Resveratrol improves insulin signaling in a tissue-specific manner under insulin-resistant conditions only: in vitro and in vivo experiments in rodents
Abstract Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin signaling has not been completely evaluated. Here, we determined whether RSV alters insulin signaling in insulin-responsive cells and tissues. The e...
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Published in | Metabolism, clinical and experimental Vol. 61; no. 3; pp. 424 - 433 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.03.2012
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Abstract | Abstract Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin signaling has not been completely evaluated. Here, we determined whether RSV alters insulin signaling in insulin-responsive cells and tissues. The effects of RSV on insulin signaling in 3T3-L1 adipocytes under both insulin-sensitive and insulin-resistant states and in insulin-sensitive tissues of high fat–fed diet-induced obese (DIO) mice were investigated. Insulin-stimulated insulin receptor substrate–1 tyrosine phosphorylation (Y612) was suppressed in RSV-treated adipocytes compared with untreated adipocytes, as was the insulin-stimulated Akt phosphorylation (Ser473). However, under an insulin-resistant condition that was made by incubating 3T3-L1 adipocytes in the conditioned medium from lipopolysaccharide-stimulated LAW264.7 cells, RSV reduced inducible nitric oxide synthase expression and I κ B α protein degradation and improved insulin-stimulated Akt phosphorylation (Ser473). In DIO mice, relatively low-dose RSV (30 mg/kg daily for 2 weeks) therapy lowered fasting blood glucose level and serum insulin, increased hepatic glycogen content, and ameliorated fatty liver without change in body weight. The insulin-stimulated Akt phosphorylation was decreased in the liver and white adipose tissue of DIO mice, but it was completely normalized by RSV treatment. However, in the skeletal muscle of DIO mice, insulin signaling was not improved by RSV treatment, whereas the phosphorylation of adenosine monophosphate–activated protein kinase α (Thr172) was improved by it. Our results show that RSV enhances insulin action only under insulin-resistant conditions and suggest that the effect of RSV may depend on the type of tissue being targeted and its metabolic status. |
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AbstractList | Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin signaling has not been completely evaluated. Here, we determined whether RSV alters insulin signaling in insulin-responsive cells and tissues. The effects of RSV on insulin signaling in 3T3-L1 adipocytes under both insulin-sensitive and insulin-resistant states and in insulin-sensitive tissues of high fat–fed diet-induced obese (DIO) mice were investigated. Insulin-stimulated insulin receptor substrate–1 tyrosine phosphorylation (Y612) was suppressed in RSV-treated adipocytes compared with untreated adipocytes, as was the insulin-stimulated Akt phosphorylation (Ser473). However, under an insulin-resistant condition that was made by incubating 3T3-L1 adipocytes in the conditioned medium from lipopolysaccharide-stimulated LAW264.7 cells, RSV reduced inducible nitric oxide synthase expression and IκBα protein degradation and improved insulin-stimulated Akt phosphorylation (Ser473). In DIO mice, relatively low-dose RSV (30 mg/kg daily for 2 weeks) therapy lowered fasting blood glucose level and serum insulin, increased hepatic glycogen content, and ameliorated fatty liver without change in body weight. The insulin-stimulated Akt phosphorylation was decreased in the liver and white adipose tissue of DIO mice, but it was completely normalized by RSV treatment. However, in the skeletal muscle of DIO mice, insulin signaling was not improved by RSV treatment, whereas the phosphorylation of adenosine monophosphate–activated protein kinase α (Thr172) was improved by it. Our results show that RSV enhances insulin action only under insulin-resistant conditions and suggest that the effect of RSV may depend on the type of tissue being targeted and its metabolic status. Abstract Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin signaling has not been completely evaluated. Here, we determined whether RSV alters insulin signaling in insulin-responsive cells and tissues. The effects of RSV on insulin signaling in 3T3-L1 adipocytes under both insulin-sensitive and insulin-resistant states and in insulin-sensitive tissues of high fat–fed diet-induced obese (DIO) mice were investigated. Insulin-stimulated insulin receptor substrate–1 tyrosine phosphorylation (Y612) was suppressed in RSV-treated adipocytes compared with untreated adipocytes, as was the insulin-stimulated Akt phosphorylation (Ser473). However, under an insulin-resistant condition that was made by incubating 3T3-L1 adipocytes in the conditioned medium from lipopolysaccharide-stimulated LAW264.7 cells, RSV reduced inducible nitric oxide synthase expression and I κ B α protein degradation and improved insulin-stimulated Akt phosphorylation (Ser473). In DIO mice, relatively low-dose RSV (30 mg/kg daily for 2 weeks) therapy lowered fasting blood glucose level and serum insulin, increased hepatic glycogen content, and ameliorated fatty liver without change in body weight. The insulin-stimulated Akt phosphorylation was decreased in the liver and white adipose tissue of DIO mice, but it was completely normalized by RSV treatment. However, in the skeletal muscle of DIO mice, insulin signaling was not improved by RSV treatment, whereas the phosphorylation of adenosine monophosphate–activated protein kinase α (Thr172) was improved by it. Our results show that RSV enhances insulin action only under insulin-resistant conditions and suggest that the effect of RSV may depend on the type of tissue being targeted and its metabolic status. |
Author | Park, Doekbae Lee, Young-Jae Han, Chang Hoon Guan, Jian Yang, Eun-Jin Lee, Dae-Ho Hong, Hyun Ju Kang, Wonyoung Koh, Gwanpyo Kim, Dong Geon |
Author_xml | – sequence: 1 fullname: Kang, Wonyoung – sequence: 2 fullname: Hong, Hyun Ju – sequence: 3 fullname: Guan, Jian – sequence: 4 fullname: Kim, Dong Geon – sequence: 5 fullname: Yang, Eun-Jin – sequence: 6 fullname: Koh, Gwanpyo – sequence: 7 fullname: Park, Doekbae – sequence: 8 fullname: Han, Chang Hoon – sequence: 9 fullname: Lee, Young-Jae – sequence: 10 fullname: Lee, Dae-Ho |
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Keywords | Pancreatic hormone Rodentia Antioxidant In vitro Insulin Stilbene derivatives Resistance In vivo Tissue Vertebrata Mammalia Animal Resveratrol Endocrinology |
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Snippet | Abstract Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin... Resveratrol (RSV) has various metabolic effects, especially with relatively high-dose therapy. However, the ability of RSV to modulate insulin signaling has... |
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SubjectTerms | 3T3-L1 Cells Adipocytes - drug effects Adipocytes - metabolism AMP-Activated Protein Kinases - metabolism Animals Anti-Inflammatory Agents - pharmacology Biological and medical sciences Blotting, Western Cells, Cultured Culture Media, Conditioned Dietary Fats - pharmacology Endocrinology & Metabolism Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology Inflammation - metabolism Insulin - physiology Insulin Resistance - physiology Liver - cytology Liver - drug effects Liver - metabolism Male Mice Mice, Inbred C57BL Mice, Obese Obesity - chemically induced Obesity - metabolism Phosphorylation Real-Time Polymerase Chain Reaction Signal Transduction - drug effects Stilbenes - pharmacology Vertebrates: anatomy and physiology, studies on body, several organs or systems |
Title | Resveratrol improves insulin signaling in a tissue-specific manner under insulin-resistant conditions only: in vitro and in vivo experiments in rodents |
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