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Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats
(R)‐ α ‐lipoic acid (ALA), an essential cofactor in mitochondrial respiration and a potential antioxidant, possesses a wide array of metabolic benefits including anti‐obesity, glucose lowering, insulin‐sensitizing, and lipid‐lowering effects. In this study, the curative effects of ALA (100 mg/kg) on...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464337/ https://www.ncbi.nlm.nih.gov/pubmed/28603627 http://dx.doi.org/10.1002/prp2.306 |
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author | Ghelani, Hardik Razmovski‐Naumovski, Valentina Nammi, Srinivas |
author_facet | Ghelani, Hardik Razmovski‐Naumovski, Valentina Nammi, Srinivas |
author_sort | Ghelani, Hardik |
collection | PubMed |
description | (R)‐ α ‐lipoic acid (ALA), an essential cofactor in mitochondrial respiration and a potential antioxidant, possesses a wide array of metabolic benefits including anti‐obesity, glucose lowering, insulin‐sensitizing, and lipid‐lowering effects. In this study, the curative effects of ALA (100 mg/kg) on a spectrum of conditions related to metabolic syndrome and type 2 diabetes (T2D) were investigated in a high‐fat diet (HFD)‐fed and low‐dose streptozotocin (STZ)‐induced rat model of metabolic syndrome and T2D. The marked rise in the levels of glucose, triglycerides, total‐cholesterol, LDL‐cholesterol, and VLDL‐cholesterol in the blood of HFD‐fed and low‐dose STZ‐injected rats were significantly reduced by ALA treatment. Furthermore, ALA treatment significantly increased the serum HDL‐cholesterol levels and tended to inhibit diabetes‐induced weight reduction. Mathematical computational analysis revealed that ALA also significantly improved insulin sensitivity and reduced the risk of atherosclerotic lesions and coronary atherogenesis. This study provides scientific evidence to substantiate the use of ALA to mitigate the glucose and lipid abnormality in metabolic syndrome and T2D. |
format | Online Article Text |
id | pubmed-5464337 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54643372017-06-09 Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats Ghelani, Hardik Razmovski‐Naumovski, Valentina Nammi, Srinivas Pharmacol Res Perspect Original Articles (R)‐ α ‐lipoic acid (ALA), an essential cofactor in mitochondrial respiration and a potential antioxidant, possesses a wide array of metabolic benefits including anti‐obesity, glucose lowering, insulin‐sensitizing, and lipid‐lowering effects. In this study, the curative effects of ALA (100 mg/kg) on a spectrum of conditions related to metabolic syndrome and type 2 diabetes (T2D) were investigated in a high‐fat diet (HFD)‐fed and low‐dose streptozotocin (STZ)‐induced rat model of metabolic syndrome and T2D. The marked rise in the levels of glucose, triglycerides, total‐cholesterol, LDL‐cholesterol, and VLDL‐cholesterol in the blood of HFD‐fed and low‐dose STZ‐injected rats were significantly reduced by ALA treatment. Furthermore, ALA treatment significantly increased the serum HDL‐cholesterol levels and tended to inhibit diabetes‐induced weight reduction. Mathematical computational analysis revealed that ALA also significantly improved insulin sensitivity and reduced the risk of atherosclerotic lesions and coronary atherogenesis. This study provides scientific evidence to substantiate the use of ALA to mitigate the glucose and lipid abnormality in metabolic syndrome and T2D. John Wiley and Sons Inc. 2017-04-03 /pmc/articles/PMC5464337/ /pubmed/28603627 http://dx.doi.org/10.1002/prp2.306 Text en © 2017 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Ghelani, Hardik Razmovski‐Naumovski, Valentina Nammi, Srinivas Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title | Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title_full | Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title_fullStr | Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title_full_unstemmed | Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title_short | Chronic treatment of (R)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in Sprague‐Dawley rats |
title_sort | chronic treatment of (r)‐α‐lipoic acid reduces blood glucose and lipid levels in high‐fat diet and low‐dose streptozotocin‐induced metabolic syndrome and type 2 diabetes in sprague‐dawley rats |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464337/ https://www.ncbi.nlm.nih.gov/pubmed/28603627 http://dx.doi.org/10.1002/prp2.306 |
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