Journal articles on the topic 'Glucose uptake'
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1
Taher, Muhammad, Fadzilah Adibah Abdul Majid, and Mohamad Roji Sarmidi. "The Effect of Cinnamtannin B1 on Cell Proliferation and Glucose Uptake of 3T3-L1 Cells." Natural Product Communications 2, no. 1 (January 2007): 1934578X0700200. http://dx.doi.org/10.1177/1934578x0700200112.
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The effects of cinnamtannin B1 on cell proliferation and glucose uptake of 3T3-L1 cells were examined. Cinnamtannin B1 promoted cell proliferation of 3T3-L1 adipocytes at a concentration range between 0.11-0.17 mM. The effect of cinnamtannin B1 on cellular 2-deoxy-D-[1-3H] glucose uptake in differentiated 3T3-L1 adipocytes, following treatment with a 0.11 mM concentration of cinnamtannin B1 for 15, 30 and 60 minutes, was an increase in the glucose uptake from a basal value to 702.0, 1111.0 and 2226.0 cpm, respectively (p<0.005). The comparable glucose uptakes with insulin treatment were 660.0, 1039.0 and 2135.0 cpm, respectively. Wortmannin and cytochalasin B were found to inhibit cinnamtannin B1-stimulated glucose uptake, but sodium orthovanadate increased the glucose uptake.
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Brozinick, J. T., G. J. Etgen, B. B. Yaspelkis, and J. L. Ivy. "Contraction-activated glucose uptake is normal in insulin-resistant muscle of the obese Zucker rat." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 382–87. http://dx.doi.org/10.1152/jappl.1992.73.1.382.
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The rates of muscle glucose uptake of lean and obese Zucker rats were assessed via hindlimb perfusion under basal conditions (no insulin), in the presence of a maximal insulin concentration (10 mU/ml), and after electrically stimulated muscle contraction in the absence of insulin. The perfusate contained 28 mM glucose and 7.5 microCi/mmol of 2-deoxy-D-[3H-(G)]glucose. Glucose uptake rates in the soleus (slow-twitch oxidative fibers), red gastrocnemius (fast-twitch oxidative-glycolytic fibers), and white gastrocnemius (fast-twitch glycolytic fibers) under basal conditions and after electrically stimulated muscle contraction were not significantly different between the lean and obese rats. However, the rate of glucose uptake during insulin stimulation was significantly lower for obese than for lean rats in all three fiber types. Significant correlations were found for insulin-stimulated glucose uptake and glucose transporter protein isoform (GLUT-4) content of soleus, red gastrocnemius, and white gastrocnemius of lean (r = 0.79) and obese (r = 0.65) rats. In contrast, the relationships between contraction-stimulated glucose uptake and muscle GLUT-4 content of lean and obese rats were negligible because of inordinately low contraction-stimulated glucose uptakes by the solei. These results suggest that maximal skeletal muscle glucose uptake of obese Zucker rats is resistant to stimulation by insulin but not to contractile activity. In addition, the relationship between contraction-stimulated glucose uptake and GLUT-4 content appears to be fiber-type specific.
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OKAMOTO, MIKIKO, MOTOZUMI OKAMOTO, HARUO NISHIMURA, ATSUSHI KOSAKI, SHIGEO KONO, GEN INOUE, IKUKO MAEDA, et al. "Insulin-Stimulated Glucose Uptake and Fasting Blood Glucose." Endocrinologia Japonica 38, no. 4 (1991): 421–27. http://dx.doi.org/10.1507/endocrj1954.38.421.
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Galassetti, Pietro, Masakazu Shiota, Brad A. Zinker, David H. Wasserman, and Alan D. Cherrington. "A negative arterial-portal venous glucose gradient decreases skeletal muscle glucose uptake." American Journal of Physiology-Endocrinology and Metabolism 275, no. 1 (July 1, 1998): E101—E111. http://dx.doi.org/10.1152/ajpendo.1998.275.1.e101.
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The effect of a negative arterial-portal venous (a-pv) glucose gradient on skeletal muscle and whole body nonhepatic glucose uptake was studied in 12 42-h-fasted conscious dogs. Each study consisted of a 110-min equilibration period, a 30-min baseline period, and two 120-min hyperglycemic (2-fold basal) periods (either peripheral or intraportal glucose infusion). Somatostatin was infused along with insulin (3 × basal) and glucagon (basal). Catheters were inserted 17 days before studies in the external iliac artery and hepatic, portal and common iliac veins. Blood flow was measured in liver and hindlimb using Doppler flow probes. The arterial blood glucose, arterial plasma insulin, arterial plasma glucagon, and hindlimb glucose loads were similar during peripheral and intraportal glucose infusions. The a-pv glucose gradient (in mg/dl) was 5 ± 1 during peripheral and −18 ± 3 during intraportal glucose infusion. The net hindlimb glucose uptakes (in mg/min) were 5.0 ± 1.2, 20.4 ± 4.5, and 14.8 ± 3.2 during baseline, peripheral, and intraportal glucose infusion periods, respectively ( P < 0.01, peripheral vs. intraportal); the hindlimb glucose fractional extractions (in %) were 2.8 ± 0.4, 4.7 ± 0.8, and 3.9 ± 0.5 during baseline, peripheral, and intraportal glucose infusions, respectively ( P < 0.05, peripheral vs. intraportal). The net whole body nonhepatic glucose uptakes (in mg ⋅ kg−1⋅ min−1) were 1.6 ± 0.1, 7.9 ± 1.3, and 5.4 ± 1.1 during baseline, peripheral, and intraportal glucose infusion, respectively ( P < 0.05, peripheral vs. intraportal). In the liver, net glucose uptake was 70% greater during intraportal than during peripheral glucose infusion (5.8 ± 0.7 vs. 3.4 ± 0.4 mg ⋅ kg−1⋅ min−1). In conclusion, despite comparable glucose loads and insulin levels, hindlimb and whole body net nonhepatic glucose uptake decreased significantly during portal venous glucose infusion, suggesting that a negative a-pv glucose gradient leads to an inhibitory signal in nonhepatic tissues, among which skeletal muscle appears to be the most important.
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Rottman, Jeffrey N., Deanna Bracy, Carlo Malabanan, Zou Yue, Jeff Clanton, and David H. Wasserman. "Contrasting effects of exercise and NOS inhibition on tissue-specific fatty acid and glucose uptake in mice." American Journal of Physiology-Endocrinology and Metabolism 283, no. 1 (July 1, 2002): E116—E123. http://dx.doi.org/10.1152/ajpendo.00545.2001.
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Isotopic techniques were used to test the hypothesis that exercise and nitric oxide synthase (NOS) inhibition have distinct effects on tissue-specific fatty acid and glucose uptakes in a conscious, chronically catheterized mouse model. Uptakes were measured using the radioactive tracers125I-labeled β-methyl- p-iodophenylpentadecanoic acid (BMIPP) and deoxy-[2-3H]glucose (DG) during treadmill exercise with and without inhibition of NOS. [125I]BMIPP uptake at rest differed substantially among tissues with the highest levels in heart. With exercise, [125I]BMIPP uptake increased in both heart and skeletal muscles. In sedentary mice, NOS inhibition induced by nitro-l-arginine methyl ester (l-NAME) feeding increased heart and soleus [125I]BMIPP uptake. In contrast, exercise, but not l-NAME feeding, resulted in increased heart and skeletal muscle [2-3H]DG uptake. Significant interactions were not observed in the effects of combined exercise and l-NAME feeding on [125I]BMIPP and [2-3H]DG uptakes. In the conscious mouse, exercise and NOS inhibition produce distinct patterns of tissue-specific fatty acid and glucose uptake; NOS is not required for important components of exercise-associated metabolic signaling, or other mechanisms compensate for the absence of this regulatory mechanism.
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Nuutila, P., M. J. Knuuti, M. Raitakari, U. Ruotsalainen, M. Teras, L. M. Voipio-Pulkki, M. Haaparanta, O. Solin, U. Wegelius, and H. Yki-Jarvinen. "Effect of antilipolysis on heart and skeletal muscle glucose uptake in overnight fasted humans." American Journal of Physiology-Endocrinology and Metabolism 267, no. 6 (December 1, 1994): E941—E946. http://dx.doi.org/10.1152/ajpendo.1994.267.6.e941.
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We quantitated how lowering of free fatty acid (FFA) by an antilipolytic agent (acipimox) in the fasting state changes glucose uptake in heart and skeletal muscles. Glucose uptake in these tissues was measured two times in seven normal subjects, once after acipimox and once after placebo, using positron emission tomography-derived [18F]fluoro-2-deoxy-D-glucose kinetics. Plasma glucose and insulin remained at their fasting concentrations in both studies. Fasting FFA concentrations were 60% lower after acipimox (238 +/- 39) than placebo (645 +/- 78 mumol/l, P < 0.001). Glucose uptake increased 6 +/- 2-fold in the heart by acipimox (344 +/- 49 vs. 108 +/- 40 mumol.kg muscle-1.min-1, P < 0.002) and 1.5-fold in arm muscles (27.7 +/- 2.6 vs. 18.6 +/- 1.2 mumol.kg muscle-1.min-1, P < 0.02). Heart (r = -0.93, P < 0.001) and arm (r = -0.82, P < 0.001) glucose uptakes were inversely related to serum FFA. We conclude that serum FFA are inversely related to glucose uptake in heart and arm skeletal muscles after an overnight fast. These data indicate that compensatory glycogenolysis, although it may occur, does not prevent operation of the glucose-FFA cycle under fasting conditions.
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Huang, Jianpan, Peter C. M. van Zijl, Xiongqi Han, Celia M. Dong, Gerald W. Y. Cheng, Kai-Hei Tse, Linda Knutsson, et al. "Altered d-glucose in brain parenchyma and cerebrospinal fluid of early Alzheimer’s disease detected by dynamic glucose-enhanced MRI." Science Advances 6, no. 20 (May 2020): eaba3884. http://dx.doi.org/10.1126/sciadv.aba3884.
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Altered cerebral glucose uptake is one of the hallmarks of Alzheimer’s disease (AD). A dynamic glucose-enhanced (DGE) magnetic resonance imaging (MRI) approach was developed to simultaneously monitor d-glucose uptake and clearance in both brain parenchyma and cerebrospinal fluid (CSF). We observed substantially higher uptake in parenchyma of young (6 months) transgenic AD mice compared to age-matched wild-type (WT) mice. Notably lower uptakes were observed in parenchyma and CSF of old (16 months) AD mice. Both young and old AD mice had an obviously slower CSF clearance than age-matched WT mice. This resembles recent reports of the hampered CSF clearance that leads to protein accumulation in the brain. These findings suggest that DGE MRI can identify altered glucose uptake and clearance in young AD mice upon the emergence of amyloid plaques. DGE MRI of brain parenchyma and CSF has potential for early AD stratification, especially at 3T clinical field strength MRI.
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de la Torre, Alejandro J., Daniela Rogoff, and Perrin C. White. "P53 and Cellular Glucose Uptake." Endocrine Research 38, no. 1 (August 2, 2012): 32–39. http://dx.doi.org/10.3109/07435800.2012.710883.
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Hutchinson, Lisa. "Novel glucose uptake imaging method." Nature Reviews Clinical Oncology 10, no. 9 (July 16, 2013): 488. http://dx.doi.org/10.1038/nrclinonc.2013.130.
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Khanna, S. "Glucose uptake by Cellulomonas fimi." World Journal of Microbiology & Biotechnology 9, no. 5 (September 1993): 559–61. http://dx.doi.org/10.1007/bf00386293.
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Teng, Cecilia, Frederick C. Battaglia, Giacomo Meschia, Michael R. Narkewicz, and Randall B. Wilkening. "Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion." American Journal of Physiology-Endocrinology and Metabolism 282, no. 3 (March 1, 2002): E542—E550. http://dx.doi.org/10.1152/ajpendo.00248.2001.
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To test the hypothesis that fetal hepatic glutamate output diverts the products of hepatic amino acid metabolism from hepatic gluconeogenesis, ovine fetal hepatic and umbilical uptakes of glucose and glucogenic substrates were measured before and during fetal glucagon-somatostatin (GS) infusion and during the combined infusion of GS, alanine, glutamine, and arginine. Before the infusions, hepatic uptake of lactate, alanine, glutamine, arginine, and other substrates was accompanied by hepatic output of pyruvate, aspartate, serine, glutamate, and ornithine. The GS infusion induced hepatic output of 1.00 ± 0.07 mol glucose carbon/mol O2 uptake, an equivalent reduction in hepatic output of pyruvate and glutamate carbon, a decrease in umbilical glucose uptake and placental uptake of fetal glutamate, an increase in hepatic alanine and arginine clearances, and a decrease in umbilical alanine, glutamine, and arginine uptakes. The latter result suggests that glucagon inhibits umbilical amino acid uptake. We conclude that fetal hepatic pyruvate and glutamate output is part of an adaptation to placental function that requires the fetal liver to maintain both a high rate of catabolism of glucogenic substrates and a low rate of gluconeogenesis.
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Galassetti, Pietro, Yoshiharu Koyama, Robert H. Coker, Drury B. Lacy, Alan D. Cherrington, and David H. Wasserman. "Role of a negative arterial-portal venous glucose gradient in the postexercise state." American Journal of Physiology-Endocrinology and Metabolism 277, no. 6 (December 1, 1999): E1038—E1045. http://dx.doi.org/10.1152/ajpendo.1999.277.6.e1038.
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Prior exercise stimulates muscle and liver glucose uptake. A negative arterial-portal venous glucose gradient (a-pv grad) stimulates resting net hepatic glucose uptake (NHGU) but reduces muscle glucose uptake. This study investigates the effects of a negative a-pv grad during glucose administration after exercise in dogs. Experimental protocol: exercise (−180 to −30 min), transition (−30 to −20 min), basal period (−20 to 0 min), and experimental period (0 to 100 min). In the experimental period, 130 mg/dl arterial hyperglycemia was induced via vena cava (Pe, n = 6) or portal vein (Po, n = 6) glucose infusions. Insulin and glucagon were replaced at fourfold basal and basal rates. During the experimental period, the a-pv grad (mg/dl) was 3 ± 1 in Pe and −10 ± 2 in Po. Arterial insulin and glucagon were similar in the two groups. In Pe, net hepatic glucose balance (mg ⋅ kg−1⋅ min−1, negative = uptake) was 4.2 ± 0.3 (basal period) and −1.2 ± 0.3 (glucose infusion); in Po it was 4.1 ± 0.5 and −3.2 ± 0.4, respectively ( P < 0.005 vs. Pe). Total glucose infusion (mg ⋅ kg−1⋅ min−1) was 11 ± 1 in Po and 8 ± 1 in Pe ( P < 0.05). Net hindlimb and whole body nonhepatic glucose uptakes were similar. Conclusions: the portal signal independently stimulates NHGU after exercise. Conversely, prior exercise eliminates the inhibitory effect of the portal signal on glucose uptake by nonhepatic tissues. The portal signal therefore increases whole body glucose disposal after exercise by an amount equal to the increase in NHGU.
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Landau, Bernard R., Chandra L. Spring-Robinson, Raymond F. Muzic, Nadia Rachdaoui, Darrell Rubin, Marc S. Berridge, William C. Schumann, Visvanathan Chandramouli, Timothy S. Kern, and Faramarz Ismail-Beigi. "6-Fluoro-6-deoxy-d-glucose as a tracer of glucose transport." American Journal of Physiology-Endocrinology and Metabolism 293, no. 1 (July 2007): E237—E245. http://dx.doi.org/10.1152/ajpendo.00022.2007.
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Glucose transport rates are estimated noninvasively in physiological and pathological states by kinetic imaging using PET. The glucose analog most often used is 18F-labeled 2FDG. Compared with glucose, 2FDG is poorly transported by intestine and kidney. We examined the possible use of 6FDG as a tracer of glucose transport. Lacking a hydroxyl at its 6th position, 6FDG cannot be phosphorylated as 2FDG is. Prior studies have shown that 6FDG competes with glucose for transport in yeast and is actively transported by intestine. Its uptake by muscle has been reported to be unresponsive to insulin, but that study is suspect. We found that insulin stimulated 6FDG uptake 1.6-fold in 3T3-L1 adipocytes and azide stimulated the uptake 3.7-fold in Clone 9 cells. Stimulations of the uptake of 3OMG, commonly used in transport assays, were similar, and the uptakes were inhibited by cyclochalasin B. Glucose transport is by GLUT1 and GLUT4 transporters in 3T3-L1 adipocyte and by the GLUT1 transporter in Clone 9 cells. Cytochalasin B inhibits those transporters. Rats were also imaged in vivo by PET using 618FDG. There was no excretion of 18F into the urinary bladder unless phlorizin, an inhibitor of active renal transport, was also injected. 18F activity in brain, liver, and heart over the time of scanning reached a constant level, in keeping with the 6FDG being distributed in body water. In contrast, 18F from 218FDG was excreted in relatively large amounts into the bladder, and 18F activity rose with time in heart and brain in accord with accumulation of 218FDG-6-P in those organs. We conclude that 6FDG is actively transported by kidney as well as intestine and is insulin responsive. In trace quantity, it appears to be distributed in body water unchanged. These results provide support for its use as a valid tracer of glucose transport.
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Richter, E. A., B. F. Hansen, and S. A. Hansen. "Glucose-induced insulin resistance of skeletal-muscle glucose transport and uptake." Biochemical Journal 252, no. 3 (June 15, 1988): 733–37. http://dx.doi.org/10.1042/bj2520733.
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The ability of glucose and insulin to modify insulin-stimulated glucose transport and uptake was investigated in perfused skeletal muscle. Here we report that perfusion of isolated rat hindlimbs for 5 h with 12 mM-glucose and 20,000 microunits of insulin/ml leads to marked, rapidly developing, impairment of insulin action on muscle glucose transport and uptake. Thus maximal insulin-stimulated glucose uptake at 12 mM-glucose decreased from 34.8 +/- 1.9 to 11.5 +/- 1.1 mumol/h per g (mean +/- S.E.M., n = 10) during 5 h perfusion. This decrease in glucose uptake was accompanied by a similar change in muscle glucose transport as measured by uptake of 3-O-[14C]-methylglucose. Simultaneously, muscle glycogen stores increased to 2-3.5 times initial values, depending on fibre type. Perfusion for 5 h in the presence of glucose but in the absence of insulin decreased subsequent insulin action on glucose uptake by 80% of the effect of glucose with insulin, but without an increase in muscle glycogen concentration. Perfusion for 5 h with insulin but without glucose, and with subsequent addition of glucose back to the perfusate, revealed glucose uptake and transport similar to initial values obtained in the presence of glucose and insulin. The data indicate that exposure to a moderately increased glucose concentration (12 mM) leads to rapidly developing resistance of skeletal-muscle glucose transport and uptake to maximal insulin stimulation. The effect of glucose is enhanced by simultaneous insulin exposure, whereas exposure for 5 h to insulin itself does not cause measurable resistance to maximal insulin stimulation.
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Li, Tingting, Jie Xu, Xinghua Qin, Zuoxu Hou, Yongzheng Guo, Zhenhua Liu, Jianjiang Wu, Hong Zheng, Xing Zhang, and Feng Gao. "Glucose oxidation positively regulates glucose uptake and improves cardiac function recovery after myocardial reperfusion." American Journal of Physiology-Endocrinology and Metabolism 313, no. 5 (November 1, 2017): E577—E585. http://dx.doi.org/10.1152/ajpendo.00014.2017.
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Myocardial reperfusion decreases glucose oxidation and uncouples glucose oxidation from glycolysis. Therapies that increase glucose oxidation lessen myocardial ischemia-reperfusion (I/R) injury. However, the regulation of glucose uptake during reperfusion remains poorly understood. We found that glucose uptake was remarkably diminished in the myocardium following reperfusion in Sprague-Dawley rats as detected by 18F–labeled and fluorescent-labeled glucose analogs, even though GLUT1 was upregulated by threefold and GLUT4 translocation remained unchanged compared with those of sham-treated rats. The decreased glucose uptake was accompanied by suppressed glucose oxidation. Interestingly, stimulating glucose oxidation by inhibition of pyruvate dehydrogenase kinase 4 (PDK4), a rate-limiting enzyme for glucose oxidation, increased glucose uptake and alleviated I/R injury. In vitro data in neonatal myocytes showed that PDK4 overexpression decreased glucose uptake, whereas its knockdown increased glucose uptake, suggesting that PDK4 has a role in regulating glucose uptake. Moreover, inhibition of PDK4 increased myocardial glucose uptake with concomitant enhancement of cardiac insulin sensitivity following myocardial I/R. These results showed that the suppressed glucose oxidation mediated by PDK4 contributes to the reduced glucose uptake in the myocardium following reperfusion, and enhancement of glucose uptake exerts cardioprotection. The findings suggest that stimulating glucose oxidation via PDK4 could be an efficient approach to improve recovery from myocardial I/R injury.
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Cheung, P. T., and M. R. Hammerman. "Na+-independent D-glucose transport in rabbit renal basolateral membranes." American Journal of Physiology-Renal Physiology 254, no. 5 (May 1, 1988): F711—F718. http://dx.doi.org/10.1152/ajprenal.1988.254.5.f711.
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To define the mechanism by which glucose is transported across the basolateral membrane of the renal proximal tubular cell, we measured D-[14C]glucose uptake in basolateral membrane vesicles from rabbit kidney. Na+-dependent D-glucose transport, demonstrable in brush-border vesicles, could not be demonstrated in basolateral membrane vesicles. In the absence of Na+, the uptake of D-[14C]glucose in basolateral vesicles was more rapid than that of L-[3H]glucose over a concentration range of 1-50 mM. Subtraction of the latter from the former uptakes revealed a saturable process with apparent Km of 9.9 mM and Vmax of 0.80 nmol.mg protein-1.s-1. To characterize the transport component of D-glucose uptake in basolateral vesicles, we measured trans stimulation of 2 mM D-[14C]glucose entry in the absence of Na+. Trans stimulation could be effected by preloading basolateral vesicles with D-glucose, 2-deoxy-D-glucose, or 3-O-methyl-D-glucose, but not with L-glucose or alpha-methyl-D-glucoside. Trans-stimulated D-[14C]glucose uptake was inhibited by 0.1 mM phloretin or cytochalasin B but not phlorizin. In contrast, Na+-dependent D-[14C]glucose transport in brush-border vesicles was inhibited by phlorizin but not phloretin or cytochalasin B. Our findings are consistent with the presence of a Na+-independent D-glucose transporter in the proximal tubular basolateral membrane with characteristics similar to those of transporters present in nonepithelial cells.
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Rosenkrantz, Ted S., Anthony F. Philipps, Isabella Knox, Edwin L. Zalneraitis, Patricia J. Porte, Peter E. Skrzypczak, and John R. Raye. "Regulation of Cerebral Glucose Metabolism in Normal and Polycythemic Newborn Lambs." Journal of Cerebral Blood Flow & Metabolism 12, no. 5 (September 1992): 856–65. http://dx.doi.org/10.1038/jcbfm.1992.117.
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In contrast to previous investigations, a recent study of polycythemic lambs suggested that cerebral glucose delivery (concentration × blood flow), not arterial glucose concentration, determined cerebral glucose uptake. In the present study, the independent effects of arterial glucose concentration and delivery on cerebral glucose uptake were examined in two groups of chronically catheterized newborn lambs (control and polycythemic). Arterial glucose concentration was varied by an infusion of insulin. CBF was reduced in one group of lambs (polycythemic) by increasing the hematocrit. At all arterial glucose concentrations, the cerebral glucose delivery of the polycythemic group was 59.6% of the control group. At arterial glucose concentrations of > 1.6 mmol/L, cerebral glucose uptake was constant and similar in both groups. At arterial glucose concentrations of ≤1.6 mmol/L, cerebral glucose uptake was unchanged in the control group, but was significantly decreased in the polycythemic group. In contrast, the cerebral glucose uptake was similar in both groups over a broad range of cerebral glucose delivery values. At cerebral glucose delivery values ≤83 μmol/min/100 g, there was a significant decrease in cerebral glucose uptake in both groups. During periods of low cerebral glucose delivery and uptake, cerebral oxygen uptake fell in the control group but remained unchanged in the polycythemic group. Maintenance of cerebral oxygen uptake in the polycythemic group was associated with an increased extraction and uptake of lactate and β-hydroxybutyrate. We conclude that cerebral glucose delivery, not arterial glucose concentration alone, determines cerebral glucose uptake.
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Leury, B. J., A. R. Bird, K. D. Chandler, and A. W. Bell. "Glucose partitioning in the pregnant ewe: Effects of undernutrition and exercise." British Journal of Nutrition 64, no. 2 (September 1990): 449–62. http://dx.doi.org/10.1079/bjn19900045.
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Maternal whole-body glucose entry rate and uterine and umbilical net uptakes of glucose and oxygen were measured in single-pregnant ewes which were either well-fed throughout, or fed at 0.3–0.4 predicted energy requirement for 7–21 d during late pregnancy. All ewes were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min. Underfed ewes suffered significant decreases in live weight and had lower fetal, but not placental, weights at 140–144 d gestation. Undernutrition also caused large decreases in maternal glycaemia and glucose entry rate, which were associated with equally large decreases in uterine and umbilical net uptakes and O2 quotients of glucose, and with a decrease in placental glucose transfer capacity. Exercise caused increases in maternal blood concentration, entry rate and uterine net uptake of glucose, the magnitudes of which were not significantly affected by plane of nutrition. Umbilical glucose uptake and placental glucose transfer capacity increased during exercise in underfed but not fed ewes. The fractional distribution of maternal glucose to the pregnant uterus, and of uterine glucose uptake to the fetus, were unaltered by undernutrition; during exercise, a disproportionately small fraction of the increased maternal glucose supply went to the uterus. The results confirm that the ovine conceptus responds to nutritional reduction in maternal glucose availability in a manner similar to non-uterine maternal tissues. Major reductions in glucose supply appear to override putative glucose-sparing mechanisms which may operate to favour the conceptus in better-nourished animals.
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Marmy-Conus, N., S. Fabris, J. Proietto, and M. Hargreaves. "Preexercise glucose ingestion and glucose kinetics during exercise." Journal of Applied Physiology 81, no. 2 (August 1, 1996): 853–57. http://dx.doi.org/10.1152/jappl.1996.81.2.853.
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The present study was undertaken to examine the effects of glucose ingestion before exercise on liver glucose output and muscle glucose uptake during exercise. On two occasions, at least 1 wk apart, six trained men (peak pulmonary O2 uptake = 5.11 +/- 0.17 l/min) ingested 400 ml of a solution containing either 75 g glucose [carbohydrate (CHO)] or a sweet placebo [control (Con)] 30 min before 60 min of exercise at 71 +/- 1% peak pulmonary O2 uptake. Glucose kinetics (rates of appearance and disappearance) were measured by a primed continuous infusion of [6,6–2H2]glucose. Liver glucose output was derived from total glucose appearance and the appearance of ingested glucose from the gut. After glucose ingestion, plasma glucose increased to 6.4 +/- 0.4 mmol/l immediately before exercise, fell to 4.2 +/- 0.5 mmol/l after 20 min of exercise, and then increased to a higher value than in the Con group (5.4 +/- 0.3 vs. 4.7 +/- 0.1 mmol/l; P < 0.05) after 60 min of exercise. In the CHO group, plasma insulin was higher immediately before exercise (P < 0.05) and, despite falling during exercise, remained higher than in the Con group after 60 min of exercise (57.0 +/- 11.4 vs. 24.8 +/- 1.7 pmol/l; P < 0.05). The rapid fall in plasma glucose in the CHO group was the result of a higher muscle glucose uptake with the onset of exercise (P < 0.05), which could not be matched by the glucose rate of appearance. Liver glucose output was decreased by glucose ingestion, and although it increased during the early stages of exercise in the CHO group, it did not rise above the basal values and was reduced by 62% over the 60 min of exercise compared with the Con group. In summary, preexercise glucose ingestion results in increased muscle glucose uptake and reduced liver glucose output during exercise.
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Chandler, K. D., B. J. Leury, A. R. Bird, and A. W. Bell. "Effects of undernutrition and exercise during late pregnancy on uterine, fetal and uteroplacental metabolism in the ewe." British Journal of Nutrition 53, no. 3 (May 1985): 625–35. http://dx.doi.org/10.1079/bjn19850072.
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1. Uterine, umbilical and, by difference, uteroplacental net uptakes of oxygen, glucose, lactate and 3-hydroxybutyrate (uterine uptake only) were measured in single-pregnant ewes which were either well-fed throughout, or severely undernourished for 8–20 d during late pregnancy. All animals were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min.2. Undernutrition did not significantly affect fetal or placental weights at 143 d gestation but caused a 14% decrease in maternal live weight. Uterine blood flow was decreased by 32% and was associated with a significant decrease in uteroplacental oxygen uptake; neither umbilical blood flow nor fetal O2, uptake were affected by maternal plane of nutrition. Maternal and fetal hypoglycaemia in underfed ewes was accompanied by 46–63 % decreases in uterine, umbilical and uteroplacental net uptakes of glucose, and similar declines in uterine and umbilical glucose/O, quotients. Moderate maternal hyperketonaemia was associated with 2.5-fold and 3-fold increases in uterine net uptake of 3-hydroxybutyrate and 3-hydroxybutyrate/O2 quotient respectively.3. Exercise caused significant decreases in uterine blood flow in fed and underfed ewes but did not affect uterine or umbilical O2 uptakes; uterine net glucose uptake increased in most ewes but umbilical uptake was not significantly affected. Umbilical net uptake of lactate was significantly reduced. In underfed ewes, the extent of hyperketonaemia was significantly reduced by exercise.4. Contrary to earlier proposals, the ovine pregnant uterus is sensitive and adaptable to long- and short-term alterations in maternal energy balance, as achieved by chronic undernutrition and exercise respectively. Thus, the fetus and placenta significantly add to, but do not necessarily have priority over the energy demands of other tissues of the ewe.
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Fueger, Patrick T. "GLUCOSE PHOSPHORYLATION AS A BARRIER TO MUSCLE GLUCOSE UPTAKE." Clinical and Experimental Pharmacology and Physiology 32, no. 4 (April 2005): 314–18. http://dx.doi.org/10.1111/j.1440-1681.2005.04190.x.
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Alatrach, Mariam, Christina Agyin, John Adams, Ralph A. DeFronzo, and Muhammad A. Abdul-Ghani. "Decreased basal hepatic glucose uptake in impaired fasting glucose." Diabetologia 60, no. 7 (March 22, 2017): 1325–32. http://dx.doi.org/10.1007/s00125-017-4252-0.
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Nedachi, Taku, and Makoto Kanzaki. "Regulation of glucose transporters by insulin and extracellular glucose in C2C12 myotubes." American Journal of Physiology-Endocrinology and Metabolism 291, no. 4 (October 2006): E817—E828. http://dx.doi.org/10.1152/ajpendo.00194.2006.
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It is well established that insulin stimulation of glucose uptake in skeletal muscle cells is mediated through translocation of GLUT4 from intracellular storage sites to the cell surface. However, the established skeletal muscle cell lines, with the exception of L6 myocytes, reportedly show minimal insulin-dependent glucose uptake and GLUT4 translocation. Using C2C12 myocytes expressing exofacial-Myc-GLUT4-enhanced cyan fluorescent protein, we herein show that differentiated C2C12 myotubes are equipped with basic GLUT4 translocation machinery that can be activated by insulin stimulation (∼3-fold increase as assessed by anti-Myc antibody uptake and immunostaining assay). However, this insulin stimulation of GLUT4 translocation was difficult to demonstrate with a conventional 2-deoxyglucose uptake assay because of markedly elevated basal glucose uptake via other glucose transporter(s). Intriguingly, the basal glucose transport activity in C2C12 myotubes appeared to be acutely suppressed within 5 min by preincubation with a pathophysiologically high level of extracellular glucose (25 mM). In contrast, this activity was augmented by acute glucose deprivation via an unidentified mechanism that is independent of GLUT4 translocation but is dependent on phosphatidylinositol 3-kinase activity. Taken together, these findings indicate that regulation of the facilitative glucose transport system in differentiated C2C12 myotubes can be achieved through surprisingly acute glucose-dependent modulation of the activity of glucose transporter(s), which apparently contributes to obscuring the insulin augmentation of glucose uptake elicited by GLUT4 translocation. We herein also describe several methods of monitoring insulin-dependent glucose uptake in C2C12 myotubes and propose this cell line to be a useful model for analyzing GLUT4 translocation in skeletal muscle.
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Milley, J. R. "Exogenous substrate uptake by fetal lambs during reduced glucose delivery." American Journal of Physiology-Endocrinology and Metabolism 264, no. 2 (February 1, 1993): E250—E256. http://dx.doi.org/10.1152/ajpendo.1993.264.2.e250.
Full textAbstract:
Normally, metabolism of exogenous glucose accounts for one-half of the normal fetal metabolic rate. When fetal glucose delivery is restricted for 2 wk, endogenous production increases to maintain glucose use. Such increased glucose production must originate either from increased uptake of other exogenous substrates (lactate or amino acids) or from use of endogenous substrates (via glycogenolysis or gluconeogenesis). Our purpose was to find if exogenous fetal substrate uptake increased during decreased fetal glucose delivery. Catheters were placed in eight lamb fetuses under general maternal anesthesia, and the animals were allowed 6 days to recover. Umbilical venoarterial blood concentration differences of antipyrine (during fetal antipyrine infusion), glucose, lactate, amino nitrogen-containing substances, and oxygen were measured before and after fetal glucose delivery was diminished by 3 h of maternal insulin infusion (5-10 mU.kg-1.m-1). Fetal substrate uptakes and substrate/oxygen quotients (i.e., the proportion of oxidative metabolism supported by complete oxidation of each exogenous substrate) were calculated. No increase occurred in the uptake of other exogenous substrates during deficient glucose delivery. Because even complete oxidation of all exogenous substrates did not meet fetal oxidative requirements, the fetus must oxidize endogenous substrates. If such a pattern of substrate use were to continue, fetal growth retardation would result.
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Moore, M. C., M. J. Pagliassotti, L. L. Swift, J. Asher, J. Murrell, D. Neal, and A. D. Cherrington. "Disposition of a mixed meal by the conscious dog." American Journal of Physiology-Endocrinology and Metabolism 266, no. 4 (April 1, 1994): E666—E675. http://dx.doi.org/10.1152/ajpendo.1994.266.4.e666.
Full textAbstract:
The disposition of a mixed meal administered intragastrically was examined in 13 24-h-fasted conscious dogs, using the arteriovenous (AV) difference technique (and isotopic methods in 6 dogs). Postprandial net gut output totaled (in g of glucose equivalents) 42 +/- 6 glucose, 3 +/- 0.3 lactate, 2 +/- 0.2 alanine, and 0.2 +/- 0.0 glycerol. The gut oxidized 2 +/- 1 g of glucose, and 0.2 +/- 0.1 g remained within the intestinal lumen. Of the administered glucose 68 +/- 6% were accounted for, and volatile fatty acid production by the gut (n = 1) accounted for at least an additional 4%. Of the labeled glucose in the meal 82 +/- 5% appeared in the systemic circulation, an apparent overestimate of absorption of glucose from the meal. Cumulative net hepatic uptakes (in g of glucose equivalents) were 4.1 +/- 3.1 glucose, 12.1 +/- 2.1 gluconeogenic amino acids, and 1.5 +/- 0.2 glycerol. Net hepatic glycogen synthesis and lactate and CO2 production accounted for 6.2 +/- 4.1, 9.3 +/- 2.8, and 1.6 +/- 0.8 g of glucose equivalents, respectively. In summary, the AV difference method could account for the gut disposition of about two-thirds of the meal glucose. Nonsplanchnic tissues disposed of threefold more glucose than the liver. Net hepatic uptake of glucose equivalents as gluconeogenic amino acids was threefold > glucose uptake, and net hepatic uptake of gluconeogenic amino acids was > net gut release of gluconeogenic amino acids. In conclusion, the net hepatic uptake of glucose and gluconeogenic substrates provided adequate carbon for net hepatic synthesis of glycogen and production of lactate and CO2. In a net sense, peripheral tissues must have been the source of some of the gluconeogenic carbon taken up by the liver after the meal.
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Hunt, Desmond G., Zhenping Ding, and John L. Ivy. "Propranolol prevents epinephrine from limiting insulin-stimulated muscle glucose uptake during contraction." Journal of Applied Physiology 93, no. 2 (August 1, 2002): 697–704. http://dx.doi.org/10.1152/japplphysiol.00017.2002.
Full textAbstract:
β-Blockade results in rapid glucose clearance and premature fatigue during exercise. To investigate the cause of this increased glucose clearance, we studied the acute effects of propranolol on insulin-stimulated muscle glucose uptake during contraction in the presence of epinephrine with an isolated rat muscle preparation. Glucose uptake increased in both fast- (epitrochlearis) and slow-twitch (soleus) muscle during insulin or contraction stimulation. In the presence of 24 nM epinephrine, glucose uptake during contraction was completely suppressed when insulin was present. This suppression of glucose uptake by epinephrine was accompanied by a decrease in insulin receptor substrate (IRS)-1-phosphatidylinositol 3 (PI3)-kinase activity. Propranolol had no direct effect on insulin-stimulated glucose uptake during contraction. However, epinephrine was ineffective in attenuating insulin-stimulated glucose uptake during contraction in the presence of propranolol. This ineffectiveness of epinephrine to suppress insulin-stimulated glucose uptake during contraction occurred in conjunction with its inability to completely suppress IRS-1-PI3-kinase activity. Results of this study indicate that the effectiveness of epinephrine to inhibit insulin-stimulated glucose uptake during contraction is severely diminished in muscle exposed to propranolol. Thus the increase in glucose clearance and premature fatigue associated with β-blockade could result from the inability of epinephrine to attenuate insulin-stimulated muscle glucose uptake.
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McMillin, Shawna L., Parker L. Evans, William M. Taylor, Luke A. Weyrauch, Tyler J. Sermersheim, Steven S. Welc, Monique R. Heitmeier, et al. "Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake." Biomolecules 12, no. 12 (November 23, 2022): 1734. http://dx.doi.org/10.3390/biom12121734.
Full textAbstract:
Glucose transporter 1 (GLUT1) is believed to solely mediate basal (insulin-independent) glucose uptake in skeletal muscle; yet recent work has demonstrated that mechanical overload, a model of resistance exercise training, increases muscle GLUT1 levels. The primary objective of this study was to determine if GLUT1 is necessary for basal or overload-stimulated muscle glucose uptake. Muscle-specific GLUT1 knockout (mGLUT1KO) mice were generated and examined for changes in body weight, body composition, metabolism, systemic glucose regulation, muscle glucose transporters, and muscle [3H]-2-deoxyglucose uptake ± the GLUT1 inhibitor BAY-876. [3H]-hexose uptake ± BAY-876 was also examined in HEK293 cells-expressing GLUT1-6 or GLUT10. mGLUT1KO mice exhibited no impairments in body weight, lean mass, whole body metabolism, glucose tolerance, basal or overload-stimulated muscle glucose uptake. There was no compensation by the insulin-responsive GLUT4. In mGLUT1KO mouse muscles, overload stimulated higher expression of mechanosensitive GLUT6, but not GLUT3 or GLUT10. In control and mGLUT1KO mouse muscles, 0.05 µM BAY-876 impaired overload-stimulated, but not basal glucose uptake. In the GLUT-HEK293 cells, BAY-876 inhibited glucose uptake via GLUT1, GLUT3, GLUT4, GLUT6, and GLUT10. Collectively, these findings demonstrate that GLUT1 does not mediate basal muscle glucose uptake and suggest that a novel glucose transport mechanism mediates overload-stimulated glucose uptake.
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Buller, Carolyn L., Robert D. Loberg, Ming-Hui Fan, Qihong Zhu, James L. Park, Eileen Vesely, Ken Inoki, Kun-Liang Guan, and Frank C. Brosius. "A GSK-3/TSC2/mTOR pathway regulates glucose uptake and GLUT1 glucose transporter expression." American Journal of Physiology-Cell Physiology 295, no. 3 (September 2008): C836—C843. http://dx.doi.org/10.1152/ajpcell.00554.2007.
Full textAbstract:
Glucose transport is a highly regulated process and is dependent on a variety of signaling events. Glycogen synthase kinase-3 (GSK-3) has been implicated in various aspects of the regulation of glucose transport, but the mechanisms by which GSK-3 activity affects glucose uptake have not been well defined. We report that basal glycogen synthase kinase-3 (GSK-3) activity regulates glucose transport in several cell types. Chronic inhibition of basal GSK-3 activity (8–24 h) in several cell types, including vascular smooth muscle cells, resulted in an approximately twofold increase in glucose uptake due to a similar increase in protein expression of the facilitative glucose transporter 1 (GLUT1). Conversely, expression of a constitutively active form of GSK-3β resulted in at least a twofold decrease in GLUT1 expression and glucose uptake. Since GSK-3 can inhibit mammalian target of rapamycin (mTOR) signaling via phosphorylation of the tuberous sclerosis complex subunit 2 (TSC2) tumor suppressor, we investigated whether chronic GSK-3 effects on glucose uptake and GLUT1 expression depended on TSC2 phosphorylation and TSC inhibition of mTOR. We found that absence of functional TSC2 resulted in a 1.5-to 3-fold increase in glucose uptake and GLUT1 expression in multiple cell types. These increases in glucose uptake and GLUT1 levels were prevented by inhibition of mTOR with rapamycin. GSK-3 inhibition had no effect on glucose uptake or GLUT1 expression in TSC2 mutant cells, indicating that GSK-3 effects on GLUT1 and glucose uptake were mediated by a TSC2/mTOR-dependent pathway. The effect of GSK-3 inhibition on GLUT1 expression and glucose uptake was restored in TSC2 mutant cells by transfection of a wild-type TSC2 vector, but not by a TSC2 construct with mutated GSK-3 phosphorylation sites. Thus, TSC2 and rapamycin-sensitive mTOR function downstream of GSK-3 to modulate effects of GSK-3 on glucose uptake and GLUT1 expression. GSK-3 therefore suppresses glucose uptake via TSC2 and mTOR and may serve to match energy substrate utilization to cellular growth.
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Hunt, Desmond G., Zhenping Ding, and John L. Ivy. "Clenbuterol prevents epinephrine from antagonizing insulin-stimulated muscle glucose uptake." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1285–92. http://dx.doi.org/10.1152/japplphysiol.01009.2001.
Full textAbstract:
In the present study, we investigated the effects of chronic clenbuterol treatment on insulin-stimulated glucose uptake in the presence of epinephrine in isolated rat skeletal muscle. Insulin (50 μU/ml) increased glucose uptake in both fast-twitch (epitrochlearis) and slow-twitch (soleus) muscles. In the presence of 24 nM epinephrine, insulin-stimulated glucose uptake was completely suppressed. This suppression of glucose uptake by epinephrine was accompanied by an increase in the intracellular concentration of glucose 6-phosphate and a decrease in insulin-receptor substrate-1-associated phosphatidylinositol 3-kinase (IRS-1/PI3-kinase) activity. Clenbuterol treatment had no direct effect on insulin-stimulated glucose uptake. However, after clenbuterol treatment, epinephrine was ineffective in attenuating insulin-stimulated muscle glucose uptake. This ineffectiveness of epinephrine to suppress insulin-stimulated glucose uptake occurred in conjunction with its inability to increase the intracellular concentration of glucose 6-phosphate and attenuate IRS-1/PI3-kinase activity. Results of this study indicate that the effectiveness of epinephrine to inhibit insulin-stimulated glucose uptake is severely diminished in muscle from rats pretreated with clenbuterol.
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Huska, Brenda, Sarah Niccoli, Christopher P. Phenix, and Simon J. Lees. "Leucine Potentiates Glucose-mediated 18F-FDG Uptake in Brown Adipose Tissue via β-Adrenergic Activation." Biomedicines 8, no. 6 (June 13, 2020): 159. http://dx.doi.org/10.3390/biomedicines8060159.
Full textAbstract:
Significant depots of brown adipose tissue (BAT) have been identified in many adult humans through positron emission tomography (PET), with the amount of BAT being inversely correlated with obesity. As dietary activation of BAT has implications for whole body glucose metabolism, leucine was used in the present study to determine its ability to promote BAT activation resulting in increased glucose uptake. In order to assess this, 2-deoxy-2-(fluorine-18)fluoro-d-glucose (18F-FDG) uptake was measured in C57BL/6 mice using microPET after treatment with leucine, glucose, or both in interscapular BAT (IBAT). Pretreatment with propranolol (PRP) was used to determine the role of β-adrenergic activation in glucose and leucine-mediated 18F-FDG uptake. Analysis of maximum standardized uptake values (SUVMAX) determined that glucose administration increased 18F-FDG uptake in IBAT by 25.3%. While leucine did not promote 18F-FDG uptake alone, it did potentiate glucose-mediated 18F-FDG uptake, increasing 18F-FDG uptake in IBAT by 22.5%, compared to glucose alone. Pretreatment with PRP prevented the increase in IBAT 18F-FDG uptake following the combination of glucose and leucine administration. These data suggest that leucine is effective in promoting BAT 18F-FDG uptake through β-adrenergic activation in combination with glucose.
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Madsen, Peter L., Rasmus Linde, Steen G. Hasselbalch, Olaf B. Paulson, and Niels A. Lassen. "Activation-Induced Resetting of Cerebral Oxygen and Glucose Uptake in the Rat." Journal of Cerebral Blood Flow & Metabolism 18, no. 7 (July 1998): 742–48. http://dx.doi.org/10.1097/00004647-199807000-00005.
Full textAbstract:
In the clinical setting it has been shown that activation will increase cerebral glucose uptake in excess of cerebral oxygen uptake. To study this phenomenon further, this study presents an experimental setup that enables precise determination of the ratio between cerebral uptake of glucose and oxygen in the awake rat. Global CBF was measured by the Kety-Schmidt technique, and the ratio between cerebral uptake rates for oxygen, glucose, and lactate was calculated from cerebral arterial—venous differences. During baseline conditions, rats were kept in a closed box designed to minimize interference. During baseline conditions CBF was 1.08 ± 0.25 mL·g−1·minute−1, and the cerebral oxygen to glucose uptake ratio was 5.5. Activation was induced by opening the sheltering box for 6 minutes. Activation increased CBF to 1.81 mL·g−1·minute−1. During activation cerebral glucose uptake increased disproportionately to cerebral oxygen uptake, and the cerebral oxygen to glucose uptake ratio was 4.2. The accumulated excess glucose uptake during 6 minutes of activation amounted to 2.4 μmol/g. Activation was terminated by closure of the sheltering box. In the postactivation period, the cerebral oxygen to glucose uptake ratio rose to a maximum of 6.4. This response is exactly opposite to the excess cerebral glucose uptake observed during activation.
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Milley, J. R., J. S. Papacostas, and B. K. Tabata. "Effect of insulin on uptake of metabolic substrates by the sheep fetus." American Journal of Physiology-Endocrinology and Metabolism 251, no. 3 (September 1, 1986): E349—E356. http://dx.doi.org/10.1152/ajpendo.1986.251.3.e349.
Full textAbstract:
To measure the effect of fetal hyperinsulinemia on fetal oxidative metabolic rate and the uptake of fetal oxidative substrates, we operated on 12 near-term ewes under spinal anesthesia and placed catheters in the fetus under local anesthesia. Four days after surgery, we began an 18-h insulin infusion, at the end of which we drew blood samples for analysis of oxygen, glucose, lactate, amino-nitrogen concentrations, blood gases, pH, hematocrit, and plasma insulin concentrations, then injected radiolabeled microspheres to measure umbilical blood flow. Three to five infusions were given to each fetus. Fetal plasma insulin concentrations varied from 0.3 to 60 microU/ml. As fetal plasma insulin concentration rose, the blood concentrations of oxygen, glucose, lactate, and amino-nitrogen fell, but the fetal uptakes of oxygen, glucose, and amino-nitrogen rose. The rise of fetal oxygen uptake occurred by increasing oxygen extraction, resulting in arterial hypoxemia. The increase of the glucose uptake was sufficient to account for an increased fraction of oxidative metabolism, allowing the increased uptake of amino acids to be used for either synthetic or oxidative purposes.
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Sofue, M., Y. Yoshimura, M. Nishida, and J. Kawada. "Possible multifunction of glucose transporter. Transport of nicotinamide by reconstituted liposomes." Biochemical Journal 288, no. 2 (December 1, 1992): 669–74. http://dx.doi.org/10.1042/bj2880669.
Full textAbstract:
A kinetic study of the uptake of nicotinamide by reconstituted liposomes containing the human erythrocyte glucose transporter, compared with that of D-glucose, demonstrated that the Km and Vmax. values were almost the same for each compound, and that the uptake of D-glucose was competitively inhibited by nicotinamide. At 20 mM concentration, 2-deoxy-D-glucose, 3-O-methyl-D-glucose and 4,6-O-ethylidene-D-glucose all caused 50% inhibition of nicotinamide uptake, but L-glucose and nicotinic acid were not inhibitory. Similar results were obtained for the uptake of D-glucose. Cytochalasin B binding to the liposomes was inhibited in a dose-dependent manner by either nicotinamide or D-glucose. Antibody for glucose transporter detected in band 4.5 by SDS/PAGE inhibited the uptake of D-glucose and nicotinamide. A possible uptake of nicotinamide by nucleoside transporter was excluded. In human erythrocytes, cytochalasin B binding was inhibited dose-dependently by either nicotinamide or D-glucose, and cytochalasin B depressed the uptake of both nicotinamide and 2-deoxy-D-glucose. These findings were well reproduced in the reconstituted liposomes. The very close similarities between uptake of nicotinamide and D-glucose suggest that the glucose transporter plays a direct role in transport of nicotinamide, which is structurally quite different from monosaccharides, and thus that the transporter is probably multifunctional.
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NIELSEN, METTE O., TORBEN G. MADSEN, and ANNE MARIE HEDEBOE. "Regulation of mammary glucose uptake in goats: role of mammary gland supply, insulin, IGF-1 and synthetic capacity." Journal of Dairy Research 68, no. 3 (August 2001): 337–49. http://dx.doi.org/10.1017/s002202990100499x.
Full textAbstract:
Variations in mammary glucose uptake were measured during the normal pregnancy-lactation cycle in dairy goats. In addition mammary glucose uptake was studied in response to somatotropin (ST) treatment in mid-lactation and acute increases in glucose concentration induced by sodium-propionate challenge in early lactation. Mammary glucose uptake was independent of arterial glucose, insulin and Insulin-like Growth Factor-1 (IGF-1) concentrations during lactation and during acute increases in arterial glucose concentration. Glucose uptake in the lactating mammary gland of the goat must therefore be carried out by an insulin-independent carrier, possible GLUT1, and glucose supply is not a limiting factor for uptake under in vivo conditions. Extraction of glucose uptake changed markedly during the normal course of lactation, following the overall changes in milk yield. Concentrations of glucose in skimmed milk, believed to reflect intracellular glucose concentration, changed in opposite directions, resulting in decreasing ratios of arterialratioskimmed milk glucose concentration with progressing lactation. Thus, mammary synthetic capacity also involves a capacity for glucose uptake, which may be influenced by variations in glucose carrier numbers, as well as mammary metabolic activity (intracellular glucose concentration). In contrast to the situation during the normal course of lactation, ST stimulated milk yield, despite less efficient glucose extraction.
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Cartee, Gregory D., Edward B. Arias, Carmen S. Yu, and Mark W. Pataky. "Novel single skeletal muscle fiber analysis reveals a fiber type-selective effect of acute exercise on glucose uptake." American Journal of Physiology-Endocrinology and Metabolism 311, no. 5 (November 1, 2016): E818—E824. http://dx.doi.org/10.1152/ajpendo.00289.2016.
Full textAbstract:
One exercise session can induce subsequently elevated insulin sensitivity that is largely attributable to greater insulin-stimulated glucose uptake by skeletal muscle. Because skeletal muscle is a heterogeneous tissue comprised of diverse fiber types, our primary aim was to determine exercise effects on insulin-independent and insulin-dependent glucose uptake by single fibers of different fiber types. We hypothesized that each fiber type featuring elevated insulin-independent glucose uptake immediately postexercise (IPEX) would be characterized by increased insulin-dependent glucose uptake at 3.5 h postexercise (3.5hPEX). Rat epitrochlearis muscles were isolated and incubated with 2-[3H]deoxyglucose. Muscles from IPEX and sedentary (SED) controls were incubated without insulin. Muscles from 3.5hPEX and SED controls were incubated ± insulin. Glucose uptake (2-[3H]deoxyglucose accumulation) and fiber type (myosin heavy chain isoform expression) were determined for single fibers dissected from the muscles. Major new findings included the following: 1) insulin-independent glucose uptake was increased IPEX in single fibers of each fiber type (types I, IIA, IIB, IIBX, and IIX), 2) glucose uptake values from insulin-stimulated type I and IIA fibers exceeded the values for the other fiber types, 3) insulin-stimulated glucose uptake for type IIX exceeded IIB fibers, and 4) the 3.5hPEX group vs. SED had greater insulin-stimulated glucose uptake in type I, IIA, IIB, and IIBX but not type IIX fibers. Insulin-dependent glucose uptake was increased at 3.5hPEX in each fiber type except for IIX fibers, although insulin-independent glucose uptake was increased IPEX in all fiber types (including type IIX). Single fiber analysis enabled the discovery of this fiber type-related difference for postexercise, insulin-stimulated glucose uptake.
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Miki, Takashi, Kohtaro Minami, Li Zhang, Mizuo Morita, Tohru Gonoi, Tetsuya Shiuchi, Yasuhiko Minokoshi, Jean-Marc Renaud, and Susumu Seino. "ATP-sensitive potassium channels participate in glucose uptake in skeletal muscle and adipose tissue." American Journal of Physiology-Endocrinology and Metabolism 283, no. 6 (December 1, 2002): E1178—E1184. http://dx.doi.org/10.1152/ajpendo.00313.2002.
Full textAbstract:
ATP-sensitive potassium (KATP) channels are known to be critical in the control of both insulin and glucagon secretion, the major hormones in the maintenance of glucose homeostasis. The involvement of KATPchannels in glucose uptake in the target tissues of insulin, however, is not known. We show here that Kir6.2(−/−) mice lacking Kir6.2, the pore-forming subunit of these channels, have no KATPchannel activity in their skeletal muscles. A 2-deoxy-[3H]glucose uptake experiment in vivo showed that the basal and insulin-stimulated glucose uptake in skeletal muscles and adipose tissues of Kir6.2(−/−) mice is enhanced compared with that in wild-type (WT) mice. In addition, in vitro measurement of glucose uptake indicates that disruption of the channel increases the basal glucose uptake in Kir6.2(−/−) extensor digitorum longus and the insulin-stimulated glucose uptake in Kir6.2(−/−) soleus muscle. In contrast, glucose uptake in adipose tissue, measured in vitro, was similar in Kir6.2(−/−) and WT mice, suggesting that the increase in glucose uptake in Kir6.2(−/−) adipocytes is mediated by altered extracellular hormonal or neuronal signals altered by disruption of the KATP channels.
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Hashimoto, K., T. Nishimura, M. Ishikawa, K. Koga, T. Mori, S. Matsuda, M. Hori, and H. Kusuoka. "Enhancement of glucose uptake in stunned myocardium: role of glucose transporter." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (March 1, 1997): H1122—H1130. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1122.
Full textAbstract:
This study quantifies the myocardial glucose uptake and clarifies the pathway of augmented glucose uptake in myocardium reperfused after a brief period of ischemia (stunned myocardium). The glucose uptake rate was determined from the time course of the sugar phosphate (SP) resonance in rat myocardium (d[SP]/dt) with 31P nuclear magnetic resonance after the substitution of glucose with its analog 2-deoxyglucose. The d[SP]/dt in stunned myocardium [1.03 +/- 0.05 (SE) micromol x g wet wt(-1) x min(-1); n = 8] increased significantly compared with nonischemic control myocardium (0.18 +/- 0.03 micromol x g wet wt(-1) x min(-1); n = 8; P < 0.0001), reaching the maximal stimulatory uptake rate during exposure to insulin (1.05 +/- 0.04 micromol x g wet wt(-1) x min(-1); n = 8). Twenty minutes after reperfusion, the d[SP]/dt was still augmented (0.41 +/- 0.05 micromol x g wet wt(-1) x min(-1); n = 5; P < 0.05 vs. control myocardium). To elucidate further the mechanism of augmented glucose uptake, N6-(L-2-phenylisopropyl)-adenosine (PIA; 100 micromol/l), a potent blocker of the glucose transporter, was administered to stunned hearts and, as a control, to insulin-stimulated hearts. PIA significantly and comparably inhibited the increase in d[SP]/dt in stunned myocardium (0.36 +/- 0.07 micromol x g wet wt(-1) x min(-1); n = 4; P < 0.0001 vs. without PIA) and in insulin-stimulated myocardium (0.38 +/- 0.02 micromol x g wet wt(-1) x min(-1); n = 4; P < 0.0001 vs. without PIA). These results indicate that the augmented glucose uptake in stunned myocardium is maintained by the glucose transporter, the amount of which is almost equal to that which can be maximally recruited by insulin.
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Heyligenberg, R., J. A. Romijn, M. J. T. Hommes, E. Endert, J. K. M. Eeftinck Schattenkerk, and H. P. Sauerwein. "Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men." Clinical Science 84, no. 2 (February 1, 1993): 209–16. http://dx.doi.org/10.1042/cs0840209.
Full textAbstract:
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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Kalliokoski, Kari K., Henning Langberg, Ann Kathrine Ryberg, Celena Scheede-Bergdahl, Simon Doessing, Andreas Kjaer, Robert Boushel, and Michael Kjaer. "The effect of dynamic knee-extension exercise on patellar tendon and quadriceps femoris muscle glucose uptake in humans studied by positron emission tomography." Journal of Applied Physiology 99, no. 3 (September 2005): 1189–92. http://dx.doi.org/10.1152/japplphysiol.00283.2005.
Full textAbstract:
Both tendon and peritendinous tissue show evidence of metabolic activity, but the effect of acute exercise on substrate turnover is unknown. We therefore examined the influence of acute exercise on glucose uptake in the patellar and quadriceps tendons during dynamic exercise in humans. Glucose uptake was measured in five healthy men in the patellar and quadriceps tendons and the quadriceps femoris muscle at rest and during dynamic knee-extension exercise (25 W) using positron emission tomography and [18F]-2-fluoro-2-deoxy-d-glucose ([18F]FDG). Glucose uptake index was calculated by dividing the tissue activity with blood activity of [18F]FDG. Exercise increased glucose uptake index by 77% in the patellar tendon (from 0.30 ± 0.09 to 0.51 ± 0.16, P = 0.03), by 106% in the quadriceps tendon (from 0.37 ± 0.15 to 0.75 ± 0.36, P = 0.02), and by 15-fold in the quadriceps femoris muscle (from 0.31 ± 0.11 to 4.5 ± 1.7, P = 0.005). The exercise-induced increase in the glucose uptake in neither tendon correlated with the increase in glucose uptake in the quadriceps muscle ( r = −0.10, P = 0.87 for the patellar tendon and r = −0.30, P = 0.62 for the quadriceps tendon). These results show that tendon glucose uptake is increased during exercise. However, the increase in tendon glucose uptake is less pronounced than in muscle and the increases are uncorrelated. Thus tendon glucose uptake is likely to be regulated by mechanisms independently of those regulating skeletal muscle glucose uptake.
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Shibata, H., F. Perusse, A. Vallerand, and L. J. Bukowiecki. "Cold exposure reverses inhibitory effects of fasting on peripheral glucose uptake in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 1 (July 1, 1989): R96—R101. http://dx.doi.org/10.1152/ajpregu.1989.257.1.r96.
Full textAbstract:
The effects of fasting and cold exposure on glucose uptake in skeletal muscles (tibialis anterior, quadriceps, and soleus), heart, and brown adipose tissue (BAT) were studied in conscious rats. Glucose uptake was estimated by determining the glucose metabolic index of individual tissues using the 2-[3H]deoxyglucose method. Fasting for 18 h at 25 degrees C decreased plasma glucose levels (-40%) and glucose uptake in heart (-95%) and skeletal muscles (-64-90%) but did not significantly affect glucose uptake in BAT. Fasting for 48 h did not further decrease these parameters. On the other hand, cold exposure (48 h at 5 degrees C) of fed animals did not alter plasma glucose levels but increased glucose uptake in heart (73%), skeletal muscles (126-326%), and particularly in BAT (95-fold). Remarkably, cold exposure stimulated glucose uptake in BAT and skeletal muscles of 18-h fasted rats by the same order of magnitude as in fed animals (percentagewise), thereby indicating that glucose represents an essential metabolite for shivering (muscles) and nonshivering (BAT) thermogeneses. In the heart of starved animals, the cold-induced increase in glucose uptake was even more important (8-fold) than in fed animals. Considering that cold exposure of fasted rats results in a severe insulinopenia, it is suggested that cold exposure stimulates glucose uptake in peripheral tissues primarily by enhancing glucose oxidation via insulin-independent pathways.
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Bashan, N., E. Burdett, H. S. Hundal, and A. Klip. "Regulation of glucose transport and GLUT1 glucose transporter expression by O2 in muscle cells in culture." American Journal of Physiology-Cell Physiology 262, no. 3 (March 1, 1992): C682—C690. http://dx.doi.org/10.1152/ajpcell.1992.262.3.c682.
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The effect of varying cellular oxygenation on L6 muscle cell 2-deoxy-D-glucose transport, glucose utilization, lactate production, and expression of GLUT1 and GLUT4 transport proteins was investigated. Incubation of L6 myotubes in 3% O2 (mimicking a state of hypoxia) elevated glucose uptake by 6.5-fold over 48 h relative to cells incubated in 21% O2 (normoxia). Incubation of L6 cells in hyperoxic conditions (50% O2) significantly depressed glucose uptake by 0.4-fold. These effects were fully reversible. Incubation in 3% O2 also caused lactate accumulation and enhanced glucose consumption from the medium. Hypoxia elevated 2-deoxy-D-glucose transport even when the concentration of glucose in the medium was kept constant, suggesting that glucose deprivation alone was not responsible for increased cellular glucose uptake. Incubation in 3% O2 also elevated 3-O-methylglucose uptake but not amino acid uptake. Cycloheximide prevented the hypoxia-induced increase in glucose uptake, indicating that de novo synthesis of glucose transport-related proteins was the major means by which cells increased glucose uptake. The content of GLUT1 glucose transporter was significantly elevated in total membranes of cells incubated in 3% O2 and depressed in membranes from cells incubated in hyperoxic conditions, whereas GLUT4 expression was not affected. These results indicate that hypoxia induces an adaptive response of increasing cellular glucose uptake through elevated expression of GLUT1 in an attempt to maintain supply of glucose for utilization by nonoxidative pathways.
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ALVIM, RAFAEL O., MARCEL R. CHEUHEN, SILMARA R. MACHADO, ANDRÉ GUSTAVO P. SOUSA, and PAULO C. J. L. SANTOS. "General aspects of muscle glucose uptake." Anais da Academia Brasileira de Ciências 87, no. 1 (March 6, 2015): 351–68. http://dx.doi.org/10.1590/0001-3765201520140225.
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Glucose uptake in peripheral tissues is dependent on the translocation of GLUT4 glucose transporters to the plasma membrane. Studies have shown the existence of two major signaling pathways that lead to the translocation of GLUT4. The first, and widely investigated, is the insulin activated signaling pathway through insulin receptor substrate-1 and phosphatidylinositol 3-kinase. The second is the insulin-independent signaling pathway, which is activated by contractions. Individuals with type 2 diabetes mellitus have reduced insulin-stimulated glucose uptake in skeletal muscle due to the phenomenon of insulin resistance. However, those individuals have normal glucose uptake during exercise. In this context, physical exercise is one of the most important interventions that stimulates glucose uptake by insulin-independent pathways, and the main molecules involved are adenosine monophosphate-activated protein kinase, nitric oxide, bradykinin, AKT, reactive oxygen species and calcium. In this review, our main aims were to highlight the different glucose uptake pathways and to report the effects of physical exercise, diet and drugs on their functioning. Lastly, with the better understanding of these pathways, it would be possible to assess, exactly and molecularly, the importance of physical exercise and diet on glucose homeostasis. Furthermore, it would be possible to assess the action of drugs that might optimize glucose uptake and consequently be an important step in controlling the blood glucose levels in diabetic patients, in addition to being important to clarify some pathways that justify the development of drugs capable of mimicking the contraction pathway.
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Caumo, A., M. Homan, H. Katz, C. Cobelli, and R. Rizza. "Glucose turnover in presence of changing glucose concentrations: error analysis for glucose disappearance." American Journal of Physiology-Endocrinology and Metabolism 269, no. 3 (September 1, 1995): E557—E567. http://dx.doi.org/10.1152/ajpendo.1995.269.3.e557.
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The present studies were undertaken to determine whether 1) the cold- and hot-GINF techniques used with Steele's model provide equivalent estimates of the rates of glucose appearance (R(a)) and disappearance (R(d)) in the presence of physiological changes in glucose and insulin concentrations, 2) the conditions for the best estimation of R(a) are the same as those for R(d), 3) the magnitude of error (if present) differs in diabetic and nondiabetic subjects, and 4) situations exist in which the knowledge of R(d) allows inferences to be made on whole body glucose uptake. To do so we performed experiments in non-insulin-dependent diabetes mellitus and nondiabetic subjects using simultaneous infusions of [6-3H]glucose and [6-14C]glucose; glucose and insulin were infused to mimic normal postprandial glucose and insulin profiles; the infused glucose contained [6-14C]glucose but not [6-3H]glucose. Compared with the hot-GINF method, the traditional cold-GINF method underestimated (P < 0.05) R(a) and R(d) by 10-15% and hepatic glucose release by 25-50% during the 1st h of the study, with the magnitude of error being the same in both diabetic and nondiabetic subjects. Error analysis demonstrated that errors in R(a) and R(d) have different analytic expressions containing common structural but different volume errors. Both R(a) and R(d) can be accurately measured in diabetic and nondiabetic subjects if glucose specific activity is kept constant and the volume of the accessible pool is used to calculate glucose disappearance. The relationship between R(d) and whole body glucose uptake was also derived. Although R(d) can be determined by relying on measurements in the accessible pool only, the assessment of whole body glucose uptake requires a model of the nonaccessible portion of the glucose system. However, knowledge of R(d) can provide useful insights into the behavior of whole body glucose uptake.
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Lappas, Martha, Sofianos Andrikopoulos, and Michael Permezel. "Hypoxanthine–xanthine oxidase down-regulates GLUT1 transcription via SIRT1 resulting in decreased glucose uptake in human placenta." Journal of Endocrinology 213, no. 1 (January 19, 2012): 49–57. http://dx.doi.org/10.1530/joe-11-0355.
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Appropriate foetal growth and development is dependent on adequate placental glucose uptake. Oxidative stress regulates glucose uptake in various tissues. The effect of oxidative stress on placental glucose transport is not known. Thus, the aim of this study was to determine the effect of oxidative stress on glucose uptake and glucose transporters (GLUTs) in human placenta. Human placenta was incubated in the absence or presence of 0.5 mM hypoxanthine+15 mU/ml xanthine oxidase (HX/XO) for 24 h. Gene and protein expressions of the GLUTs were analysed by quantitative RT-PCR and western blotting respectively. Glucose uptake was measured using radiolabelled (14C) glucose. HX/XO significantly decreased GLUT1 gene and protein expression and resultant glucose uptake. There was no effect of the antioxidants N-acetylcysteine, catalase and superoxide dismutase or the NF-κB inhibitor BAY 11-0782 on HX/XO-induced decrease in glucose uptake. However, HX/XO treatment significantly decreased both gene and protein expression of SIRT1. In the presence of the SIRT1 activator resveratrol, the decrease in GLUT1 expression and glucose uptake mediated by HX/XO was abolished. Collectively, the data presented here demonstrate that oxidative stress reduces placental glucose uptake and GLUT1 expression by a SIRT1-dependent mechanism.
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de Lima, Juliana Bezerra Medeiros, Lucas Kniess Debarba, Alan C. Rupp, Nathan Qi, Chidera Ubah, Manal Khan, Olesya Didyuk, et al. "ARCGHR Neurons Regulate Muscle Glucose Uptake." Cells 10, no. 5 (May 3, 2021): 1093. http://dx.doi.org/10.3390/cells10051093.
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The growth hormone receptor (GHR) is expressed in brain regions that are known to participate in the regulation of energy homeostasis and glucose metabolism. We generated a novel transgenic mouse line (GHRcre) to characterize GHR-expressing neurons specifically in the arcuate nucleus of the hypothalamus (ARC). Here, we demonstrate that ARCGHR+ neurons are co-localized with agouti-related peptide (AgRP), growth hormone releasing hormone (GHRH), and somatostatin neurons, which are activated by GH stimulation. Using the designer receptors exclusively activated by designer drugs (DREADD) technique to control the ARCGHR+ neuronal activity, we demonstrate that the activation of ARCGHR+ neurons elevates a respiratory exchange ratio (RER) under both fed and fasted conditions. However, while the activation of ARCGHR+ promotes feeding, under fasting conditions, the activation of ARCGHR+ neurons promotes glucose over fat utilization in the body. This effect was accompanied by significant improvements in glucose tolerance, and was specific to GHR+ versus GHRH+ neurons. The activation of ARCGHR+ neurons increased glucose turnover and whole-body glycolysis, as revealed by hyperinsulinemic-euglycemic clamp studies. Remarkably, the increased insulin sensitivity upon the activation of ARCGHR+ neurons was tissue-specific, as the insulin-stimulated glucose uptake was specifically elevated in the skeletal muscle, in parallel with the increased expression of muscle glycolytic genes. Overall, our results identify the GHR-expressing neuronal population in the ARC as a major regulator of glycolysis and muscle insulin sensitivity in vivo.
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Leung, Po Sing. "Angiotensin II and intestinal glucose uptake." Physiology News, Autumn 2008 (September 1, 2008): 21–22. http://dx.doi.org/10.36866/pn.72.21.
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Levin, P., T. Bistritzer, L. Hanukoglu, S. Max, and L. Roeder. "ACTH1-24Stimulates Muscle Cell Glucose Uptake." Hormone and Metabolic Research 22, no. 12 (December 1990): 608–11. http://dx.doi.org/10.1055/s-2007-1004984.
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Kovi, D., K. F. Rinehardt, R. S. Axtell, D. Upson, J. M. Weitzner, S. V. Klein, and T. Quill. "ERYTHROCYTE GLUCOSE UPTAKE DURING GRADED SWIMMING." Medicine & Science in Sports & Exercise 35, Supplement 1 (May 2003): S367. http://dx.doi.org/10.1097/00005768-200305001-02039.
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Liu, Li-Zhong, Ai-Bin He, Xiao-Jun Liu, Yi Li, Yong-Sheng Chang, and Fu-De Fang. "Protein kinase Cζ and glucose uptake." Biochemistry (Moscow) 71, no. 7 (July 2006): 701–6. http://dx.doi.org/10.1134/s0006297906070017.
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Hartl, W. H. "Prostaglandins and skeletal muscle glucose uptake." Biochemical Journal 248, no. 2 (December 1, 1987): 621–23. http://dx.doi.org/10.1042/bj2480621.
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