93)90100-k.

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19

Sugawara, Akira, Akira Uruno, Masataka Kudo, Ken Matsuda, Chul Woo Yang, and Sadayoshi Ito. "PPARγ Agonist Beyond Glucose Lowering Effect." Korean Journal of Internal Medicine 26, no. 1 (2011): 19. http://dx.doi.org/10.3904/kjim.2011.26.1.19.

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20

Wittig, Rainer, and Johannes F. Coy. "The Role of Glucose Metabolism and Glucose-Associated Signalling in Cancer." Perspectives in Medicinal Chemistry 1 (January 2007): 1177391X0700100. http://dx.doi.org/10.1177/1177391x0700100006.

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Aggressive carcinomas ferment glucose to lactate even in the presence of oxygen. This particular metabolism, termed aerobic glycolysis, the glycolytic phenotype, or the Warburg effect, was discovered by Nobel laureate Otto Warburg in the 1920s. Since these times, controversial discussions about the relevance of the fermentation of glucose by tumours took place; however, a majority of cancer researchers considered the Warburg effect as a non-causative epiphenomenon. Recent research demonstrated, that several common oncogenic events favour the expression of the glycolytic phenotype. Moreover, a suppression of the phenotypic features by either substrate limitation, pharmacological intervention, or genetic manipulation was found to mediate potent tumour-suppressive effects. The discovery of the transketolase-like 1 (TKTL1) enzyme in aggressive cancers may deliver a missing link in the interpretation of the Warburg effect. TKTL1-activity could be the basis for a rapid fermentation of glucose in aggressive carcinoma cells via the pentose phosphate pathway, which leads to matrix acidification, invasive growth, and ultimately metastasis. TKTL1 expression in certain non-cancerous tissues correlates with aerobic formation of lactate and rapid fermentation of glucose, which may be required for the prevention of advanced glycation end products and the suppression of reactive oxygen species. There is evidence, that the activity of this enzyme and the Warburg effect can be both protective or destructive for the organism. These results place glucose metabolism to the centre of pathogenesis of several civilisation related diseases and raise concerns about the high glycaemic index of various food components commonly consumed in western diets.

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21

Vissing, J., J. L. Wallace, and H. Galbo. "Effect of liver glycogen content on glucose production in running rats." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 318–22. http://dx.doi.org/10.1152/jappl.1989.66.1.318.

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The influence of supranormal compared with normal hepatic glycogen levels on hepatic glucose production (Ra) during exercise was investigated in chronically catheterized rats. Supranormal hepatic glycogen levels were obtained by a 24-h fast-24-h refeeding regimen. During treadmill running for 35 min at a speed of 21 m/min, Ra and plasma glucose increased more (P less than 0.05) and liver glucogen breakdown was larger in fasted-refed compared with control rats, although the stimuli for Ra were higher in control rats, the plasma concentrations of insulin and glucose being lower (P less than 0.05) in control compared with fasted-refed rats. Also, plasma concentrations of glucagon and both catecholamines tended to be higher and muscle glycogenolysis lower in control compared with fasted-refed rats. Lipid metabolism was similar in the two groups. The results indicate that hepatic glycogenolysis during exercise is directly related to hepatic glycogen content. The smaller endocrine glycogenolytic signal in face of higher plasma glucose concentrations in fasted-refed compared with control rats is indicative of metabolic feedback control of glucose mobilization during exercise. However, the higher exercise-induced increase in Ra, plasma glucose, and liver glycogen breakdown in fasted-refed compared with control rats indicates that metabolic feedback mechanisms are not able to accurately match Ra to the metabolic needs of working muscles.

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22

Kunicka-Styczyńska, A. "Glucose, l-Malic Acid and pH Effect on Fermentation Products in Biological Deacidification." Czech Journal of Food Sciences 27, Special Issue 1 (June 24, 2009): S319—S322. http://dx.doi.org/10.17221/604-cjfs.

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Industrial wine yeasts <I>Saccharomyces cerevisiae</I> Syrena, an interspecies hybrid (<I>S. cerevisiae × S. bayanus</I>) HW2-3 and <I>Schizosaccharomyces pombe</I> met 3–15 h<sup>+>/sup> were examined to determine changes in fermentation profiles in different environmental conditions in YG medium with different concentrations of glucose (2, 6, 40 or 100 g/l), L-malic acid (4, 7 or 11 g/l) and at pH 3.0, 3.5 and 5.0. The results were obtained by HPLC method (organic acids, acetaldehyde, glycerol, diacetyl) and enzymatically (L-malic acid, ethanol). In anaerobic conditions (100 g/l glucose), the optimal parameters for L-malic acid decomposition for <I>S. cerevisiae</I> Syrena and the hybrid HW2-3 were 11 g/l L-malic acid and pH 3.0 and 3.5, respectively. <I>S. pombe</I> expressed the highest demalication activity at 40 and 100 g/l glucose, 7 g/l L-malic acid and pH 3.0. The fermentation profiles of selected metabolites of yeast were unique for specific industrial strains. These profiles may help in the proper selection of yeast strains to fermentation and make it possible to predict the organoleptic changes in the course of fruit must fermentation.

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23

Sharma, Anjali. "Effect of Glucose on Biosurfactant Production using Bacterial Isolates from Oil Contaminated Sites." International Journal of Trend in Scientific Research and Development Volume-3, Issue-1 (December 31, 2018): 730–32. http://dx.doi.org/10.31142/ijtsrd19033.

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24

Talaei, Afsaneh, Masoud Amini, Mansour Siavash, and Maryam Zare. "The effect of Dehydroepiandrosterone on insulin resistance in patients with impaired glucose tolerance." HORMONES 9, no. 4 (October 15, 2010): 326–31. http://dx.doi.org/10.14310/horm.2002.1284.

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25

Vloshchinskiy, Pavel, Natalya Klebleeva, Arkadiy Kolpakov, and Irina Berezovikova. "Effect of Multicomponent Cereal Mixtures on Glucose Level in Blood of Experimental Animals." Foods and Raw Materials 2, no. 1 (May 26, 2014): 82–85. http://dx.doi.org/10.12737/4140.

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26

Hu, Shiling, Shuya Wang, and Beth E. Dunning. "Glucose-dependent and Glucose-sensitizing Insulinotropic Effect of Nateglinide: Comparison to Sulfonylureas and Repaglinide." International Journal of Experimental Diabetes Research 2, no. 1 (2001): 63–72. http://dx.doi.org/10.1155/edr.2001.63.

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Nateglinide, a novel D-phenylalanine derivative, stimulates insulin releaseviaclosure ofKATPchannels in pancreaticβ-cell, a primary mechanism of action it shares with sulfonylureas (SUs) and repaglinide. This study investigated (1) the influence of ambient glucose levels on the insulinotropic effects of nateglinide, glyburide and repaglinide, and (2) the influence of the antidiabetic agents on glucose-stimulated insulin secretion (GSIS)in vitrofrom isolated rat islets. TheEC50of nateglinide to stimulate insulin secretion was 14 μM in the presence of 3mM glucose and was reduced by 6-fold in 8mM glucose and by 16-fold in 16mM glucose, indicating a glucose-dependent insulinotropic effect. The actions of glyburide and repaglinide failed to demonstrate such a glucose concentration-dependent sensitization. When tested at fixed and equipotent concentrations (~2xEC50in the presence of 8mM glucose) nateglinide and repaglinide shifted theEC50s for GSIS to the left by 1.7mM suggesting an enhancement of islet glucose sensitivity, while glimepiride and glyburide caused, respectively, no change and a right shift of theEC50. These data demonstrate that despite a common basic mechanism of action, the insulinotropic effects of different agents can be influenced differentially by ambient glucose and can differentially influence the islet responsiveness to glucose. Further, the present findings suggest that nateglinide may exert a more physiologic effect on insulin secretion than comparator agents and thereby have less propensity to elicit hypoglycemiain vivo.

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27

Yamazaki, Hanae, William Philbrick, Kathleen C. Zawalich, and Walter S. Zawalich. "Acute and chronic effects of glucose and carbachol on insulin secretion and phospholipase C activation: studies with diazoxide and atropine." American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (January 2006): E26—E33. http://dx.doi.org/10.1152/ajpendo.00149.2005.

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The acute and chronic effects of 20 mM glucose and 10 μM carbachol on β-cell responses were investigated. Acute exposure of rat islets to 20 mM glucose increased glucose usage rates and resulted in a large insulin-secretory response during a dynamic perifusion. The secretory, but not the metabolic, effect of 20 mM glucose was abolished by simultaneous exposure to 100 μM diazoxide. Glucose (20 mM) significantly increased inositol phosphate (IP) accumulation, an index of phospholipase C (PLC) activation, from [3H]inositol-prelabeled islets. Diazoxide, but not atropine, abolished this effect as well. Unlike 20 mM glucose, 10 μM carbachol (in the presence of 5 mM glucose) increased IP accumulation but had no effect on insulin secretion or glucose (5 mM) metabolism. The IP effect was abolished by 50 μM atropine but not by diazoxide. Chronic 3-h exposure of islets to 20 mM glucose or 10 μM carbachol profoundly reduced both the insulin-secretory and PLC responses to a subsequent 20 mM glucose stimulus. The adverse effects of chronic glucose exposure were abolished by diazoxide but not by atropine. In contrast, the adverse effects of carbachol were abolished by atropine but not by diazoxide. Prior 3 h of exposure to 20 mM glucose or carbachol had no inhibitory effect on glucose metabolism. Significant secretory responses could be evoked from 20 mM glucose- or carbachol-pretreated islets by the inclusion of forskolin. These findings support the concept that an early event in the evolution of β-cell desensitization is the impaired activation of islet PLC.

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28

Messier, Claude, and Norman M. White. "Memory improvement by glucose, fructose, and two glucose analogs: A possible effect on peripheral glucose transport." Behavioral and Neural Biology 48, no. 1 (July 1987): 104–27. http://dx.doi.org/10.1016/s0163-1047(87)90634-0.

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29

WOOD, David M., Amanda L. BRENNAN, Barbara J. PHILIPS, and Emma H. BAKER. "Effect of hyperglycaemia on glucose concentration of human nasal secretions." Clinical Science 106, no. 5 (May 1, 2004): 527–33. http://dx.doi.org/10.1042/cs20030333.

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Glucose is not detectable in airways secretions of normoglycaemic volunteers, but is present at 1–9 mmol·l-1 in airways secretions from people with hyperglycaemia. These observations suggest the existence of a blood glucose threshold at which glucose appears in airways secretions, similar to that seen in renal and salivary epithelia. In the present study we determined the blood glucose threshold at which glucose appears in nasal secretions. Blood glucose concentrations were raised in healthy human volunteers by 20% dextrose intravenous infusion or 75 g oral glucose load. Nasal glucose concentrations were measured using modified glucose oxidase sticks as blood glucose concentrations were raised. Glucose appeared rapidly in nasal secretions once blood glucose was clamped at approx. 12 mmol·l-1 (n=6). On removal of the clamp, nasal glucose fell to baseline levels in parallel with blood glucose concentrations. An airway glucose threshold of 6.7–9.7 mmol·l-1 was identified (n=12). In six subjects with normal glucose tolerance, blood glucose concentrations rose above the airways threshold and nasal glucose became detectable following an oral glucose load. The presence of an airway glucose threshold suggests that active glucose transport by airway epithelial cells normally maintains low glucose concentrations in airways secretions. Blood glucose exceeds the airway threshold after a glucose load even in people with normal glucose tolerance, so it is likely that people with diabetes or hyperglycaemia spend a significant proportion of each day with glucose in their airways secretions.

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30

McConell, G., S. Fabris, J. Proietto, and M. Hargreaves. "Effect of carbohydrate ingestion on glucose kinetics during exercise." Journal of Applied Physiology 77, no. 3 (September 1, 1994): 1537–41. http://dx.doi.org/10.1152/jappl.1994.77.3.1537.

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Six well-trained men (peak pulmonary oxygen uptake = 5.03 +/- 0.11 l/min) were studied during 2 h of exercise at 69 +/- 1% peak pulmonary oxygen uptake to examine the effect of carbohydrate (CHO) ingestion on glucose kinetics. Subjects ingested 250 ml of either a 10% glucose solution containing 6-[3H]glucose (CHO) or a sweet placebo every 15 min during exercise. Glucose kinetics were assessed by 6,6-[2H]glucose infusion corrected for gut-derived glucose in CHO. Plasma glucose was higher (P < 0.05) in CHO from 20 min. Total glucose appearance was higher in CHO due to glucose delivery from the gut (68 +/- 7 g), since hepatic glucose production was reduced by 51% (29 +/- 5 vs. 59 +/- 5 g). Glucose uptake was higher in CHO (96 +/- 7 vs. 60 +/- 6 g) with the ingested glucose supplying 67 +/- 4 g and, with the assumption that it was fully oxidized, accounted for 14 +/- 1% of total energy expenditure. In conclusion, CHO ingestion during prolonged exercise results in suppression of hepatic glucose production and increased glucose uptake. These effects appear to be mediated mainly by increased plasma glucose and insulin levels.

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31

Iverson, Jennifer F., Mary C. Gannon, and Frank Q. Nuttall. "Ingestion of Leucine + Phenylalanine with Glucose Produces an Additive Effect on Serum Insulin but Less than Additive Effect on Plasma Glucose." Journal of Amino Acids 2013 (July 29, 2013): 1–6. http://dx.doi.org/10.1155/2013/964637.

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Most individual amino acids stimulate insulin secretion and attenuate the plasma glucose response when ingested with glucose. We determined whether ingestion of two amino acids simultaneously with glucose would result in an additive effect on the glucose area response compared with ingestion of amino acids individually. Leucine and phenylalanine were chosen because they were two of the most potent glucose-lowering amino acids when given individually. Eight healthy subjects were studied on four separate days. Test meals were given at 0800. The first meal was a water control. Subjects then received 25 g glucose or leucine + phenylalanine (1 mmol/kg fat free body mass each) ±25 g glucose in random order. Glucose, insulin and glucagon were measured frequently for 2.5 hours thereafter. Net areas under the curves were calculated using the mean fasting value as baseline. The insulin response to leucine + phenylalanine was additive. In contrast, the decrease in glucose response to leucine + phenylalanine + glucose was less than additive compared to the individual amino acids ingested with glucose. Interestingly, the insulin response to the combination was largely due to the leucine component, whereas the glucose response was largely due to the phenylalanine component. Glucose was unchanged when leucine or phenylalanine, alone or in combination, was ingested without glucose. This trial is registered with ClinicalTrials.gov NCT01471509.

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32

Koop, Brenda L., Alan G. Harris, and Shereen Ezzat. "Effect of octreotide on glucose tolerance in acromegaly." European Journal of Endocrinology 130, no. 6 (June 1994): 581–86. http://dx.doi.org/10.1530/eje.0.1300581.

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Koop BL, Harris AG. Ezzat S. Effect of octreotide on glucose tolerance in acromegaly. Eur J Endocrinol 1994;130:581–6. ISSN 0804–4643 To determine the effect of the somatostatin analog octreotide on glucose tolerance in acromegaly, we examined glucose profiles, oral glucose tolerance and the insulinogenic index in patients treated with this analog. Ninety patients participated in a long-term, prospective, open-label study. There was no significant change between mean daily blood glucose profiles at baseline or during octreotide treatment. Using glucose tolerance test criteria, 61% of 90 patients had normal baseline glucose tolerance. While on octreotide, 20% and 29% of these patients, respectively, developed impaired glucose tolerance or became frankly diabetic. Conversely, three of the patients who were diabetic at baseline (N = 11) became normal (18%) or developed impaired glucose tolerance (9%) during octreotide therapy. There was no relationship between the dose of octreotide and change in glycemic state. The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Female patients and those with elevated baseline insulin levels were more likely to develop diabetes mellitus during octreotide therapy. In conclusion, octreotide significantly alters glucose tolerance in patients with acromegaly, mandating glucose monitoring during this form of therapy. Alan G Harris, Division of Clinical Pharmacology, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA 90048, USA

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33

Kaufmann, Robert, Francis Khosho, Steven Verhulst, and Kofi Amankwah. "Effect of Pregnancy on Glucose Metabolism in Glucose Intolerant ‘BB’ WISTAR RATS." American Journal of Perinatology 8, no. 01 (January 1991): 11–14. http://dx.doi.org/10.1055/s-2007-999328.

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Reaven, G. M., N. Chen, C. Hollenbeck, and Y. D. I. Chen. "Effect of Age on Glucose Tolerance and Glucose Uptake in Healthy Individuals." Journal of the American Geriatrics Society 37, no. 8 (August 1989): 735–40. http://dx.doi.org/10.1111/j.1532-5415.1989.tb02235.x.

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35

Rosenblatt, Sidney. "Effect of Pioglitazone on blood glucose following an oral glucose tolerance test." Diabetes Research and Clinical Practice 50 (September 2000): 60. http://dx.doi.org/10.1016/s0168-8227(00)81663-0.

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36

Messier, C. "Effect of Glucose and Peripheral Glucose Regulation on Memory in the Elderly." Neurobiology of Aging 18, no. 3 (May 6, 1997): 297–304. http://dx.doi.org/10.1016/s0197-4580(97)80311-9.

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37

Tiina, M. "Antibacterial effect of the glucose oxidase-glucose system on food-poisoning organisms." International Journal of Food Microbiology 8, no. 2 (May 1989): 165–74. http://dx.doi.org/10.1016/0168-1605(89)90071-8.

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Zhao, K., H. Y. Liu, H. F. Wang, M. M. Zhou, and J. X. Liu. "Effect of glucose availability on glucose transport in bovine mammary epithelial cells." Animal 6, no. 3 (2012): 488–93. http://dx.doi.org/10.1017/s1751731111001893.

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39

Messier, Claude, Alain Desrochers, and Michèle Gagnon. "Effect of glucose, glucose regulation, and word imagery value on human memory." Behavioral Neuroscience 113, no. 3 (1999): 431–38. http://dx.doi.org/10.1037/0735-7044.113.3.431.

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40

Shi, Ting, Yiming Zhang, and Luo Lu. "Effect of physiological parameters on glucose microcirculation compartmental model in glucose monitoring." Biotechnology & Biotechnological Equipment 32, no. 4 (December 12, 2017): 1047–52. http://dx.doi.org/10.1080/13102818.2017.1413595.

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41

Kozacz, Agnieszka, Paulina Grunt, Marta Steczkowska, Tomasz Mikulski, Jan Dąbrowski, Monika Górecka, Urszula Sanocka, and Andrzej Wojciech Ziemba. "Thermogenic Effect of Glucose in Hypothyroid Subjects." International Journal of Endocrinology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/308017.

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The importance of thyroid hormone, catecholamines, and insulin in modification of the thermogenic effect of glucose (TEG) was examined in 34 healthy and 32 hypothyroid subjects. We calculated the energy expenditure at rest and during oral glucose tolerance test. Blood samples for determinations of glucose, plasma insulin, adrenaline (A), and noradrenaline (NA) were collected. It was found that TEG was lower in hypothyroid than in control group (19.68±3.90versus55.40±7.32 kJ, resp.,P<0.0004). Mean values of glucose and insulin areas under the curve were higher in women with hypothyroidism than in control group (286.79±23.65versus188.41±15.84 mmol/L·min,P<0.003and7563.27±863.65versus4987.72±583.88 mU/L·min,P<0.03resp.). Maximal levels of catecholamines after glucose ingestion were higher in hypothyroid patients than in control subjects (Amax—0.69±0.08versus0.30±0.07 nmol/L,P<0.0001, and NAmax—6.42±0.86versus2.54±0.30 nmol/L,P<0.0002). It can be concluded that in hypothyroidism TEG and glucose tolerance are decreased while the adrenergic response to glucose administration is enhanced. Presumably, these changes are related to decreased insulin sensitivity and responsiveness to catecholamine action.

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Schmid, R., V. Schusdziarra, and M. Classen. "Modulatory effect of glucose on VIP-induced gastric somatostatin release." American Journal of Physiology-Endocrinology and Metabolism 254, no. 6 (June 1, 1988): E756—E759. http://dx.doi.org/10.1152/ajpendo.1988.254.6.e756.

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The present study was designed to examine the effect of increasing perfusate glucose concentrations on vasoactive intestinal peptide (VIP)-induced somatostatin (SLI) release from the isolated rat stomach. The stomach of overnight-fasted rats was perfused with Krebs-Ringer buffer containing 100, 150, or 200 mg/dl glucose, respectively. VIP was administered at 10(-12), 10(-11), 10(-9), and 10(-8) M. At a normal glucose concentration of 100 mg/dl, VIP at doses of 10(-12), 10(-11), and 10(-9) M elicited a small inhibitory effect on SLI release by 200-300 pg/min (P less than 0.01). As reported previously at 10(-8) M, VIP stimulated gastric SLI secretion by 500 pg/min (P less than 0.01). Increasing perfusate glucose to 150 mg/dl resulted in a stimulation of SLI release by all four concentrations of VIP with a maximal effect at 10(-9) M. During 200 mg/dl glucose, VIP had no effect in concentrations below 10(-9) M, and only the two highest doses (10(-9) and 10(-8) M) stimulated SLI release significantly. In the absence of VIP, glucose had no effect on gastric SLI release. In conclusion, the present data demonstrate for the first time that at normal glucose levels VIP has not only stimulatory but also inhibitory effects on gastric SLI, and second, a modest elevation of glucose has a modulatory effect on gastric D-cell function.

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43

Fraeyman, A., G. Claeys, and Z. Zaman. "Effect of non-glucose sugars and haematocrit on glucose measurements with Roche Accu-Chek Performa glucose strips." Annals of Clinical Biochemistry 47, no. 5 (August 2, 2010): 494–96. http://dx.doi.org/10.1258/acb.2010.010091.

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44

DiGiacomo, J. E., and W. W. Hay. "Effect of hypoinsulinemia and hyperglycemia on fetal glucose utilization." American Journal of Physiology-Endocrinology and Metabolism 259, no. 4 (October 1, 1990): E506—E512. http://dx.doi.org/10.1152/ajpendo.1990.259.4.e506.

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The present studies were performed to determine the effect of normal levels of insulin on fetal glucose metabolism and to measure the acute changes in insulin secretion and concentration that occur in response to a hyperglycemia stimulus. In fetal sheep, infusion of somatostatin alone decreased fetal insulin concentration 4 microU/ml (33%) from the basal value without a significant change in fetal glucose concentration, umbilical glucose uptake (UGU), or fetal glucose utilization rate (GUR). Glucose plus somatostatin infusion produced a significantly lower insulin concentration (54% lower, P less than 0.005) and GUR (22% lower, P less than 0.05) at glucose concentration approximately 40 mg/dl compared with glucose infusion alone. No significant difference was seen at glucose concentration of approximately 30 mg/dl. These results indicate that fetal glucose metabolism is responsive not only to changes in glucose but also insulin concentrations; however, a relatively large change in insulin (greater than 5 microU/ml) is necessary to produce a measurable response. These quantitative aspects of fetal insulin effect must be considered when assessing the role of insulin in the regulation of fetal glucose metabolism.

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45

Elnour, Rehab Omer, Omar Musa EzzEldin, Abdalbasit Adam Mariod, Reem Hassan Ahmed, and Ahlam Salih Eltahir. "Effect of Raphanus sativus on Glucose, Cholesterol and Triglycerides Levels in Glucose Loaded Rats." Functional Foods in Health and Disease 12, no. 3 (March 25, 2022): 134. http://dx.doi.org/10.31989/ffhd.v12i3.883.

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Background: In fact, diabetes is now a serious health concern, and the import of medications from other countries consumes a significant amount of foreign cash each year. The effects of Raphanus satives (Radish) in the treatment of diabetes mellitus were evaluated scientifically in this study. Thyroid hormone increases metabolic actions in almost every tissue, and the current study was an attempt to evaluate scientifically the effects of Raphanus satives (Radish) in the treatment of diabetes mellitus.Objectives: The main objective of this study is to evaluate the hypoglycemic effect of Raphanus sativus (Radish) on induced hyperglycemic rats.Methods: An oral administration of ethanolic extract of Radish in glucose loaded rats at dose of 250mg/k body weight, standard group was administered with 10mg/kg of hypoglycemic drug glibenclamide for 2 consecutive weeks. The control group was given distilled water only. After the two weeks' time, the groups were subjected to a glucose tolerance test and measurement of plasma cholesterol and triglyceride levels. Results: significant reduction of blood glucose was observed (P <0.001), when compared with the control group at 2 hours after glucose loud. Radish ethanolic extract did not present any significant difference in cholesterol level after 2 weeks compared with start point. No significant difference was seen in triglyceride level after 2 weeks of administration of Radish extract compared with start point. Radish extract(250 mg/kg) did not affect kidney function creatinin and urea, also liver function were not affected Glutamic-Oxaloacetic Transaminase (GOT), Glutamic-Pyruvate Transaminase (GPT), albumin, total protein and bilirubin, this means administration of increased doses to hyperglycemic subjects can be considered safe. CONCLUSION: In this investigation, doses of radish extract (250 mg/kg) had no effect on renal function, creatinin, and urea, as well as liver function. Glutamic-Oxaloacetic Transaminase (GOT), Glutamic-Pyruvate Transaminase (GPT), albumin, total protein, and bilirubin .Keywords: Raphanus sativus, extract, hypoglycemic, glucose, rats

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46

Verspohl, E. J., I. Breuning, and H. P. Ammon. "Effect of CCK-8 on pentose phosphate shunt activity, pyridine nucleotides, and glucokinase of rat islets." American Journal of Physiology-Endocrinology and Metabolism 256, no. 1 (January 1, 1989): E68—E73. http://dx.doi.org/10.1152/ajpendo.1989.256.1.e68.

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In rat pancreatic islets the effects of cholecystokinin octapeptide (CCK-8) on pentose phosphate shunt (PPS) activity, glucokinase and hexokinase activity, and NADPH, NADP+, NADH, and NAD+ were studied. By elevating the glucose concentration from 3.0 to 8.3 and 16.7 mM the oxidation of [1-14C]- and [6-14C]glucose and the calculated PPS activity were increased in a concentration-dependent manner; 10 nM CCK-8 enhanced selectively the effect on [1-14C]glucose oxidation thereby increasing the PPS activity but only at an intermediate glucose concentration (8.3 mM). CCK-8 had no effect on glucokinase or hexokinase activity and CCK-8 did not influence glucose utilization. By elevating the glucose concentration, total NADPH and NADH were increased and total NADP+ and NAD+ were decreased. CCK-8 (10 nM) increased selectively NADPH and decreased NADP+ but did not change NADH or NAD+; the effect of CCK-8 on NADPH and NADH was only observed in the presence of an intermediate stimulatory glucose concentration (8.3 mM) but not at either a substimulatory glucose concentration or a maximally stimulatory glucose concentration for insulin release (3.0 or 16.7 mM). The data indicate first that CCK-8 does not act on glucose phosphorylation or glucose utilization and second that CCK-8 increases PPS activity and NADPH levels in rat pancreatic islets. Since the concentrations of glucose necessary for these CCK-8 effects are in the range of 8.3 mM and parallel with those necessary for insulin release as shown in earlier observations, glucose oxidation via pentose phosphate shunt and NADPH are suggested to be related to the CCK-8-modulated insulin release.

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47

Zawalich, W. S., K. C. Zawalich, S. Ganesan, R. Calle, and H. Rasmussen. "Influence of staurosporine on glucose-mediated and glucose-conditioned insulin secretion." Biochemical Journal 279, no. 3 (November 1, 1991): 807–13. http://dx.doi.org/10.1042/bj2790807.

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The effect of staurosporine, a putative inhibitor of protein kinase C (PKC), on insulin secretion induced by glucose and 4-methyl-2-oxopentanoate (KIC) was examined. In addition, the effects of staurosporine on the actions of other agonists, for which glucose acts as a conditional modifier, were also examined. At 20 nM, staurosporine caused a marked inhibition of second-phase insulin secretion, whether it was stimulated by 10 mM- or 20 mM-glucose, by 15 mM-KIC, or by carbachol or tolbutamide in islets co-perifused with 7.0 mM-glucose. In each case, the second-phase secretory response was inhibited by 70-85%. In contrast, in all cases there was no effect of staurosporine on the magnitude of the first phase of insulin secretion, nor on the time course of first-phase secretion, except when glucose alone was the secretagogue. With either 10 mM- or 20 mM-glucose, the peak of the first phase of insulin secretion was delayed. Staurosporine does not alter glucose metabolism, or the ability of glucose to activate phosphoinositide hydrolysis or to cause the translocation of alpha-PKC to the membrane. These findings support the concept that PKC activation plays an important role in fuel-induced or fuel-conditioned insulin secretion.

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48

Ya Su, Ya Su, Zhuo Meng Zhuo Meng, Longzhi Wang Longzhi Wang, Haimin Yu Haimin Yu, and Tiegen Liu Tiegen Liu. "Effect of temperature on noninvasive blood glucose monitoring in vivo using optical coherence tomography." Chinese Optics Letters 12, no. 11 (2014): 111701–5. http://dx.doi.org/10.3788/col201412.111701.

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49

Cheng, Hui, Fumiko Isoda, Denise D. Belsham, and Charles V. Mobbs. "Inhibition of Agouti-Related Peptide Expression by Glucose in a Clonal Hypothalamic Neuronal Cell Line Is Mediated by Glycolysis, Not Oxidative Phosphorylation." Endocrinology 149, no. 2 (November 1, 2007): 703–10. http://dx.doi.org/10.1210/en.2007-0772.

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The regulation of neuroendocrine electrical activity and gene expression by glucose is mediated through several distinct metabolic pathways. Many studies have implicated AMP and ATP as key metabolites mediating neuroendocrine responses to glucose, especially through their effects on AMP-activated protein kinase (AMPK), but other studies have suggested that glycolysis, and in particular the cytoplasmic conversion of nicotinamide adenine dinucleotide (NAD+) to reduced NAD (NADH), may play a more important role than oxidative phosphorylation for some effects of glucose. To address these molecular mechanisms further, we have examined the regulation of agouti-related peptide (AgRP) in a clonal hypothalamic cell line, N-38. AgRP expression was induced monotonically as glucose concentrations decreased from 10 to 0.5 mm glucose and with increasing concentrations of glycolytic inhibitors. However, neither pyruvate nor 3-β-hydroxybutyrate mimicked the effect of glucose to reduce AgRP mRNA, but on the contrary, produced the opposite effect of glucose and actually increased AgRP mRNA. Nevertheless, 3β-hydroxybutyrate mimicked the effect of glucose to increase ATP and to decrease AMPK phosphorylation. Similarly, inhibition of AMPK by RNA interference increased, and activation of AMPK decreased, AgRP mRNA. Additional studies demonstrated that neither the hexosamine nor the pentose/carbohydrate response element-binding protein pathways mediate the effects of glucose on AgRP expression. These studies do not support that either ATP or AMPK mediate effects of glucose on AgRP in this hypothalamic cell line but support a role for glycolysis and, in particular, NADH. These studies support that cytoplasmic or nuclear NADH, uniquely produced by glucose metabolism, mediates effects of glucose on AgRP expression.

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50

Nesher, R., I. E. Karl, and D. M. Kipnis. "Dissociation of effects of insulin and contraction on glucose transport in rat epitrochlearis muscle." American Journal of Physiology-Cell Physiology 249, no. 3 (September 1, 1985): C226—C232. http://dx.doi.org/10.1152/ajpcell.1985.249.3.c226.

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The effects of insulin and contraction on glucose transport and metabolism were investigated in rat epitrochlearis muscles in vitro. Insulin dose-response curves showed a threshold (approximately 50 microunits/ml) and saturation-type (approximately 1 mU/ml) kinetics, whereas isometric contraction activated glucose transport and metabolism in a linear fashion with no evidence of a threshold. Insulin and contraction increased the apparent maximal rate of uptake of the hexose transport system with minimal effect on its apparent Km. The stimulatory effects of insulin and contraction were additive; similar results were obtained with 2-deoxy-D-glucose. Contraction stimulated glucose transport in three different preparations of muscles depleted of insulin: 1) exhaustively washed for 2 h, 2) rats infused with anti-insulin serum, and 3) chronically (streptozotocin-induced) diabetic rats. Prostaglandin E2 augmented the effect of a submaximal concentration of insulin on glucose transport without exerting any effect by itself but had no effect on contraction-augmented glucose transport. It is concluded that insulin and contraction activate glucose transport and metabolism via independent mechanisms.

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