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Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes
BACKGROUND: Progressive insulin resistance in a prediabetic state has been reported to be the predominant causative factor for the development of nonalcoholic fatty liver disease. The combination of dietary modification and pharmacotherapy has been recommended to manage diabetic liver complications....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911857/ https://www.ncbi.nlm.nih.gov/pubmed/31871510 http://dx.doi.org/10.1016/j.curtheres.2019.100570 |
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author | Mabuza, Lindokuhle Patience Gamede, Mlindeli Wilkinson Maikoo, Sanam Booysen, Irvin Noel Nguban, Phikelelani Siphosethu Khathi, Andile |
author_facet | Mabuza, Lindokuhle Patience Gamede, Mlindeli Wilkinson Maikoo, Sanam Booysen, Irvin Noel Nguban, Phikelelani Siphosethu Khathi, Andile |
author_sort | Mabuza, Lindokuhle Patience |
collection | PubMed |
description | BACKGROUND: Progressive insulin resistance in a prediabetic state has been reported to be the predominant causative factor for the development of nonalcoholic fatty liver disease. The combination of dietary modification and pharmacotherapy has been recommended to manage diabetic liver complications. However, poor patient compliance and toxicity of current drug therapy on liver function still results; thus, newer alternative drugs are required. OBJECTIVE: This study sought to investigate the hepatoprotective effects of the ruthenium(II) Schiff base complex in the presence and absence of dietary intervention in a diet-induced pre-diabetic rat model. METHODS: Prediabetic rats were randomly allocated to respective treatment groups. The ruthenium-based compound (15 mg/kg) was administered to the prediabetic rats in both the presence and absence of dietary intervention once a day every third day for 12 weeks. RESULTS: The administration of the ruthenium compound in both the presence and absence of dietary intervention resulted in the restoration of liver and body weights. This treatment also reduced liver damage enzyme biomarkers, bilirubin, and sterol regulatory element binding protein 1c concentrations in the plasma. CONCLUSIONS: The ruthenium(II) complex showed beneficial effects as it ameliorated and prevented the progression of diabetes-related liver derangements while eliminating the hepatotoxicity associated with the use of metal compounds. However, further studies are still required to further determine the physiological mechanisms behind this effect. |
format | Online Article Text |
id | pubmed-6911857 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-69118572019-12-23 Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes Mabuza, Lindokuhle Patience Gamede, Mlindeli Wilkinson Maikoo, Sanam Booysen, Irvin Noel Nguban, Phikelelani Siphosethu Khathi, Andile Curr Ther Res Clin Exp Original Research BACKGROUND: Progressive insulin resistance in a prediabetic state has been reported to be the predominant causative factor for the development of nonalcoholic fatty liver disease. The combination of dietary modification and pharmacotherapy has been recommended to manage diabetic liver complications. However, poor patient compliance and toxicity of current drug therapy on liver function still results; thus, newer alternative drugs are required. OBJECTIVE: This study sought to investigate the hepatoprotective effects of the ruthenium(II) Schiff base complex in the presence and absence of dietary intervention in a diet-induced pre-diabetic rat model. METHODS: Prediabetic rats were randomly allocated to respective treatment groups. The ruthenium-based compound (15 mg/kg) was administered to the prediabetic rats in both the presence and absence of dietary intervention once a day every third day for 12 weeks. RESULTS: The administration of the ruthenium compound in both the presence and absence of dietary intervention resulted in the restoration of liver and body weights. This treatment also reduced liver damage enzyme biomarkers, bilirubin, and sterol regulatory element binding protein 1c concentrations in the plasma. CONCLUSIONS: The ruthenium(II) complex showed beneficial effects as it ameliorated and prevented the progression of diabetes-related liver derangements while eliminating the hepatotoxicity associated with the use of metal compounds. However, further studies are still required to further determine the physiological mechanisms behind this effect. Elsevier 2019-11-13 /pmc/articles/PMC6911857/ /pubmed/31871510 http://dx.doi.org/10.1016/j.curtheres.2019.100570 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Research Mabuza, Lindokuhle Patience Gamede, Mlindeli Wilkinson Maikoo, Sanam Booysen, Irvin Noel Nguban, Phikelelani Siphosethu Khathi, Andile Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title | Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title_full | Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title_fullStr | Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title_full_unstemmed | Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title_short | Hepatoprotective Effects of a Ruthenium(II) Schiff Base Complex in Rats with Diet-Induced Prediabetes |
title_sort | hepatoprotective effects of a ruthenium(ii) schiff base complex in rats with diet-induced prediabetes |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911857/ https://www.ncbi.nlm.nih.gov/pubmed/31871510 http://dx.doi.org/10.1016/j.curtheres.2019.100570 |
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