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N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress
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Zeitschriftentitel: | American Journal of Physiology-Endocrinology and Metabolism |
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Personen und Körperschaften: | , , , , , , , |
In: | American Journal of Physiology-Endocrinology and Metabolism, 285, 2003, 4, S. E744-E753 |
Format: | E-Article |
Sprache: | Englisch |
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American Physiological Society
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author_facet |
Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George |
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author |
Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George |
spellingShingle |
Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George American Journal of Physiology-Endocrinology and Metabolism N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism |
author_sort |
haber, c. andrew |
spelling |
Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George 0193-1849 1522-1555 American Physiological Society Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism http://dx.doi.org/10.1152/ajpendo.00355.2002 <jats:p>Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (R<jats:sub>d</jats:sub>), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered R<jats:sub>d</jats:sub>. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.</jats:p> <i>N</i>-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress American Journal of Physiology-Endocrinology and Metabolism |
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10.1152/ajpendo.00355.2002 |
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American Physiological Society |
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title |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_unstemmed |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_full |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_fullStr |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_full_unstemmed |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_short |
N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_sort |
<i>n</i>-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
topic |
Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism |
url |
http://dx.doi.org/10.1152/ajpendo.00355.2002 |
publishDate |
2003 |
physical |
E744-E753 |
description |
<jats:p>Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (R<jats:sub>d</jats:sub>), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered R<jats:sub>d</jats:sub>. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.</jats:p> |
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author | Haber, C. Andrew, Lam, Tony K. T., Yu, Zhiwen, Gupta, Neehar, Goh, Tracy, Bogdanovic, Elena, Giacca, Adria, Fantus, I. George |
author_facet | Haber, C. Andrew, Lam, Tony K. T., Yu, Zhiwen, Gupta, Neehar, Goh, Tracy, Bogdanovic, Elena, Giacca, Adria, Fantus, I. George, Haber, C. Andrew, Lam, Tony K. T., Yu, Zhiwen, Gupta, Neehar, Goh, Tracy, Bogdanovic, Elena, Giacca, Adria, Fantus, I. George |
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container_title | American Journal of Physiology-Endocrinology and Metabolism |
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description | <jats:p>Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (R<jats:sub>d</jats:sub>), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered R<jats:sub>d</jats:sub>. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.</jats:p> |
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spelling | Haber, C. Andrew Lam, Tony K. T. Yu, Zhiwen Gupta, Neehar Goh, Tracy Bogdanovic, Elena Giacca, Adria Fantus, I. George 0193-1849 1522-1555 American Physiological Society Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism http://dx.doi.org/10.1152/ajpendo.00355.2002 <jats:p>Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (R<jats:sub>d</jats:sub>), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg<jats:sup>–</jats:sup><jats:sup>1</jats:sup>· min<jats:sup>–</jats:sup><jats:sup>1</jats:sup>). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered R<jats:sub>d</jats:sub>. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.</jats:p> <i>N</i>-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress American Journal of Physiology-Endocrinology and Metabolism |
spellingShingle | Haber, C. Andrew, Lam, Tony K. T., Yu, Zhiwen, Gupta, Neehar, Goh, Tracy, Bogdanovic, Elena, Giacca, Adria, Fantus, I. George, American Journal of Physiology-Endocrinology and Metabolism, N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress, Physiology (medical), Physiology, Endocrinology, Diabetes and Metabolism |
title | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_full | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_fullStr | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_full_unstemmed | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_short | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_sort | <i>n</i>-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
title_unstemmed | N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress |
topic | Physiology (medical), Physiology, Endocrinology, Diabetes and Metabolism |
url | http://dx.doi.org/10.1152/ajpendo.00355.2002 |