Impact of a high-fat diet on dyslipidemia and gene expression of low-density lipoprotein receptors in male rats
Dyslipidemia is one of the leading causes of heart disease in human and pet animals. This study aimed to induce experimental dyslipidemia in adult male rats by a simple method via a high-fat diet. The 30 adult male rats were grouped as follows: The first group (G1) was feds a standard diet orally fo...
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Published in: | Iraqi journal of veterinary sciences Vol. 38; no. 1; pp. 133 - 138 |
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Main Authors: | , |
Format: | Journal Article |
Language: | English |
Published: |
University of Mosul, College of Veterinary Medicine
01-01-2024
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Subjects: | |
Online Access: | Get full text |
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Summary: | Dyslipidemia is one of the leading causes of heart disease in human and pet animals. This study aimed to induce experimental dyslipidemia in adult male rats by a simple method via a high-fat diet. The 30 adult male rats were grouped as follows: The first group (G1) was feds a standard diet orally for five weeks as a control, while the second group (G2) was given a high-fat diet (dyslipidemia group) for five weeks. Serum lipid profile confirmed the induction, in which there were elevated cholesterol, triacylglycerol, very low-density lipoproteins, low-density lipoproteins, and depressed high-density lipoprotein, so, the atherogenic index in the dyslipidemic group was more significant than the control rat group. Low-density lipoprotein receptor plays an essential role in the metabolism of lipids in the blood. Thus, there was an upregulation (about seven folds) in the expression of genes of the receptor of low-density lipoprotein corresponding with the elevated receptor protein concentration (18.6 ng/ml) when compared with the control group (1.91 ng/ml). It could be concluded that experimental dyslipidemia could be induced in adult rats by consuming a high-fat diet within five weeks, and it is related to gene expression upregulation and protein elevation of a receptor of low-density lipoprotein, and this may be a compensatory mechanism to challenge hyperlipidemia. |
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ISSN: | 2071-1255 1607-3894 2071-1255 |
DOI: | 10.33899/ijvs.2023.140070.3017 |