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Artykuły w czasopismach na temat „Glucose-mediated”

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Data publikacji: 6 września 2023

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1

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption". Endocrinology and Disorders 2, nr 2 (27.02.2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets could lead to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies we demonstrated that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoproteinB concentrations were also increased in subjects consuming fructose, but not those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high fructose corn syrup (HFCS) and sucrose, suggest that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable to that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences fructose consumption in carefully controlled experiments.

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2

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption". Endocrinology and Disorders 2, nr 2 (15.02.2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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Seaquist, E. R., K. Pyzdrowski, A. Moran, A. U. Teuscher i R. P. Robertson. "Insulin-mediated and glucose-mediated glucose uptake following hemipancreatectomy in healthy human donors". Diabetologia 37, nr 10 (1.09.1994): 1036–43. http://dx.doi.org/10.1007/s001250050214.

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4

Seaquist, E. R., K. Pyzdrowski, A. Moran, A. U. Teuscher i R. P. Robertson. "Insulin-mediated and glucose-mediated glucose uptake following hemipancreatectomy in healthy human donors". Diabetologia 37, nr 10 (październik 1994): 1036–43. http://dx.doi.org/10.1007/bf00400467.

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5

Fink, R. I., P. Wallace i J. M. Olefsky. "Effects of aging on glucose-mediated glucose disposal and glucose transport." Journal of Clinical Investigation 77, nr 6 (1.06.1986): 2034–41. http://dx.doi.org/10.1172/jci112533.

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Mohsin, Mahmoud A., Yousef Haik i Tahir Abdulrehman. "Glucose-Mediated Insulin Release Carrier". Polymer Science, Series A 60, nr 5 (wrzesień 2018): 618–27. http://dx.doi.org/10.1134/s0965545x18050097.

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7

Atanasov, P., A. Kaisheva, S. Gamburzev, I. Iliev i S. Bobrin. "Nickelocene-mediated glucose oxidase electrode". Electroanalysis 5, nr 1 (styczeń 1993): 91–97. http://dx.doi.org/10.1002/elan.1140050114.

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8

Patolsky, Fernando, Guoliang Tao, Eugenii Katz i Itamar Willner. "C60-mediated bioelectrocatalyzed oxidation of glucose with glucose oxidase". Journal of Electroanalytical Chemistry 454, nr 1-2 (sierpień 1998): 9–13. http://dx.doi.org/10.1016/s0022-0728(98)00257-5.

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9

Regittnig, W., Z. Trajanoski, G. Brunner, H. J. Leis, T. Pieber i P. Wach. "Glucose-Mediated Glucose Dynamics after Intravenous Glucose Injection in Insulin-Dependent Diabetic Subjects". IFAC Proceedings Volumes 30, nr 2 (marzec 1997): 85–87. http://dx.doi.org/10.1016/s1474-6670(17)44547-2.

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10

Jeon, Won-Yong, Young-Bong Choi, Bo-Hee Lee, Ho-Jin Jo, Soo-Yeon Jeon, Chang-Jun Lee i Hyug-Han Kim. "Glucose detection via Ru-mediated catalytic reaction of glucose dehydrogenase". Advanced Materials Letters 9, nr 3 (2.03.2018): 220–24. http://dx.doi.org/10.5185/amlett.2018.1947.

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11

Murthy, A. Surya N., i Anita. "Benzoquinone-mediated glucose/glucose oxidase reaction at pyrolytic graphite electrode". Electroanalysis 5, nr 3 (kwiecień 1993): 265–68. http://dx.doi.org/10.1002/elan.1140050313.

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12

Taguchi, Masashige, Andre Ptitsyn, Eric S. McLamore i Jonathan C. Claussen. "Nanomaterial-mediated Biosensors for Monitoring Glucose". Journal of Diabetes Science and Technology 8, nr 2 (marzec 2014): 403–11. http://dx.doi.org/10.1177/1932296814522799.

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13

Del Prato, S., P. Castellino, D. C. Simonson i R. A. DeFronzo. "Hyperglucagonemia and insulin-mediated glucose metabolism." Journal of Clinical Investigation 79, nr 2 (1.02.1987): 547–56. http://dx.doi.org/10.1172/jci112846.

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14

Nguyen, An-Lac, i John H. T. Luong. "Mediated glucose biosensor based on polyvinylferrocene". Applied Biochemistry and Biotechnology 43, nr 2 (listopad 1993): 117–32. http://dx.doi.org/10.1007/bf02916436.

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15

Claremont, D. J., Claire Penton i J. C. Pickup. "Potentially-implantable, ferrocene-mediated glucose sensor". Journal of Biomedical Engineering 8, nr 3 (lipiec 1986): 272–74. http://dx.doi.org/10.1016/0141-5425(86)90095-6.

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16

LANNER, J., J. BRUTON, A. KATZ i H. WESTERBLAD. "Ca2+ and insulin-mediated glucose uptake". Current Opinion in Pharmacology 8, nr 3 (czerwiec 2008): 339–45. http://dx.doi.org/10.1016/j.coph.2008.01.006.

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17

Walters, J. M., G. M. Ward, A. Kalfas, J. D. Best i F. P. Alford. "The effect of epinephrine on glucose-mediated and insulin-mediated glucose disposal in insulin-dependent diabetes". Metabolism 41, nr 6 (czerwiec 1992): 671–77. http://dx.doi.org/10.1016/0026-0495(92)90062-f.

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18

Yesudas, Rekha, Russell Snyder, Thomas Abbruscato i Thomas Thekkumkara. "Functional role of sodium glucose transporter in high glucose-mediated angiotensin type 1 receptor downregulation in human proximal tubule cells". American Journal of Physiology-Renal Physiology 303, nr 5 (1.09.2012): F766—F774. http://dx.doi.org/10.1152/ajprenal.00651.2011.

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Previously, we have demonstrated human angiotensin type 1 receptor (hAT1R) promoter architecture with regard to the effect of high glucose (25 mM)-mediated transcriptional repression in human proximal tubule epithelial cells (hPTEC; Thomas BE, Thekkumkara TJ. Mol Biol Cell 15: 4347–4355, 2004). In the present study, we investigated the role of glucose transporters in high glucose-mediated hAT1R repression in primary hPTEC. Cells were exposed to normal glucose (5.5 mM) and high glucose (25 mM), followed by determination of hyperglycemia-mediated changes in receptor expression and glucose transporter activity. Exposure of cells to high glucose resulted in downregulation of ANG II binding (4,034 ± 163.3 to 1,360 ± 154.3 dpm/mg protein) and hAT1R mRNA expression (reduced 60.6 ± 4.643%) at 48 h. Under similar conditions, we observed a significant increase in glucose uptake (influx) in cells exposed to hyperglycemia. Our data indicated that the magnitude of glucose influx is concentration and time dependent. In euglycemic cells, inhibiting sodium-glucose cotransporters (SGLTs) with phlorizin and facilitative glucose transporters (GLUTs) with phloretin decreased glucose influx by 28.57 ± 0.9123 and 54.33 ± 1.202%, respectively. However, inhibiting SGLTs in cells under hyperglycemic conditions decreased glucose influx by 53.67 ± 2.906%, while GLUT-mediated glucose uptake remained unaltered (57.67 ± 3.180%). Furthermore, pretreating cells with an SGLT inhibitor reversed high glucose-mediated downregulation of the hAT1R, suggesting an involvement of SGLT in high glucose-mediated hAT1R repression. Our results suggest that in hPTEC, hyperglycemia-induced hAT1R downregulation is largely mediated through SGLT-dependent glucose influx. As ANG II is an important modulator of hPTEC transcellular sodium reabsorption and function, glucose-mediated changes in hAT1R gene expression may participate in the pathogenesis of diabetic renal disease.

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19

Alatrach, Mariam, Christina Agyin, Rucha Mehta, John Adams, Ralph A. DeFronzo i Muhammad Abdul-Ghani. "Glucose-Mediated Glucose Disposal at Baseline Insulin Is Impaired in IFG". Journal of Clinical Endocrinology & Metabolism 104, nr 1 (26.10.2018): 163–71. http://dx.doi.org/10.1210/jc.2017-01866.

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20

Xianzheng, Sha, Huo Jiwen i Wang Xiuzhang. "Amperometric determination of glucose with a ferrocene-mediated glucose oxidase electrode". Sensors and Actuators B: Chemical 12, nr 1 (marzec 1993): 33–36. http://dx.doi.org/10.1016/0925-4005(93)85009-y.

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21

Zawalich, W. S., K. C. Zawalich, S. Ganesan, R. Calle i H. Rasmussen. "Influence of staurosporine on glucose-mediated and glucose-conditioned insulin secretion". Biochemical Journal 279, nr 3 (1.11.1991): 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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22

Saiepour, Daniel, Janove Sehlin i Per-Arne Oldenborg. "Hyperglycemia-Induced Protein Kinase C Activation Inhibits Phagocytosis of C3b- and Immunoglobulin G–Opsonized Yeast Particles in Normal Human Neutrophils". Experimental Diabesity Research 4, nr 2 (2003): 125–32. http://dx.doi.org/10.1155/edr.2003.125.

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The aim of this study was to investigate the effects of elevated glucose concentrations on complement receptor– and Fcγreceptor–mediated phagocytosis in normal human neutrophils. D-Glucose at 15 or 25 mM dose-dependently inhibited both complement receptor– and Fcγreceptor– mediated phagocytosis, as compared to that at a normal physiological glucose concentration. The protein kinase C (PKC) inhibitors GF109203X and Go6976 both dose dependently and completely reversed the inhibitory effect of 25 mM D-glucose on phagocytosis. Complement receptor– mediated phagocytosis was dose-dependently inhibited by the cell permeable diacylglycerol analogue 1,2-dioctanoylsn- glycerol (DAG), an effect that was abolished by PKC inhibitors. Furthermore, suboptimal inhibitory concentrations of DAG and glucose showed an additive inhibitory effect on complement receptor–mediated phagocytosis. The authors conclude that elevated glucose concentrations can inhibit complement receptor and Fcγreceptor–mediated phagocytosis in normal human neutrophils by activating PKCαand/or PKCβ, an effect possibly mediated by DAG.

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23

Garcia-Ocaña, Adolfo. "Glucose Mediated Regulation of Beta Cell Proliferation". Open Endocrinology Journal 4, nr 1 (1.11.2010): 55–65. http://dx.doi.org/10.2174/1874216501004010055.

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24

Díez, Paula, Berta Esteban-Fernández de Ávila, Doris E. Ramírez-Herrera, Reynaldo Villalonga i Joseph Wang. "Biomedical nanomotors: efficient glucose-mediated insulin release". Nanoscale 9, nr 38 (2017): 14307–11. http://dx.doi.org/10.1039/c7nr05535h.

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Ultrasound-propelled gold/mesoporous silica nanomotors loaded with insulin and functionalized with pH-responsive supramolecular nanovalves are able to release the entrapped hormone autonomously in the presence of d-glucose.

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25

Scampicchio, Matteo, Alessandra Arecchi, Nathan S. Lawrence i Saverio Mannino. "Nylon nanofibrous membrane for mediated glucose biosensing". Sensors and Actuators B: Chemical 145, nr 1 (4.03.2010): 394–97. http://dx.doi.org/10.1016/j.snb.2009.12.042.

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Bagherzadeh-Yazdi, M., M. Bohlooli, M. Khajeh, F. Ghamari, M. Ghaffari-Moghaddam, N. Poormolaie, A. Khatibi, P. Hasanein i N. Sheibani. "Acetoacetate enhancement of glucose mediated DNA glycation". Biochemistry and Biophysics Reports 25 (marzec 2021): 100878. http://dx.doi.org/10.1016/j.bbrep.2020.100878.

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Loisel-Meyer, S., L. Swainson, M. Craveiro, L. Oburoglu, C. Mongellaz, C. Costa, M. Martinez i in. "Glut1-mediated glucose transport regulates HIV infection". Proceedings of the National Academy of Sciences 109, nr 7 (30.01.2012): 2549–54. http://dx.doi.org/10.1073/pnas.1121427109.

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Yokoyama, Kenji, Soo Mi Lee, Eiichi Tamiya, Isao Karube, Kenji Nakajima, Shunichi Uchiyama, Shuichi Suzuki, Minaru Akiyama i Yuzo Masuda. "Mediated glucose sensor using a cylindrical microelectrode". Analytica Chimica Acta 263, nr 1-2 (czerwiec 1992): 101–10. http://dx.doi.org/10.1016/0003-2670(92)85431-5.

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Zheng, Weiran, Yong Li, Chui-Shan Tsang, Liangsheng Hu, Mengjie Liu, Bolong Huang, Lawrence Yoon Suk Lee i Kwok-Yin Wong. "CuII -Mediated Ultra-efficient Electrooxidation of Glucose". ChemElectroChem 4, nr 11 (5.09.2017): 2788–92. http://dx.doi.org/10.1002/celc.201700712.

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Kulys, J., L. Wang, H. E. Hansen, T. Buch-Rasmussen, J. Wang i M. Ozsoz. "Methylene-green-mediated carbon paste glucose biosensor". Electroanalysis 7, nr 1 (styczeń 1995): 92–94. http://dx.doi.org/10.1002/elan.1140070112.

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ROSE, MICHAEL T., FUMIAKI ITOH, MITSUTO MATSUMOTO, YUJI TAKAHASHI i YOSHIAKI OBARA. "Insulin-independent glucose uptake in growth hormone treated dairy cows". Journal of Dairy Research 65, nr 3 (sierpień 1998): 423–31. http://dx.doi.org/10.1017/s0022029998002908.

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Our aim was to determine the effect of growth hormone on non-insulin-mediated glucose disposal in lactating dairy cows. Following 5 d of subcutaneous injections of either saline or growth hormone, insulin, somatostatin or insulin plus somatostatin were infused for 2 h each, in a series of experiments. Coincident with this, unlabelled glucose was infused at a variable rate to maintain a constant plasma glucose concentration. Glucose, doubly labelled with deuterium, was also infused for the calculations of glucose turnover. Plasma insulin levels were reduced to nearly zero by the infusion of somatostatin; under such conditions whole body glucose disposal should be non-insulin-mediated. Dairy cows treated with growth hormone, which had significantly increased milk yields on the day before the experimental infusions, did not have different levels of whole body non-insulin-mediated glucose disposal when expressed in absolute terms. Growth hormone did not affect non-mammary non-insulin-mediated glucose uptake estimated by calculation. Growth hormone significantly inhibited insulin-mediated glucose uptake when plasma insulin levels were elevated. Glucose uptake during insulin plus somatostatin infusion was not significantly different from that of the insulin only infusion.

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Skov-Jensen, Camilla, Mette Skovbro, Anne Flint, Jørn Wulff Helge i Flemming Dela. "Contraction-mediated glucose uptake is increased in men with impaired glucose tolerance". Applied Physiology, Nutrition, and Metabolism 32, nr 1 (luty 2007): 115–24. http://dx.doi.org/10.1139/h06-098.

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Exercise superimposed on insulin stimulation is shown to increase muscle glucose metabolism and these two stimuli have synergistic effects. The objective of this study was to investigate glucose infusion rates (GIR) in groups with a wide variation in terms of insulin sensitivity during insulin stimulation alone and with superimposed exercise. Patients with type 2 diabetes, subjects with impaired glucose tolerance (IGT), healthy controls, and endurance-trained subjects were studied. The groups were matched for age and lean body mass (LBM), and differed in peak oxygen uptake (VO2 peak), body fat percentage, body mass index (BMI), fasting plasma glucose concentration, and oral glucose-tolerance test (OGTT). Each subject underwent a two-step sequential hyperinsulinemic, euglycemic clamp. During the last 30 min of the 2nd clamp step, subjects exercised on a bicycle at 43% ± 2% of VO2 peak. In agreement with the OGTT data, the presence of different GIR during insulin stimulation alone demonstrated varying levels of insulin sensitivity between groups. However, the impairment of GIR in IGT observed during insulin stimulation alone was abolished compared to controls when exercise was superimposed on insulin stimulation. Humans with IGT are resistant to insulin-stimulated but not to exercise-induced glucose uptake.

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Kolka, C. M., S. Rattigan, S. M. Richards, E. J. Barrett i M. G. Clark. "Endothelial Na+-D-glucose Cotransporter: No Role in Insulin-mediated Glucose Uptake". Hormone and Metabolic Research 37, nr 11 (listopad 2005): 657–61. http://dx.doi.org/10.1055/s-2005-870574.

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Caviedes-Vidal, E., i W. H. Karasov. "Glucose and amino acid absorption in house sparrow intestine and its dietary modulation". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, nr 3 (1.09.1996): R561—R568. http://dx.doi.org/10.1152/ajpregu.1996.271.3.r561.

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We acclimated house sparrows (Passer domesticus; 26 g) to high-starch (HS), high-protein (HP), and high-lipid (HL) diets and tested the predictions that uptake of D-glucose and amino acids will be increased with increased levels of dietary carbohydrate and protein, respectively. HS birds had lower mediated D-glucose uptake rate than HP birds. Total uptake of L-leucine at low concentration (0.01 mM), but not of L-proline at 50mM, was increased by dietary protein. Measures of D-glucose maximal mediated uptake (1.2 +/- 0.2 nmol.min-1.mg-1) and intestinal mass (1 g) indicated that the intestine's mediated uptake capacity was only approximately 10% of the D-glucose absorbed at the whole animal level. This implied that nonmediated glucose absorption predominated. We applied a pharmacokinetic technique to measure in vivo absorption of L-glucose, the stereoisomer that does not interact with the Na(+)-glucose cotransporter. At least 75% of L-glucose that was ingested was apparently absorbed. This adds to the increasing evidence that substantial passive glucose absorption occurs in birds and may explain why mediated D-glucose uptake does not increase on high-carbohydrate diets.

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Edelman, S. V., M. Laakso, P. Wallace, G. Brechtel, J. M. Olefsky i A. D. Baron. "Kinetics of Insulin-Mediated and Non-Insulin-Mediated Glucose Uptake in Humans". Diabetes 39, nr 8 (1.08.1990): 955–64. http://dx.doi.org/10.2337/diab.39.8.955.

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Edelman, S. V., M. Laakso, P. Wallace, G. Brechtel, J. M. Olefsky i A. D. Baron. "Kinetics of insulin-mediated and non-insulin-mediated glucose uptake in humans". Diabetes 39, nr 8 (1.08.1990): 955–64. http://dx.doi.org/10.2337/diabetes.39.8.955.

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Heyligenberg, R., J. A. Romijn, M. J. T. Hommes, E. Endert, J. K. M. Eeftinck Schattenkerk i H. P. Sauerwein. "Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men". Clinical Science 84, nr 2 (1.02.1993): 209–16. http://dx.doi.org/10.1042/cs0840209.

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1. One of the metabolic features of acquired immunodeficiency syndrome is increased tissue glucose uptake documented by euglycaemic-hyperinsulinaemic clamp studies, suggesting increased insulin sensitivity. However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. To study the contribution of non-insulin-mediated glucose uptake to total tissue glucose uptake in acquired immunodeficiency syndrome, we conducted a hypoinsulinaemic clamp study in clinically stable human immunodeficiency virus-infected (Centers for Disease Control class IV) men (n = 7) and healthy subjects (n = 5). Glucose uptake was measured by a primed, continuous infusion of [3-3H]glucose in the postabsorptive state and during somatostatin-induced insulinopenia at euglycaemic (≈5.3 mmol/l) and hyperglycaemic (≈11 mmol/l) glucose concentrations. 2. Basal glucose concentration (patients, 5.2 ± 0.1 mmol/l; control subjects, 5.3 ± 0.1 mmol/l) and basal glucose tissue uptake (patients, 15.9 ± 0.5 μmol min−1 kg−1 fat-free mass; control subjects, 15.2 ± 0.4 μmol min−1 kg−1 fat-free mass) were not different between the two groups. 3. Euglycaemic glucose uptake during somatostatin infusion, reflecting non-insulin-mediated glucose uptake, decreased to 82 ± 3% in patients and 78 ± 2% in control subjects (not significant). Under hyperglycaemic (≈11 mmol/l) conditions with sustained insulinopenia, no differences in glucose uptake existed between the two groups (patients, 16.8 ± 0.6 μmol min−1 kg−1 fat-free mass; control subjects, 16.1 ± 0.3 μmol min−1 kg−1 fat-free mass). 4. Our results indicate that non-insulin-mediated glucose uptake is not increased in acquired immunodeficiency syndrome. Therefore the previously described increase in insulin sensitivity in acquired immunodeficiency syndrome during hyperinsulinaemia is explained by a real increase in insulin sensitivity and not by augmented non-insulin-mediated glucose uptake.

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Moreno-Aliaga, M. J., M. M. Swarbrick, S. Lorente-Cebrián, K. L. Stanhope, P. J. Havel i J. A. Martínez. "Sp1-mediated transcription is involved in the induction of leptin by insulin-stimulated glucose metabolism". Journal of Molecular Endocrinology 38, nr 5 (maj 2007): 537–46. http://dx.doi.org/10.1677/jme-06-0034.

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We have previously demonstrated that insulin-stimulated glucose metabolism, and not insulin per se, mediates the effects of insulin to increase the transcriptional activity of the leptin promoter in adipocytes. Here, we sought to identify the specific cis-acting DNA elements required for the upregulation of leptin gene transcription in response to insulin-mediated glucose metabolism. To accomplish this, 3T3-L1 cells and primary rat adipocytes were transfected with a series of luciferase reporter genes containing portions of the mouse leptin promoter. Using this method, we identified an element between −135 and −95 bp (relative to the transcriptional start site) that mediated transcription in response to insulin-stimulated glucose metabolism in adipocytes. This effect was abolished by incubation with 2-deoxy-d-glucose, a competitive inhibitor of glucose metabolism. Gel shift electrophoretic mobility shift assays confirmed that the stimulatory effect of insulin-mediated glucose metabolism on leptin transcription was mediated by a previously identified Sp1 site. Consistent with these findings, incubation of primary rat adipocytes with WP631, a specific inhibitor of specificity protein (Sp)1-dependent transcription, inhibited glucose- and insulin-stimulated, but not basal, leptin secretion. Together, these findings support a key role for Sp1 in the transcriptional activation of the leptin gene promoter by insulin-mediated glucose metabolism.

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Katz, Abram. "Modulation of glucose transport in skeletal muscle by reactive oxygen species". Journal of Applied Physiology 102, nr 4 (kwiecień 2007): 1671–76. http://dx.doi.org/10.1152/japplphysiol.01066.2006.

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Glucose transport is an essential physiological process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the GLUT-4 protein under conditions of increased carbohydrate utilization. The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.

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Yamada, Takashi, Shi-Jin Zhang, Håkan Westerblad i Abram Katz. "β-Hydroxybutyrate inhibits insulin-mediated glucose transport in mouse oxidative muscle". American Journal of Physiology-Endocrinology and Metabolism 299, nr 3 (wrzesień 2010): E364—E373. http://dx.doi.org/10.1152/ajpendo.00142.2010.

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Blood ketone body levels increase during starvation and untreated diabetes. Here we tested the hypothesis that ketone bodies directly inhibit insulin action in skeletal muscle. We investigated the effect of d,l-β-hydroxybutyrate (BOH; the major ketone body in vivo) on insulin-mediated glucose uptake (2-deoxyglucose) in isolated mouse soleus (oxidative) and extensor digitorum longus (EDL; glycolytic) muscle. BOH inhibited insulin-mediated glucose uptake in soleus (but not in EDL) muscle in a time- and concentration-dependent manner. Following 19.5 h of exposure to 5 mM BOH, insulin-mediated (20 mU/ml) glucose uptake was inhibited by ∼90% (substantial inhibition was also observed in 3- O-methylglucose transport). The inhibitory effect of BOH was reproduced with d- but not l-BOH. BOH did not significantly affect hypoxia- or AICAR-mediated (activates AMP-dependent protein kinase) glucose uptake. The BOH effect did not require the presence/utilization of glucose since it was also seen when glucose in the medium was substituted with pyruvate. To determine whether the BOH effect was mediated by oxidative stress, an exogenous antioxidant (1 mM tempol) was used; however, tempol did not reverse the BOH effect on insulin action. BOH did not alter the levels of total tissue GLUT4 protein or insulin-mediated tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 but blocked insulin-mediated phosphorylation of protein kinase B by ∼50%. These data demonstrate that BOH inhibits insulin-mediated glucose transport in oxidative muscle by inhibiting insulin signaling. Thus ketone bodies may be potent diabetogenic agents in vivo.

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Matsumoto, Hitoshi, Yan Xie, Susan Kennedy, Jianyang Luo i Nicholas O. Davidson. "1105 Blocking Intestinal Chylomicron Assembly Improves Systemic Glucose Tolerance Through Incretin Mediated Effects on Glucose Absorption and FGF-15 Mediated Alterations of Hepatic Glucose Metabolism". Gastroenterology 142, nr 5 (maj 2012): S—199—S—200. http://dx.doi.org/10.1016/s0016-5085(12)60748-3.

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KOBAYASHI, Akira, Atsuhiro KOYAMA, Mitsuaki GOTO, Kazukiyo KOBAYASHI, Chia-Wun CHANG, Kosuke TOMITA i Toshihiro AKAIKE. "Glucose Transporter-mediated Dynamic Attachment of Erythrocytes onto a Reducing Glucose-carrying Polystyrene." Proceedings of the Japan Academy. Ser. B: Physical and Biological Sciences 69, nr 4 (1993): 89–94. http://dx.doi.org/10.2183/pjab.69.89.

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Johnston, M., i J. H. Kim. "Glucose as a hormone: receptor-mediated glucose sensing in the yeast Saccharomyces cerevisiae". Biochemical Society Transactions 33, nr 1 (1.02.2005): 247–52. http://dx.doi.org/10.1042/bst0330247.

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Because glucose is the principal carbon and energy source for most cells, most organisms have evolved numerous and sophisticated mechanisms for sensing glucose and responding to it appropriately. This is especially apparent in the yeast Saccharomyces cerevisiae, where these regulatory mechanisms determine the distinctive fermentative metabolism of yeast, a lifestyle it shares with many kinds of tumour cells. Because energy generation by fermentation of glucose is inefficient, yeast cells must vigorously metabolize glucose. They do this, in part, by carefully regulating the first, rate-limiting step of glucose utilization: its transport. Yeast cells have learned how to sense the amount of glucose that is available and respond by expressing the most appropriate of its 17 glucose transporters. They do this through a signal transduction pathway that begins at the cell surface with the Snf3 and Rgt2 glucose sensors and ends in the nucleus with the Rgt1 transcription factor that regulates expression of genes encoding glucose transporters. We explain this glucose signal transduction pathway, and describe how it fits into a highly interconnected regulatory network of glucose sensing pathways that probably evolved to ensure rapid and sensitive response of the cell to changing levels of glucose.

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Mizuma, T. "Intestinal Na+/glucose cotransporter-mediated transport of glucose conjugate formed from disaccharide conjugate". Biochimica et Biophysica Acta (BBA) - General Subjects 1379, nr 1 (8.01.1998): 1–6. http://dx.doi.org/10.1016/s0304-4165(97)00074-3.

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Lange, Mark A., i James Q. Chambers. "Amperometric determination of glucose with a ferrocene-mediated glucose oxidase/polyacrylamide gel electrode". Analytica Chimica Acta 175 (1985): 89–97. http://dx.doi.org/10.1016/s0003-2670(00)82720-8.

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Ching, Congo Tak-Shing, Tai-Ping Sun, Su-Hua Huang, Hsiu-Li Shieh i Chung-Yuan Chen. "A Mediated Glucose Biosensor Incorporated with Reverse Iontophoresis Function for Noninvasive Glucose Monitoring". Annals of Biomedical Engineering 38, nr 4 (20.01.2010): 1548–55. http://dx.doi.org/10.1007/s10439-010-9918-4.

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Liu, Yi, Vishal Javvaji, Srinivasa R. Raghavan, William E. Bentley i Gregory F. Payne. "Glucose Oxidase-Mediated Gelation: A Simple Test To Detect Glucose in Food Products". Journal of Agricultural and Food Chemistry 60, nr 36 (28.08.2012): 8963–67. http://dx.doi.org/10.1021/jf301376b.

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Mangiafico, Salvatore P., Shueh H. Lim, Sandra Neoh, Helene Massinet, Christos N. Joannides, Joseph Proietto, Sofianos Andrikopoulos i Barbara C. Fam. "A primary defect in glucose production alone cannot induce glucose intolerance without defects in insulin secretion". Journal of Endocrinology 210, nr 3 (23.06.2011): 335–47. http://dx.doi.org/10.1530/joe-11-0126.

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Increased glucose production is associated with fasting hyperglycaemia in type 2 diabetes but whether or not it causes glucose intolerance is unclear. This study sought to determine whether a primary defect in gluconeogenesis (GNG) resulting in elevated glucose production is sufficient to induce glucose intolerance in the absence of insulin resistance and impaired insulin secretion. Progression of glucose intolerance was assessed in phosphoenolpyruvate carboxykinase (PEPCK) transgenic rats, a genetic model with a primary increase in GNG. Young (4–5 weeks of age) and adult (12–14 weeks of age) PEPCK transgenic and Piebald Virol Glaxo (PVG/c) control rats were studied. GNG, insulin sensitivity, insulin secretion and glucose tolerance were assessed by intraperitoneal and intravascular substrate tolerance tests and hyperinsulinaemic/euglycaemic clamps. Despite elevated GNG and increased glucose appearance, PEPCK transgenic rats displayed normal glucose tolerance due to adequate glucose disposal and robust glucose-mediated insulin secretion. Glucose intolerance only became apparent in the PEPCK transgenic rats following the development of insulin resistance (both hepatic and peripheral) and defective glucose-mediated insulin secretion. Taken together, a single genetic defect in GNG leading to increased glucose production does not adversely affect glucose tolerance. Insulin resistance and impaired glucose-mediated insulin secretion are required to precipitate glucose intolerance in a setting of chronic glucose oversupply.

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Kubo, K., i J. E. Foley. "Rate-limiting steps for insulin-mediated glucose uptake into perfused rat hindlimb". American Journal of Physiology-Endocrinology and Metabolism 250, nr 1 (1.01.1986): E100—E102. http://dx.doi.org/10.1152/ajpendo.1986.250.1.e100.

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To determine the glucose and insulin concentrations at which glucose transport is rate limiting for insulin-mediated glucose uptake and metabolism in muscle, glucose clearance was determined in the presence of glucose concentrations ranging from trace to 20 mM and in the absence or presence of insulin in the perfused rat hindlimb. In the absence of insulin and at submaximally stimulating insulin concentrations glucose clearance was constant up to 7 mM glucose and then decreased as the glucose concentration was raised. At maximally stimulating insulin concentrations glucose clearance was constant up to 2 mM glucose and then decreased. The decrease in glucose clearance between 2 and 7 mM glucose in the presence of maximally stimulating insulin concentrations could not be accounted for by competition among glucose molecules for the glucose transport system. The results suggest that at physiological glucose concentrations in the presence of maximally stimulating insulin concentrations the rate-limiting step for insulin-mediated glucose uptake and metabolism in muscle shifts from glucose transport to some step beyond transport.

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Agbu, Pamela, i Richard W. Carthew. "MicroRNA-mediated regulation of glucose and lipid metabolism". Nature Reviews Molecular Cell Biology 22, nr 6 (26.03.2021): 425–38. http://dx.doi.org/10.1038/s41580-021-00354-w.

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