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Paresh Dandona - One of the best experts on this subject based on the ideXlab platform.
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Glucose ingestion induces an increase in intranuclear nuclear factor κB, a fall in cellular inhibitor κB, and an increase in tumor necrosis factor α messenger RNA by mononuclear cells in healthy human subjects
Metabolism: clinical and experimental, 2006Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Jay Friedman, Deborah Hofmeyer, Ajay Chaudhuri, Paresh DandonaAbstract:Abstract Because hyperglycemia is a major detrimental factor in the prognosis of acute cardiovascular conditions such as acute myocardial infarction (AMI) and stroke, and because an acute Glucose challenge in healthy subjects has been shown to induce oxidative stress in mononuclear cells (MNCs), we have now investigated whether Glucose induces inflammatory stress at the cellular and molecular level. Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor κ B (NF- κ B) binding, the reduction of inhibitor κ B α (I κ B α ) protein, and an increase in the activity of inhibitor κ B kinase (IKK) and the expression of IKK α and IKK β , the enzymes that phosphorylate I κ B α , in MNCs. Glucose Intake caused an increase in NF- κ B binding to NF- κ B2, NF- κ B2a, and NF- κ B3 sequences in the promoter site of tumor necrosis factor α (TNF- α ) gene along with an increase in the expression of TNF- α messenger RNA in MNCs. Membranous p47 phox subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after Glucose Intake. We conclude that Glucose Intake induces an immediate increase in intranuclear NF- κ B binding, a fall in I κ B α , an increase in IKK α , IKK β , IKK activity, and messenger RNA expression of TNF- α in MNCs in healthy subjects. These data are consistent with profound acute pro-inflammatory changes in MNCs after Glucose Intake.
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Glucose Intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase c
The American journal of clinical nutrition, 2004Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Tufail Syed, Arindam Bandyopadhyay, Paresh DandonaAbstract:Background: Glucose Intake has been shown to cause an increase in intranuclear nuclear factor-B and a decrease in inhibitor B that are consistent with a proinflammatory effect. We investigated the effect of Glucose Intake on 2 other proinflammatory transcription factors, activator protein 1 (AP-1) and early growth response 1 (Egr-1), and on the genes regulated by them, ie, the genes for matrix metalloproteinases 2 (MMP-2 )a nd 9( MMP-9) and tissue factor (TF), respectively. Objective: The objective of the study was to ascertain whether the Intake of 75 g Glucose induces an increase in AP-1, Egr-1, and the genes regulated by them. Design: Eight healthy subjects were given 75 g Glucose dissolved in 300 mL water to drink. Blood samples were collected before and 1, 2, and 3 h after Glucose Intake. Four weeks later, the same subjects were given 300 mL water sweetened with saccharine, and blood samples were collected at the same time points. Mononuclear cells (MNCs) were separated, and nuclear fractions were isolated. Results: AP-1 and Egr-1 binding activities were significantly higher 1 and 2 h after Glucose Intake and then decreased toward the baseline by 3 h. The expression of MMP-2 and TF in MNC homogenates also was significantly higher at 2 and 3 h. Plasma concentrations of MMP-2 were significantly higher at 3 h, whereas those of MMP-9 were significantly higher at 1, 2, and 3 h. In addition, TF was significantly higher at 2 and 3 h. Intake of saccharine-sweetened water had no significant effect on the inflammatory mediators measured in this study. Conclusion: Glucose induces proinflammatory changes, including increases in AP-1, Egr-1, MMPs, and TF, the factors that regulate processes that are potentially relevant to atherosclerotic plaque rupture and thrombosis. Am J Clin Nutr 2004;80:51–7.
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Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes.
The Journal of clinical endocrinology and metabolism, 2000Co-Authors: Priya Mohanty, Ahmad Aljada, Husam Ghanim, Wael Hamouda, Rajesh Garg, Paresh DandonaAbstract:Diabetes mellitus is associated with increased ROS generation, oxidative injury and obesity. To elucidate the relationship between nutrition and ROS generation, we have investigated the effect of Glucose challenge on ROS generation by leucocytes, p47phox protein, a key protein in the enzyme NADPH oxidase and α-tocopherol levels. Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g Glucose. ROS generation by polymorphonuclear leucocytes (PMNL) and mononuclear cells (MNC) increased to a peak of 244 ± 42% and 233 ± 34% of the basal respectively at 2 h. The levels of p47phox in MNC homogenates increased significantly at 2 h and 3 h after Glucose Intake. α-Tocopherol levels decreased significantly at 1 h, 2 h, and 3 h. We conclude that Glucose Intake stimulates ROS generation and p47phox of NADPH oxidase; increases oxidative load and causes a fall in α-tocopherol concentration.
Takeo Hashiguchi - One of the best experts on this subject based on the ideXlab platform.
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Acute Changes in Arterial Stiffness with Palatinose Versus Glucose Intake in Elderly
Cardiology and Cardiovascular Medicine, 2020Co-Authors: Ryota Kobayashi, Kaori Sato, Miki Sakazaki, Yukie Nagai, Soichiro Iwanuma, Nobuyuki Ohashi, Toshihiko Takahashi, Kenji Asaki, Takeo HashiguchiAbstract:Background: We assessed acute effects of palatinose (isomaltulose) consumption on arterial stiffness. Increased arterial stiffness due to elevated postprandial blood Glucose levels increases the risk of cardiovascular disease. Palatinose appears to suppress an increase in BG levels while securing energy, and might decrease acute increases in arterial stiffness during hyperglycemia. However, the acute effects of palatinose consumption on arterial stiffness are unknown. Methods: Ten older adults had two interventions in the following cross-over design: (i) ingestion of 25 g of Glucose solution (GSI trial) and (ii) ingestion of 25 g of palatinose solution (PSI trial). Participants fasted for 12 h and then visited the laboratory. We assessed brachialankle (ba) and heartbrachial (hb) pulse wave velocity (PWV), the cardio-ankle vascular index (CAVI), brachial and ankle blood pressure, heart rate, and blood Glucose levels at baseline (before ingestion) and 30, 60, and 90 min after ingestion. Results: Changes in baPWV, hbPWV, the CAVI, and ankle systolic blood pressure were significantly increased from baseline at 30, 60, and 90 min after ingestion in the GSI trial (p < 0.05), but not in the PSI trial. The changes in baPWV, hbPWV, and CAVI were significantly lower after ingestion in the PSI trial compared with the GSI trial. Blood Glucose levels were significantly lower at 30 and 60 min after ingestion in the PSI trial compared with the GSI trial (p < 0.01). Conclusions: We conclude that arterial stiffness may increase after Glucose ingestion, but it is not elevated after palatinose ingestion.
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Acute effects of difference in Glucose Intake on arterial stiffness in healthy subjects
Cardiology journal, 2019Co-Authors: Ryota Kobayashi, Kaori Sato, Miki Sakazaki, Yukie Nagai, Soichiro Iwanuma, Nobuyuki Ohashi, Takeo HashiguchiAbstract:Background: Post-prandial hyperglycemia is associated with higher cardiovascular risk, which causes arterial stiffening and impaired function. Although post-prandial increases in blood Glucose are proportional to the level of Intake, the acute effects of different Glucose Intakes on arterial stiffness have not been fully characterized. The present study aimed to determine the acute effects of differences in Glucose Intake on arterial stiffness. Methods: Six healthy middle-aged and elderly individuals (mean age, 60.0 ± 12.1 years) were orally administered 15, 20, and 25 g of Glucose on separate days in a randomized, controlled, cross-over fashion. Brachial-ankle pulse wave velocity, heart-brachial pulse wave velocity, cardio-ankle vascular index, brachial and ankle blood pressure, heart rate, and blood Glucose and serum insulin concentrations before and 30, 60, and 90 min after Glucose ingestion were measured. Results: Compared to baseline, brachial-ankle pulse wave velocity was higher at 30, 60 and 90 min after ingestion of 25 g Glucose, and higher at 90 min after ingestion of 20 g Glucose, but at no time points after ingestion of 15 g. Cardio-ankle vascular index was higher at 60 min than at baseline after ingestion of 25 g Glucose, but not after ingestion of 15 or 20 g. Conclusions: These results suggest that brachial-ankle pulse wave velocity and cardio-ankle vascular index is affected by the quantity of Glucose ingested. Proposed presently is that Glucose Intake should be reduced at each meal to avoid increases in brachial-ankle pulse wave velocity and cardio-ankle vascular index during acute hyperglycemia.
Ahmad Aljada - One of the best experts on this subject based on the ideXlab platform.
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Glucose ingestion induces an increase in intranuclear nuclear factor κB, a fall in cellular inhibitor κB, and an increase in tumor necrosis factor α messenger RNA by mononuclear cells in healthy human subjects
Metabolism: clinical and experimental, 2006Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Jay Friedman, Deborah Hofmeyer, Ajay Chaudhuri, Paresh DandonaAbstract:Abstract Because hyperglycemia is a major detrimental factor in the prognosis of acute cardiovascular conditions such as acute myocardial infarction (AMI) and stroke, and because an acute Glucose challenge in healthy subjects has been shown to induce oxidative stress in mononuclear cells (MNCs), we have now investigated whether Glucose induces inflammatory stress at the cellular and molecular level. Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor κ B (NF- κ B) binding, the reduction of inhibitor κ B α (I κ B α ) protein, and an increase in the activity of inhibitor κ B kinase (IKK) and the expression of IKK α and IKK β , the enzymes that phosphorylate I κ B α , in MNCs. Glucose Intake caused an increase in NF- κ B binding to NF- κ B2, NF- κ B2a, and NF- κ B3 sequences in the promoter site of tumor necrosis factor α (TNF- α ) gene along with an increase in the expression of TNF- α messenger RNA in MNCs. Membranous p47 phox subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after Glucose Intake. We conclude that Glucose Intake induces an immediate increase in intranuclear NF- κ B binding, a fall in I κ B α , an increase in IKK α , IKK β , IKK activity, and messenger RNA expression of TNF- α in MNCs in healthy subjects. These data are consistent with profound acute pro-inflammatory changes in MNCs after Glucose Intake.
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Glucose Intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase c
The American journal of clinical nutrition, 2004Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Tufail Syed, Arindam Bandyopadhyay, Paresh DandonaAbstract:Background: Glucose Intake has been shown to cause an increase in intranuclear nuclear factor-B and a decrease in inhibitor B that are consistent with a proinflammatory effect. We investigated the effect of Glucose Intake on 2 other proinflammatory transcription factors, activator protein 1 (AP-1) and early growth response 1 (Egr-1), and on the genes regulated by them, ie, the genes for matrix metalloproteinases 2 (MMP-2 )a nd 9( MMP-9) and tissue factor (TF), respectively. Objective: The objective of the study was to ascertain whether the Intake of 75 g Glucose induces an increase in AP-1, Egr-1, and the genes regulated by them. Design: Eight healthy subjects were given 75 g Glucose dissolved in 300 mL water to drink. Blood samples were collected before and 1, 2, and 3 h after Glucose Intake. Four weeks later, the same subjects were given 300 mL water sweetened with saccharine, and blood samples were collected at the same time points. Mononuclear cells (MNCs) were separated, and nuclear fractions were isolated. Results: AP-1 and Egr-1 binding activities were significantly higher 1 and 2 h after Glucose Intake and then decreased toward the baseline by 3 h. The expression of MMP-2 and TF in MNC homogenates also was significantly higher at 2 and 3 h. Plasma concentrations of MMP-2 were significantly higher at 3 h, whereas those of MMP-9 were significantly higher at 1, 2, and 3 h. In addition, TF was significantly higher at 2 and 3 h. Intake of saccharine-sweetened water had no significant effect on the inflammatory mediators measured in this study. Conclusion: Glucose induces proinflammatory changes, including increases in AP-1, Egr-1, MMPs, and TF, the factors that regulate processes that are potentially relevant to atherosclerotic plaque rupture and thrombosis. Am J Clin Nutr 2004;80:51–7.
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Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes.
The Journal of clinical endocrinology and metabolism, 2000Co-Authors: Priya Mohanty, Ahmad Aljada, Husam Ghanim, Wael Hamouda, Rajesh Garg, Paresh DandonaAbstract:Diabetes mellitus is associated with increased ROS generation, oxidative injury and obesity. To elucidate the relationship between nutrition and ROS generation, we have investigated the effect of Glucose challenge on ROS generation by leucocytes, p47phox protein, a key protein in the enzyme NADPH oxidase and α-tocopherol levels. Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g Glucose. ROS generation by polymorphonuclear leucocytes (PMNL) and mononuclear cells (MNC) increased to a peak of 244 ± 42% and 233 ± 34% of the basal respectively at 2 h. The levels of p47phox in MNC homogenates increased significantly at 2 h and 3 h after Glucose Intake. α-Tocopherol levels decreased significantly at 1 h, 2 h, and 3 h. We conclude that Glucose Intake stimulates ROS generation and p47phox of NADPH oxidase; increases oxidative load and causes a fall in α-tocopherol concentration.
Priya Mohanty - One of the best experts on this subject based on the ideXlab platform.
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Glucose ingestion induces an increase in intranuclear nuclear factor κB, a fall in cellular inhibitor κB, and an increase in tumor necrosis factor α messenger RNA by mononuclear cells in healthy human subjects
Metabolism: clinical and experimental, 2006Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Jay Friedman, Deborah Hofmeyer, Ajay Chaudhuri, Paresh DandonaAbstract:Abstract Because hyperglycemia is a major detrimental factor in the prognosis of acute cardiovascular conditions such as acute myocardial infarction (AMI) and stroke, and because an acute Glucose challenge in healthy subjects has been shown to induce oxidative stress in mononuclear cells (MNCs), we have now investigated whether Glucose induces inflammatory stress at the cellular and molecular level. Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor κ B (NF- κ B) binding, the reduction of inhibitor κ B α (I κ B α ) protein, and an increase in the activity of inhibitor κ B kinase (IKK) and the expression of IKK α and IKK β , the enzymes that phosphorylate I κ B α , in MNCs. Glucose Intake caused an increase in NF- κ B binding to NF- κ B2, NF- κ B2a, and NF- κ B3 sequences in the promoter site of tumor necrosis factor α (TNF- α ) gene along with an increase in the expression of TNF- α messenger RNA in MNCs. Membranous p47 phox subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after Glucose Intake. We conclude that Glucose Intake induces an immediate increase in intranuclear NF- κ B binding, a fall in I κ B α , an increase in IKK α , IKK β , IKK activity, and messenger RNA expression of TNF- α in MNCs in healthy subjects. These data are consistent with profound acute pro-inflammatory changes in MNCs after Glucose Intake.
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Glucose Intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase c
The American journal of clinical nutrition, 2004Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Tufail Syed, Arindam Bandyopadhyay, Paresh DandonaAbstract:Background: Glucose Intake has been shown to cause an increase in intranuclear nuclear factor-B and a decrease in inhibitor B that are consistent with a proinflammatory effect. We investigated the effect of Glucose Intake on 2 other proinflammatory transcription factors, activator protein 1 (AP-1) and early growth response 1 (Egr-1), and on the genes regulated by them, ie, the genes for matrix metalloproteinases 2 (MMP-2 )a nd 9( MMP-9) and tissue factor (TF), respectively. Objective: The objective of the study was to ascertain whether the Intake of 75 g Glucose induces an increase in AP-1, Egr-1, and the genes regulated by them. Design: Eight healthy subjects were given 75 g Glucose dissolved in 300 mL water to drink. Blood samples were collected before and 1, 2, and 3 h after Glucose Intake. Four weeks later, the same subjects were given 300 mL water sweetened with saccharine, and blood samples were collected at the same time points. Mononuclear cells (MNCs) were separated, and nuclear fractions were isolated. Results: AP-1 and Egr-1 binding activities were significantly higher 1 and 2 h after Glucose Intake and then decreased toward the baseline by 3 h. The expression of MMP-2 and TF in MNC homogenates also was significantly higher at 2 and 3 h. Plasma concentrations of MMP-2 were significantly higher at 3 h, whereas those of MMP-9 were significantly higher at 1, 2, and 3 h. In addition, TF was significantly higher at 2 and 3 h. Intake of saccharine-sweetened water had no significant effect on the inflammatory mediators measured in this study. Conclusion: Glucose induces proinflammatory changes, including increases in AP-1, Egr-1, MMPs, and TF, the factors that regulate processes that are potentially relevant to atherosclerotic plaque rupture and thrombosis. Am J Clin Nutr 2004;80:51–7.
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Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes.
The Journal of clinical endocrinology and metabolism, 2000Co-Authors: Priya Mohanty, Ahmad Aljada, Husam Ghanim, Wael Hamouda, Rajesh Garg, Paresh DandonaAbstract:Diabetes mellitus is associated with increased ROS generation, oxidative injury and obesity. To elucidate the relationship between nutrition and ROS generation, we have investigated the effect of Glucose challenge on ROS generation by leucocytes, p47phox protein, a key protein in the enzyme NADPH oxidase and α-tocopherol levels. Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g Glucose. ROS generation by polymorphonuclear leucocytes (PMNL) and mononuclear cells (MNC) increased to a peak of 244 ± 42% and 233 ± 34% of the basal respectively at 2 h. The levels of p47phox in MNC homogenates increased significantly at 2 h and 3 h after Glucose Intake. α-Tocopherol levels decreased significantly at 1 h, 2 h, and 3 h. We conclude that Glucose Intake stimulates ROS generation and p47phox of NADPH oxidase; increases oxidative load and causes a fall in α-tocopherol concentration.
Husam Ghanim - One of the best experts on this subject based on the ideXlab platform.
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Glucose ingestion induces an increase in intranuclear nuclear factor κB, a fall in cellular inhibitor κB, and an increase in tumor necrosis factor α messenger RNA by mononuclear cells in healthy human subjects
Metabolism: clinical and experimental, 2006Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Jay Friedman, Deborah Hofmeyer, Ajay Chaudhuri, Paresh DandonaAbstract:Abstract Because hyperglycemia is a major detrimental factor in the prognosis of acute cardiovascular conditions such as acute myocardial infarction (AMI) and stroke, and because an acute Glucose challenge in healthy subjects has been shown to induce oxidative stress in mononuclear cells (MNCs), we have now investigated whether Glucose induces inflammatory stress at the cellular and molecular level. Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor κ B (NF- κ B) binding, the reduction of inhibitor κ B α (I κ B α ) protein, and an increase in the activity of inhibitor κ B kinase (IKK) and the expression of IKK α and IKK β , the enzymes that phosphorylate I κ B α , in MNCs. Glucose Intake caused an increase in NF- κ B binding to NF- κ B2, NF- κ B2a, and NF- κ B3 sequences in the promoter site of tumor necrosis factor α (TNF- α ) gene along with an increase in the expression of TNF- α messenger RNA in MNCs. Membranous p47 phox subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after Glucose Intake. We conclude that Glucose Intake induces an immediate increase in intranuclear NF- κ B binding, a fall in I κ B α , an increase in IKK α , IKK β , IKK activity, and messenger RNA expression of TNF- α in MNCs in healthy subjects. These data are consistent with profound acute pro-inflammatory changes in MNCs after Glucose Intake.
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Glucose Intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase c
The American journal of clinical nutrition, 2004Co-Authors: Ahmad Aljada, Husam Ghanim, Priya Mohanty, Tufail Syed, Arindam Bandyopadhyay, Paresh DandonaAbstract:Background: Glucose Intake has been shown to cause an increase in intranuclear nuclear factor-B and a decrease in inhibitor B that are consistent with a proinflammatory effect. We investigated the effect of Glucose Intake on 2 other proinflammatory transcription factors, activator protein 1 (AP-1) and early growth response 1 (Egr-1), and on the genes regulated by them, ie, the genes for matrix metalloproteinases 2 (MMP-2 )a nd 9( MMP-9) and tissue factor (TF), respectively. Objective: The objective of the study was to ascertain whether the Intake of 75 g Glucose induces an increase in AP-1, Egr-1, and the genes regulated by them. Design: Eight healthy subjects were given 75 g Glucose dissolved in 300 mL water to drink. Blood samples were collected before and 1, 2, and 3 h after Glucose Intake. Four weeks later, the same subjects were given 300 mL water sweetened with saccharine, and blood samples were collected at the same time points. Mononuclear cells (MNCs) were separated, and nuclear fractions were isolated. Results: AP-1 and Egr-1 binding activities were significantly higher 1 and 2 h after Glucose Intake and then decreased toward the baseline by 3 h. The expression of MMP-2 and TF in MNC homogenates also was significantly higher at 2 and 3 h. Plasma concentrations of MMP-2 were significantly higher at 3 h, whereas those of MMP-9 were significantly higher at 1, 2, and 3 h. In addition, TF was significantly higher at 2 and 3 h. Intake of saccharine-sweetened water had no significant effect on the inflammatory mediators measured in this study. Conclusion: Glucose induces proinflammatory changes, including increases in AP-1, Egr-1, MMPs, and TF, the factors that regulate processes that are potentially relevant to atherosclerotic plaque rupture and thrombosis. Am J Clin Nutr 2004;80:51–7.
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Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes.
The Journal of clinical endocrinology and metabolism, 2000Co-Authors: Priya Mohanty, Ahmad Aljada, Husam Ghanim, Wael Hamouda, Rajesh Garg, Paresh DandonaAbstract:Diabetes mellitus is associated with increased ROS generation, oxidative injury and obesity. To elucidate the relationship between nutrition and ROS generation, we have investigated the effect of Glucose challenge on ROS generation by leucocytes, p47phox protein, a key protein in the enzyme NADPH oxidase and α-tocopherol levels. Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g Glucose. ROS generation by polymorphonuclear leucocytes (PMNL) and mononuclear cells (MNC) increased to a peak of 244 ± 42% and 233 ± 34% of the basal respectively at 2 h. The levels of p47phox in MNC homogenates increased significantly at 2 h and 3 h after Glucose Intake. α-Tocopherol levels decreased significantly at 1 h, 2 h, and 3 h. We conclude that Glucose Intake stimulates ROS generation and p47phox of NADPH oxidase; increases oxidative load and causes a fall in α-tocopherol concentration.