The Experts below are selected from a list of 12642 Experts worldwide ranked by ideXlab platform
Glenn K Mcconell - One of the best experts on this subject based on the ideXlab platform.
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Acute exercise does not cause sustained elevations in AMPK Signaling or expression.
Medicine and Science in Sports and Exercise, 2008Co-Authors: Robert S. Lee-young, Benedict J Canny, George Koufogiannis, Glenn K McconellAbstract:ABSTRACTPurpose:No study has examined the response of skeletal muscle AMP-activated protein kinase (AMPK) Signaling beyond the first 3 h after an acute exercise bout in humans. The purpose of this study was to assess AMPK Signaling in human skeletal muscle immediately after a single bout of moderate
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Carbohydrate ingestion does not alter skeletal muscle AMPK Signaling during exercise in humans.
American journal of physiology. Endocrinology and metabolism, 2006Co-Authors: Robert S. Lee-young, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Glenn D. Wadley, Matthew J Palmer, Kelly C Linden, Kieran Leplastrier, Glenn K McconellAbstract:There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKalpha2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKalpha2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK Signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 +/- 1% V(O2 peak). In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly (P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPKalpha2 activity, AMPKalpha2 Thr(172) phosphorylation and acetyl-CoA Ser(222) phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK Signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.
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Effect of exercise intensity and hypoxia on skeletal muscle AMPK Signaling and substrate metabolism in humans.
American Journal of Physiology-endocrinology and Metabolism, 2005Co-Authors: Glenn D. Wadley, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Robert S. Lee-young, Chanchira Wasuntarawat, Zejian Chen, Glenn K McconellAbstract:We compared in human skeletal muscle the effect of absolute vs. relative exercise intensity on AMP-activated protein kinase (AMPK) Signaling and substrate metabolism under normoxic and hypoxic cond...
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effect of exercise intensity on skeletal muscle AMPK Signaling in humans
Diabetes, 2003Co-Authors: Zhiping Chen, Sid Murthy, Mark Hargreaves, Lee A Witters, Benedict J Canny, Bruce E Kemp, Terry J. Stephens, Glenn K McconellAbstract:The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) Signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 ± 2% Vo2 peak), medium (59 ± 1% Vo2 peak), and high (79 ± 1% Vo2 peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P
Chang Liu - One of the best experts on this subject based on the ideXlab platform.
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resveratrol protects against spinal cord injury by activating autophagy and inhibiting apoptosis mediated by the sirt1 AMPK Signaling pathway
Neuroscience, 2017Co-Authors: Haosen Zhao, Kai Gao, Shurui Chen, Zipeng Zhou, Chen Wang, Zhaoliang Shen, Yue Guo, Zhanghui Wan, Chang Liu, Xifan MeiAbstract:Abstract Spinal cord injury (SCI) is a devastating condition with few effective treatments. Resveratrol, a polyphenolic compound, has exhibited neuroprotective effects in many neurodegenerative diseases. However, the explicit effect and mechanism of resveratrol on SCI is still unclear. Adenosine 5′ monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1), the downstream protein, play key roles in metabolizing of energy, resisting of resistance, and cellular protein homeostasis. In this study, we determined the effects of resveratrol on SCI and their potential relationship with SIRT1/AMPK Signaling pathway, autophagy and apoptosis. To determine the effect of resveratrol on SCI recovery, a spinal cord contusion model was employed. Rats received treatment with resveratrol or DMSO immediately following contusion. We determined that Basso, Beattie, and Bresnahan (BBB) scores were significantly higher for injured rats treated with resveratrol. Nissl and HE staining revealed that resveratrol treatment significantly reduced the loss of motor neurons and lesion size in the spinal cord of injured rats when compared to vehicle-treated animals. Spinal cord tissue was assessed by Western blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical analyses 7 days after injury for changes in expression of SIRT1/AMPK Signaling pathway, autophagy and apoptosis proteins. Expression of SIRT1, p-AMPK, Beclin-1, LC3-B, and Bcl-2 was elevated in resveratrol-treated animals, whereas expression of p62, Cleaved Caspase-3, Caspase-9, and Bcl-2 associated X protein (Bax) was inhibited. Immunofluorescence analysis of primary neurons treated with resveratrol alone or in combination with Compound C (AMPK inhibitor) or EX527 (SIRT1 inhibitor) revealed that treatment with the inhibitors blocks the increased LC3-B expression in cells and increases the portion of TUNEL-positive cells. Taken together, these results suggest that resveratrol exerts neuroprotective effects on SCI by regulating autophagy and apoptosis mediated by the SIRT1-AMPK Signaling pathway.
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Resveratrol protects against spinal cord injury by activating autophagy and inhibiting apoptosis mediated by the SIRT1/AMPK Signaling pathway
Neuroscience, 2017Co-Authors: Haosen Zhao, Kai Gao, Shurui Chen, Zipeng Zhou, Chen Wang, Zhaoliang Shen, Yue Guo, Zhanghui Wan, Chang LiuAbstract:Abstract Spinal cord injury (SCI) is a devastating condition with few effective treatments. Resveratrol, a polyphenolic compound, has exhibited neuroprotective effects in many neurodegenerative diseases. However, the explicit effect and mechanism of resveratrol on SCI is still unclear. Adenosine 5′ monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1), the downstream protein, play key roles in metabolizing of energy, resisting of resistance, and cellular protein homeostasis. In this study, we determined the effects of resveratrol on SCI and their potential relationship with SIRT1/AMPK Signaling pathway, autophagy and apoptosis. To determine the effect of resveratrol on SCI recovery, a spinal cord contusion model was employed. Rats received treatment with resveratrol or DMSO immediately following contusion. We determined that Basso, Beattie, and Bresnahan (BBB) scores were significantly higher for injured rats treated with resveratrol. Nissl and HE staining revealed that resveratrol treatment significantly reduced the loss of motor neurons and lesion size in the spinal cord of injured rats when compared to vehicle-treated animals. Spinal cord tissue was assessed by Western blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical analyses 7 days after injury for changes in expression of SIRT1/AMPK Signaling pathway, autophagy and apoptosis proteins. Expression of SIRT1, p-AMPK, Beclin-1, LC3-B, and Bcl-2 was elevated in resveratrol-treated animals, whereas expression of p62, Cleaved Caspase-3, Caspase-9, and Bcl-2 associated X protein (Bax) was inhibited. Immunofluorescence analysis of primary neurons treated with resveratrol alone or in combination with Compound C (AMPK inhibitor) or EX527 (SIRT1 inhibitor) revealed that treatment with the inhibitors blocks the increased LC3-B expression in cells and increases the portion of TUNEL-positive cells. Taken together, these results suggest that resveratrol exerts neuroprotective effects on SCI by regulating autophagy and apoptosis mediated by the SIRT1-AMPK Signaling pathway.
Haosen Zhao - One of the best experts on this subject based on the ideXlab platform.
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resveratrol protects against spinal cord injury by activating autophagy and inhibiting apoptosis mediated by the sirt1 AMPK Signaling pathway
Neuroscience, 2017Co-Authors: Haosen Zhao, Kai Gao, Shurui Chen, Zipeng Zhou, Chen Wang, Zhaoliang Shen, Yue Guo, Zhanghui Wan, Chang Liu, Xifan MeiAbstract:Abstract Spinal cord injury (SCI) is a devastating condition with few effective treatments. Resveratrol, a polyphenolic compound, has exhibited neuroprotective effects in many neurodegenerative diseases. However, the explicit effect and mechanism of resveratrol on SCI is still unclear. Adenosine 5′ monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1), the downstream protein, play key roles in metabolizing of energy, resisting of resistance, and cellular protein homeostasis. In this study, we determined the effects of resveratrol on SCI and their potential relationship with SIRT1/AMPK Signaling pathway, autophagy and apoptosis. To determine the effect of resveratrol on SCI recovery, a spinal cord contusion model was employed. Rats received treatment with resveratrol or DMSO immediately following contusion. We determined that Basso, Beattie, and Bresnahan (BBB) scores were significantly higher for injured rats treated with resveratrol. Nissl and HE staining revealed that resveratrol treatment significantly reduced the loss of motor neurons and lesion size in the spinal cord of injured rats when compared to vehicle-treated animals. Spinal cord tissue was assessed by Western blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical analyses 7 days after injury for changes in expression of SIRT1/AMPK Signaling pathway, autophagy and apoptosis proteins. Expression of SIRT1, p-AMPK, Beclin-1, LC3-B, and Bcl-2 was elevated in resveratrol-treated animals, whereas expression of p62, Cleaved Caspase-3, Caspase-9, and Bcl-2 associated X protein (Bax) was inhibited. Immunofluorescence analysis of primary neurons treated with resveratrol alone or in combination with Compound C (AMPK inhibitor) or EX527 (SIRT1 inhibitor) revealed that treatment with the inhibitors blocks the increased LC3-B expression in cells and increases the portion of TUNEL-positive cells. Taken together, these results suggest that resveratrol exerts neuroprotective effects on SCI by regulating autophagy and apoptosis mediated by the SIRT1-AMPK Signaling pathway.
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Resveratrol protects against spinal cord injury by activating autophagy and inhibiting apoptosis mediated by the SIRT1/AMPK Signaling pathway
Neuroscience, 2017Co-Authors: Haosen Zhao, Kai Gao, Shurui Chen, Zipeng Zhou, Chen Wang, Zhaoliang Shen, Yue Guo, Zhanghui Wan, Chang LiuAbstract:Abstract Spinal cord injury (SCI) is a devastating condition with few effective treatments. Resveratrol, a polyphenolic compound, has exhibited neuroprotective effects in many neurodegenerative diseases. However, the explicit effect and mechanism of resveratrol on SCI is still unclear. Adenosine 5′ monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1), the downstream protein, play key roles in metabolizing of energy, resisting of resistance, and cellular protein homeostasis. In this study, we determined the effects of resveratrol on SCI and their potential relationship with SIRT1/AMPK Signaling pathway, autophagy and apoptosis. To determine the effect of resveratrol on SCI recovery, a spinal cord contusion model was employed. Rats received treatment with resveratrol or DMSO immediately following contusion. We determined that Basso, Beattie, and Bresnahan (BBB) scores were significantly higher for injured rats treated with resveratrol. Nissl and HE staining revealed that resveratrol treatment significantly reduced the loss of motor neurons and lesion size in the spinal cord of injured rats when compared to vehicle-treated animals. Spinal cord tissue was assessed by Western blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical analyses 7 days after injury for changes in expression of SIRT1/AMPK Signaling pathway, autophagy and apoptosis proteins. Expression of SIRT1, p-AMPK, Beclin-1, LC3-B, and Bcl-2 was elevated in resveratrol-treated animals, whereas expression of p62, Cleaved Caspase-3, Caspase-9, and Bcl-2 associated X protein (Bax) was inhibited. Immunofluorescence analysis of primary neurons treated with resveratrol alone or in combination with Compound C (AMPK inhibitor) or EX527 (SIRT1 inhibitor) revealed that treatment with the inhibitors blocks the increased LC3-B expression in cells and increases the portion of TUNEL-positive cells. Taken together, these results suggest that resveratrol exerts neuroprotective effects on SCI by regulating autophagy and apoptosis mediated by the SIRT1-AMPK Signaling pathway.
Robert S. Lee-young - One of the best experts on this subject based on the ideXlab platform.
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Obesity impairs skeletal muscle AMPK Signaling during exercise: role of AMPKα2 in the regulation of exercise capacity in vivo.
International Journal of Obesity, 2010Co-Authors: Robert S. Lee-young, Julio E. Ayala, Patrick T. Fueger, Wesley H. Mayes, Li Kang, David H. WassermanAbstract:Obesity impairs skeletal muscle AMPK Signaling during exercise: role of AMPKα2 in the regulation of exercise capacity in vivo
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Acute exercise does not cause sustained elevations in AMPK Signaling or expression.
Medicine and Science in Sports and Exercise, 2008Co-Authors: Robert S. Lee-young, Benedict J Canny, George Koufogiannis, Glenn K McconellAbstract:ABSTRACTPurpose:No study has examined the response of skeletal muscle AMP-activated protein kinase (AMPK) Signaling beyond the first 3 h after an acute exercise bout in humans. The purpose of this study was to assess AMPK Signaling in human skeletal muscle immediately after a single bout of moderate
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Carbohydrate ingestion does not alter skeletal muscle AMPK Signaling during exercise in humans.
American journal of physiology. Endocrinology and metabolism, 2006Co-Authors: Robert S. Lee-young, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Glenn D. Wadley, Matthew J Palmer, Kelly C Linden, Kieran Leplastrier, Glenn K McconellAbstract:There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKalpha2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKalpha2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK Signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 +/- 1% V(O2 peak). In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly (P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPKalpha2 activity, AMPKalpha2 Thr(172) phosphorylation and acetyl-CoA Ser(222) phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK Signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.
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Effect of exercise intensity and hypoxia on skeletal muscle AMPK Signaling and substrate metabolism in humans.
American Journal of Physiology-endocrinology and Metabolism, 2005Co-Authors: Glenn D. Wadley, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Robert S. Lee-young, Chanchira Wasuntarawat, Zejian Chen, Glenn K McconellAbstract:We compared in human skeletal muscle the effect of absolute vs. relative exercise intensity on AMP-activated protein kinase (AMPK) Signaling and substrate metabolism under normoxic and hypoxic cond...
Bruce E Kemp - One of the best experts on this subject based on the ideXlab platform.
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Carbohydrate ingestion does not alter skeletal muscle AMPK Signaling during exercise in humans.
American journal of physiology. Endocrinology and metabolism, 2006Co-Authors: Robert S. Lee-young, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Glenn D. Wadley, Matthew J Palmer, Kelly C Linden, Kieran Leplastrier, Glenn K McconellAbstract:There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKalpha2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKalpha2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK Signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 +/- 1% V(O2 peak). In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly (P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPKalpha2 activity, AMPKalpha2 Thr(172) phosphorylation and acetyl-CoA Ser(222) phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK Signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.
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Effect of exercise intensity and hypoxia on skeletal muscle AMPK Signaling and substrate metabolism in humans.
American Journal of Physiology-endocrinology and Metabolism, 2005Co-Authors: Glenn D. Wadley, Mark Hargreaves, Benedict J Canny, Bruce E Kemp, Robert S. Lee-young, Chanchira Wasuntarawat, Zejian Chen, Glenn K McconellAbstract:We compared in human skeletal muscle the effect of absolute vs. relative exercise intensity on AMP-activated protein kinase (AMPK) Signaling and substrate metabolism under normoxic and hypoxic cond...
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Intensified exercise training does not alter AMPK Signaling in human skeletal muscle.
American journal of physiology. Endocrinology and metabolism, 2003Co-Authors: S A Clark, Bruce E Kemp, Z-p Chen, K T Murphy, R J Aughey, M J Mckenna, J A HawleyAbstract:The AMP-activated protein kinase (AMPK) cascade has been linked to many of the acute effects of exercise on skeletal muscle substrate metabolism, as well as to some of the chronic training-induced adaptations. We determined the effect of 3 wk of intensified training (HIT; 7 sessions of 8 x 5 min at 85% Vo2 peak) in skeletal muscle from well-trained athletes on AMPK responsiveness to exercise. Rates of whole body substrate oxidation were determined during a 90-min steady-state ride (SS) pre- and post-HIT. Muscle metabolites and AMPK Signaling were determined from biopsies taken at rest and immediately after exercise during the first and seventh HIT sessions, performed at the same (absolute) pre-HIT work rate. HIT decreased rates of whole body carbohydrate oxidation (P < 0.05) and increased rates of fat oxidation (P < 0.05) during SS. Resting muscle glycogen and its utilization during intense exercise were unaffected by HIT. However, HIT induced a twofold decrease in muscle [lactate] (P < 0.05) and resulted in tighter metabolic regulation, i.e., attenuation of the decrease in the PCr/(PCr + Cr) ratio and of the increase in [AMPfree]/ATP. Resting activities of AMPKalpha1 and -alpha2 were similar post-HIT, with the magnitude of the rise in response to exercise similar pre- and post-HIT. AMPK phosphorylation at Thr172 on both the alpha1 and alpha2 subunits increased in response to exercise, with the magnitude of this rise being similar post-HIT. Acetyl-coenzyme A carboxylase-beta phosphorylation was similar at rest and, despite HIT-induced increases in whole body rates of fat oxidation, did not increase post-HIT. Our results indicate that, in well-trained individuals, short-term HIT improves metabolic control but does not blunt AMPK Signaling in response to intense exercise.
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effect of exercise intensity on skeletal muscle AMPK Signaling in humans
Diabetes, 2003Co-Authors: Zhiping Chen, Sid Murthy, Mark Hargreaves, Lee A Witters, Benedict J Canny, Bruce E Kemp, Terry J. Stephens, Glenn K McconellAbstract:The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) Signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 ± 2% Vo2 peak), medium (59 ± 1% Vo2 peak), and high (79 ± 1% Vo2 peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P