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The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid

AIMS: This study aimed to examine the effect of high fat diet (HFD) to modulate brain dysfunction, and understand the linkages between obesity, metabolic disturbances and the brain oxidative stress (BOS) dysfunction and modulation with hydroxyl citric acid of G. Cambogia. METHODS: Rats were divided...

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Detalles Bibliográficos
Autores principales: Amin, Kamal A, Kamel, Hamdy H, Abd Eltawab, Mohamed A
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104359/
https://www.ncbi.nlm.nih.gov/pubmed/21569551
http://dx.doi.org/10.1186/1476-511X-10-74
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author Amin, Kamal A
Kamel, Hamdy H
Abd Eltawab, Mohamed A
author_facet Amin, Kamal A
Kamel, Hamdy H
Abd Eltawab, Mohamed A
author_sort Amin, Kamal A
collection PubMed
description AIMS: This study aimed to examine the effect of high fat diet (HFD) to modulate brain dysfunction, and understand the linkages between obesity, metabolic disturbances and the brain oxidative stress (BOS) dysfunction and modulation with hydroxyl citric acid of G. Cambogia. METHODS: Rats were divided into 3 groups; 1(st )control, maintained on standard normal rat chow diet, 2(nd )HFD, maintained on high fat diet along 12 week and 3(rd )HFD+G, administered G. Cambogia for 4 weeks and each group include 8 rats. Blood, brain and abdominal fat were collected for biochemical measurements. RESULTS: HFD group showed significant increase in energy intake, final BW and BW gain. Also significant increase in weight of abdominal fat in HFD group. HFD induce metabolic disturbance through increasing the lipid profile (LDL, TG, TC), γGT and α-amylase activity, uric acid level and hyperglycemia, while decreasing creatine kinase (CK) activity. These changes associated with lowering in brain nitric oxide (NO) level and rising in serum butyrylcholinesterase (BChE), brain catalase activity and MDA levels as oxidative stress markers. These alterations improved by G. Cambogia that decrease BOS and increased NO level. CONCLUSIONS: Rats fed HFD showed, metabolic disturbances produce hyperglycemia, hypertriglyceridemia, hypercholesterolemia and increased LDL associated with increased BOS. Involvement of BuChE, NO and oxidative stress associated with metabolic disturbances in the pathophysiological progression in brain, suggesting association between obesity, metabolic disorders and brain alteration while, using G. Cambogia, ameliorate the damaging effects of the HFD via lowering feed intake and BOS.
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spelling pubmed-31043592011-06-01 The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid Amin, Kamal A Kamel, Hamdy H Abd Eltawab, Mohamed A Lipids Health Dis Research AIMS: This study aimed to examine the effect of high fat diet (HFD) to modulate brain dysfunction, and understand the linkages between obesity, metabolic disturbances and the brain oxidative stress (BOS) dysfunction and modulation with hydroxyl citric acid of G. Cambogia. METHODS: Rats were divided into 3 groups; 1(st )control, maintained on standard normal rat chow diet, 2(nd )HFD, maintained on high fat diet along 12 week and 3(rd )HFD+G, administered G. Cambogia for 4 weeks and each group include 8 rats. Blood, brain and abdominal fat were collected for biochemical measurements. RESULTS: HFD group showed significant increase in energy intake, final BW and BW gain. Also significant increase in weight of abdominal fat in HFD group. HFD induce metabolic disturbance through increasing the lipid profile (LDL, TG, TC), γGT and α-amylase activity, uric acid level and hyperglycemia, while decreasing creatine kinase (CK) activity. These changes associated with lowering in brain nitric oxide (NO) level and rising in serum butyrylcholinesterase (BChE), brain catalase activity and MDA levels as oxidative stress markers. These alterations improved by G. Cambogia that decrease BOS and increased NO level. CONCLUSIONS: Rats fed HFD showed, metabolic disturbances produce hyperglycemia, hypertriglyceridemia, hypercholesterolemia and increased LDL associated with increased BOS. Involvement of BuChE, NO and oxidative stress associated with metabolic disturbances in the pathophysiological progression in brain, suggesting association between obesity, metabolic disorders and brain alteration while, using G. Cambogia, ameliorate the damaging effects of the HFD via lowering feed intake and BOS. BioMed Central 2011-05-14 /pmc/articles/PMC3104359/ /pubmed/21569551 http://dx.doi.org/10.1186/1476-511X-10-74 Text en Copyright ©2011 Amin et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Amin, Kamal A
Kamel, Hamdy H
Abd Eltawab, Mohamed A
The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title_full The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title_fullStr The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title_full_unstemmed The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title_short The relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
title_sort relation of high fat diet, metabolic disturbances and brain oxidative dysfunction: modulation by hydroxy citric acid
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104359/
https://www.ncbi.nlm.nih.gov/pubmed/21569551
http://dx.doi.org/10.1186/1476-511X-10-74
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