The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome

Aims. To determine the effect of two different diets (high-sucrose (HS) and high-fat (HF)) on the main metabolic pathways potentially contributing to the development of steatosis: (1) activity of the liver lysosomal and heparin-releasable lipases; (2) fatty acid (FFA) oxidation; (3) FFA synthesis de...

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Main Authors: Monika Cahova, Helena Dankova, Eliska Palenickova, Zuzana Papackova, Ludmila Kazdova
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Journal of Nutrition and Metabolism
Online Access:http://dx.doi.org/10.1155/2012/757205
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author Monika Cahova
Helena Dankova
Eliska Palenickova
Zuzana Papackova
Ludmila Kazdova
author_facet Monika Cahova
Helena Dankova
Eliska Palenickova
Zuzana Papackova
Ludmila Kazdova
author_sort Monika Cahova
collection DOAJ
description Aims. To determine the effect of two different diets (high-sucrose (HS) and high-fat (HF)) on the main metabolic pathways potentially contributing to the development of steatosis: (1) activity of the liver lysosomal and heparin-releasable lipases; (2) fatty acid (FFA) oxidation; (3) FFA synthesis de novo; (4) VLDL output in vivo in a rat model of metabolic syndrome (MetS), hereditary hypertriglyceridemic (HHTg) rats fed HS or HF diets. Results. Both diets resulted in triacylglycerol (TAG) accumulation in the liver (HF > HS). The intracellular TAG lipolysis by lysosomal lipase was increased in both groups and positively correlated with the liver TAG content. Diet type significantly affected partitioning of intracellular TAG-derived fatty acids among FFA-utilizing metabolic pathways as HS feeding accentuated VLDL secretion and downregulated FFA oxidation while the HF diet had an entirely opposite effect. FFA de novo synthesis from glucose was significantly enhanced in the HS group (fed ≫ fasted) while being completely eradicated in the HF group. Conclusions. We found that in rats prone to the development of MetS associated diseases dietary-induced steatosis is not simply a result of impaired TAG degradation but that it depends on other mechanisms (elevated FFA synthesis or attenuated VLDL secretion) that are specific according to diet composition.
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spelling doaj-art-9e7fc9c5b17943e092fb3d193c744d6a2025-02-03T06:11:42ZengWileyJournal of Nutrition and Metabolism2090-07242090-07322012-01-01201210.1155/2012/757205757205The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic SyndromeMonika Cahova0Helena Dankova1Eliska Palenickova2Zuzana Papackova3Ludmila Kazdova4Department of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 14021 Prague, Czech RepublicDepartment of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 14021 Prague, Czech RepublicDepartment of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 14021 Prague, Czech RepublicDepartment of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 14021 Prague, Czech RepublicDepartment of Metabolism and Diabetes, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 14021 Prague, Czech RepublicAims. To determine the effect of two different diets (high-sucrose (HS) and high-fat (HF)) on the main metabolic pathways potentially contributing to the development of steatosis: (1) activity of the liver lysosomal and heparin-releasable lipases; (2) fatty acid (FFA) oxidation; (3) FFA synthesis de novo; (4) VLDL output in vivo in a rat model of metabolic syndrome (MetS), hereditary hypertriglyceridemic (HHTg) rats fed HS or HF diets. Results. Both diets resulted in triacylglycerol (TAG) accumulation in the liver (HF > HS). The intracellular TAG lipolysis by lysosomal lipase was increased in both groups and positively correlated with the liver TAG content. Diet type significantly affected partitioning of intracellular TAG-derived fatty acids among FFA-utilizing metabolic pathways as HS feeding accentuated VLDL secretion and downregulated FFA oxidation while the HF diet had an entirely opposite effect. FFA de novo synthesis from glucose was significantly enhanced in the HS group (fed ≫ fasted) while being completely eradicated in the HF group. Conclusions. We found that in rats prone to the development of MetS associated diseases dietary-induced steatosis is not simply a result of impaired TAG degradation but that it depends on other mechanisms (elevated FFA synthesis or attenuated VLDL secretion) that are specific according to diet composition.http://dx.doi.org/10.1155/2012/757205
spellingShingle Monika Cahova
Helena Dankova
Eliska Palenickova
Zuzana Papackova
Ludmila Kazdova
The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
Journal of Nutrition and Metabolism
title The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
title_full The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
title_fullStr The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
title_full_unstemmed The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
title_short The Opposite Effects of High-Sucrose and High-Fat Diet on Fatty Acid Oxidation and Very Low Density Lipoprotein Secretion in Rat Model of Metabolic Syndrome
title_sort opposite effects of high sucrose and high fat diet on fatty acid oxidation and very low density lipoprotein secretion in rat model of metabolic syndrome
url http://dx.doi.org/10.1155/2012/757205
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