We are analyzing https://link.springer.com/article/10.1007/s001250050047.

Title:
Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by α-lipoic acid in 3T3-L1 adipocytes | Diabetologia
Description:
Aims/hypothesis. A natural cofactor of mitochondrial dehydrogenase complexes and a potent antioxidant, α-lipoic acid improves glucose metabolism in people with Type II (non-insulin-dependent) diabetes mellitus and in animal models of diabetes. In this study we investigated the cellular mechanism of action of α-lipoic acid in 3T3-L1 adipocytes.¶Methods. We treated 3T3-L1 adipocytes with 2.5 mmol/l R (+) α-lipoic acid for 2 to 60 min, followed by assays of: 2-deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate-1 in cell lysates; association of phosphatidylinositol 3-kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate-1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3-kinase with phosphotyrosine proteins or with insulin receptor substrate-1; and in vitro activity of immunoprecipitated Akt1. The effect of R (+) α-lipoic acid was also compared with that of S(–) α-lipoic acid.¶Results. Short-term treatment of 3T3-L1 adipocytes with R (+) α-lipoic acid rapidly stimulated glucose uptake in a wortmannin-sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate-1 and of the insulin receptor, increased the antiphosphotyrosine-associated and insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity and stimulated Akt activity.¶Conclusion/interpretation. These results indicate that R (+) α-lipoic acid directly activates lipid, tyrosine and serine/threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor. These properties are unique among all agents currently used to lower glycaemia in animals and humans with diabetes. [Diabetologia (2000) 43: 294–303]
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Keywords {🔍}

insulin, article, αlipoic, acid, receptor, glucose, adipocytes, diabetes, substrate, privacy, cookies, kinase, content, information, publish, search, diabetologia, transport, glut, phosphatidylinositol, data, journal, research, stimulation, download, yaworsky, somwar, ramlal, type, mechanism, uptake, tyrosine, activity, akt, signalling, discover, optional, personal, parties, policy, find, track, engagement, insulinsensitive, pathway, cite, pdf, manuscript, tritschler, klip,

Topics {✒️}

treated 3t3-l1 adipocytes α-lipoic acid adipose tissue signalling privacy choices/manage cookies 3t3-l1 adipocytes klip asta-medica stimulated akt activity insulin receptor substrate-1 main content log glucose uptake induced european economic area mitochondrial dehydrogenase complexes short-term treatment wortmannin-sensitive manner serine/threonine kinases related subjects insulin-sensitive pathway reduce insulin sensitivity subsequent insulin therapy conditions privacy policy insulin-dependent accepting optional cookies vitro kinase assay scope submit manuscript type 1 diabetes phosphatidylinositol 3-kinase activity caused tyrosine phosphorylation search search journal finder publish cellular mechanism type ii article cite article yaworsky glucose transport 2-deoxyglucose uptake privacy policy personal data insulin receptor action glucose transporter 1 books a diabetes mellitus vitro activity optional cookies phosphatidylinositol 3-kinase manage preferences insulin withdrawal data protection essential cookies cookies skip

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WebPage:
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         headline:Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by α-lipoic acid in 3T3-L1 adipocytes
         description: Aims/hypothesis. A natural cofactor of mitochondrial dehydrogenase complexes and a potent antioxidant, α-lipoic acid improves glucose metabolism in people with Type II (non-insulin-dependent) diabetes mellitus and in animal models of diabetes. In this study we investigated the cellular mechanism of action of α-lipoic acid in 3T3-L1 adipocytes.¶Methods. We treated 3T3-L1 adipocytes with 2.5 mmol/l R (+) α-lipoic acid for 2 to 60 min, followed by assays of: 2-deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate-1 in cell lysates; association of phosphatidylinositol 3-kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate-1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3-kinase with phosphotyrosine proteins or with insulin receptor substrate-1; and in vitro activity of immunoprecipitated Akt1. The effect of R (+) α-lipoic acid was also compared with that of S(–) α-lipoic acid.¶Results. Short-term treatment of 3T3-L1 adipocytes with R (+) α-lipoic acid rapidly stimulated glucose uptake in a wortmannin-sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate-1 and of the insulin receptor, increased the antiphosphotyrosine-associated and insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity and stimulated Akt activity.¶Conclusion/interpretation. These results indicate that R (+) α-lipoic acid directly activates lipid, tyrosine and serine/threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor. These properties are unique among all agents currently used to lower glycaemia in animals and humans with diabetes. [Diabetologia (2000) 43: 294–303]
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      headline:Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by α-lipoic acid in 3T3-L1 adipocytes
      description: Aims/hypothesis. A natural cofactor of mitochondrial dehydrogenase complexes and a potent antioxidant, α-lipoic acid improves glucose metabolism in people with Type II (non-insulin-dependent) diabetes mellitus and in animal models of diabetes. In this study we investigated the cellular mechanism of action of α-lipoic acid in 3T3-L1 adipocytes.¶Methods. We treated 3T3-L1 adipocytes with 2.5 mmol/l R (+) α-lipoic acid for 2 to 60 min, followed by assays of: 2-deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate-1 in cell lysates; association of phosphatidylinositol 3-kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate-1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3-kinase with phosphotyrosine proteins or with insulin receptor substrate-1; and in vitro activity of immunoprecipitated Akt1. The effect of R (+) α-lipoic acid was also compared with that of S(–) α-lipoic acid.¶Results. Short-term treatment of 3T3-L1 adipocytes with R (+) α-lipoic acid rapidly stimulated glucose uptake in a wortmannin-sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate-1 and of the insulin receptor, increased the antiphosphotyrosine-associated and insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity and stimulated Akt activity.¶Conclusion/interpretation. These results indicate that R (+) α-lipoic acid directly activates lipid, tyrosine and serine/threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor. These properties are unique among all agents currently used to lower glycaemia in animals and humans with diabetes. [Diabetologia (2000) 43: 294–303]
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         Human Physiology
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