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8		<title>Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats</title>
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15					<meta name="description" content="Diabetes is the predominant metabolic condition in humans and animals, particularly in pets; it frequently coexists with many other metabolic abnormalities involving carbohydrates, proteins, and lipids. This study was conducted to investigate the correlation between experimentally generated diabetes and dyslipidemia concerning the gene expression of low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), apolipoprotein-E (APOE), and lipoprotein lipase (LPL) in adipose tissue. Sixty-four adult male albino rats were divided into four groups: the first group (control group), receiving a standard diet, while the second group became the dyslipidemia group, which was fed accordingly high-fat diet (HFD), the third group was the diabetes and dyslipidemia group or mixed group fed HFD. Taking a single dosage of 50 mg/kg of streptozotocin (STZ) intraperitoneally, the fourth group became the diabetic group. fed a standard diet and using a single-dose of 50 mg/kg STZ. Results demonstrated that diabetes and dyslipidemia cause significant changes in lipid profile, insulin resistance, and body weight parameters. Dyslipidemia exhibited a significant elevation in total cholesterol and triglycerides relative to the control group. STZ caused a notable elevation in glucose levels and a reduction in insulin levels, those changes resulted in upregulation or downregulation in gene expression of LPL, LDLR, APOB, and APOE. LPL gene expression is downregulated except in the diabetes group, which is slightly upregulated. LDLR gene expression significantly increased in dyslipidemia. It could be concluded that the coexistence of diabetes and dyslipidemia worsens most biochemical markers and gene expression, appearing to be more synergistically harmful than either condition alone." />
16					<meta name="title" content="Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats" />
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18					<meta name="citation_title" content="Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats" />
19					<meta name="citation_author" content="Mahmood, Harikar Salih" />
20					<meta name="citation_author_institution" content="Dept. of Physiology, Biochemistry, and Pharmacology, College of Veterinary Medicine, University of Mosul" />
21					<meta name="citation_author" content="Mustafa, Nashaat Ghalib" />
22					<meta name="citation_author_institution" content="Alkendey" />
23					<meta name="citation_abstract" content="Diabetes is the predominant metabolic condition in humans and animals, particularly in pets; it frequently coexists with many other metabolic abnormalities involving carbohydrates, proteins, and lipids. This study was conducted to investigate the correlation between experimentally generated diabetes and dyslipidemia concerning the gene expression of low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), apolipoprotein-E (APOE), and lipoprotein lipase (LPL) in adipose tissue. Sixty-four adult male albino rats were divided into four groups: the first group (control group), receiving a standard diet, while the second group became the dyslipidemia group, which was fed accordingly high-fat diet (HFD), the third group was the diabetes and dyslipidemia group or mixed group fed HFD. Taking a single dosage of 50 mg/kg of streptozotocin (STZ) intraperitoneally, the fourth group became the diabetic group. fed a standard diet and using a single-dose of 50 mg/kg STZ. Results demonstrated that diabetes and dyslipidemia cause significant changes in lipid profile, insulin resistance, and body weight parameters. Dyslipidemia exhibited a significant elevation in total cholesterol and triglycerides relative to the control group. STZ caused a notable elevation in glucose levels and a reduction in insulin levels, those changes resulted in upregulation or downregulation in gene expression of LPL, LDLR, APOB, and APOE. LPL gene expression is downregulated except in the diabetes group, which is slightly upregulated. LDLR gene expression significantly increased in dyslipidemia. It could be concluded that the coexistence of diabetes and dyslipidemia worsens most biochemical markers and gene expression, appearing to be more synergistically harmful than either condition alone." />
24					<meta name="citation_id" content="190465" />
25					<meta name="citation_publication_date" content="2026/07/05" />
26					<meta name="citation_date" content="2026-07-05" />
27					<meta name="citation_journal_title" content="Iraqi Journal of Veterinary Scie
27nces" />
28					<meta name="citation_issn" content="1607-3894" />
29					<meta name="citation_volume" content="40" />
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33					<meta name="citation_publisher" content="College of Veterinary Medicine / University of Mosul" />
34					<meta name="citation_doi" content="10.33899/ijvs.2025.159710.4269" />
35					<meta name="DC.Identifier" content="10.33899/ijvs.2025.159710.4269" />
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38					<meta name="DC.Title" content="Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats" />
39					<meta name="DC.Source" content="Iraqi Journal of Veterinary Sciences" />
40					<meta name="DC.Date" content="05/07/2026" />
41					<meta name="DC.Date.issued" content="2026-07-05" />
42					<meta name="DC.Format" content="application/pdf" />
43					<meta name="DC.Contributor" content="Mahmood, Harikar Salih" />
44					<meta name="DC.Contributor" content="Mustafa, Nashaat Ghalib" />
45					<meta name="og:title" content="Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats" />
46					<meta name="og:description" content="Diabetes is the predominant metabolic condition in humans and animals, particularly in pets; it frequently coexists with many other metabolic abnormalities involving carbohydrates, proteins, and lipids. This study was conducted to investigate the correlation between experimentally generated diabetes and dyslipidemia concerning the gene expression of low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), apolipoprotein-E (APOE), and lipoprotein lipase (LPL) in adipose tissue. Sixty-four adult male albino rats were divided into four groups: the first group (control group), receiving a standard diet, while the second group became the dyslipidemia group, which was fed accordingly high-fat diet (HFD), the third group was the diabetes and dyslipidemia group or mixed group fed HFD. Taking a single dosage of 50 mg/kg of streptozotocin (STZ) intraperitoneally, the fourth group became the diabetic group. fed a standard diet and using a single-dose of 50 mg/kg STZ. Results demonstrated that diabetes and dyslipidemia cause significant changes in lipid profile, insulin resistance, and body weight parameters. Dyslipidemia exhibited a significant elevation in total cholesterol and triglycerides relative to the control group. STZ caused a notable elevation in glucose levels and a reduction in insulin levels, those changes resulted in upregulation or downregulation in gene expression of LPL, LDLR, APOB, and APOE. LPL gene expression is downregulated except in the diabetes group, which is slightly upregulated. LDLR gene expression significantly increased in dyslipidemia. It could be concluded that the coexistence of diabetes and dyslipidemia worsens most biochemical markers and gene expression, appearing to be more synergistically harmful than either condition alone." />
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439                                    <h1 class="ltr"><a href="./article_190465_eef340b0309c6cf38def21bc617753e1.pdf" target="_blank">Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats</a></h1>
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452                                    <a href="./?_action=article&amp;au=478364&amp;_au=Harikar+Salih+Mahmood">Harikar Salih Mahmood</a>
453            
454                                                
455                                                                            <sup><a class="inline-block text-green" href="https://orcid.org/0009-0000-1279-3640" data-toggle="tooltip" data-placement="bottom" title="OrcID: 0009-0000-1279-3640" target="_blank"><i class="ai ai-orcid size-16" ></i></a></sup>
456                                                
457                                                                            <sup><a class="inline-block" href="#aff1" >1</a></sup>                                                                    </li>
458                                                            <li class="padding-3">
459                                    <a href="./?_action=article&amp;au=469656&amp;_au=Nashaat+Ghalib+Mustafa">Nashaat Ghalib Mustafa</a>
460            
461                                                                            <sup><a class="inline-block" href="/cdn-cgi/l/email-protection#402e213328212134777400352f2d2f33352c6e2524356e2931" data-toggle="tooltip" data-placement="bottom" title="Email to Corresponding Author"><i class="fa fa-envelope-o" ></i></a></sup>
462                                                
463                                                                            <sup><a class="inline-block text-green" href="https://orcid.org/0000-0002-8351-1230" data-toggle="tooltip" data-placement="bottom" title="OrcID: 0000-0002-8351-1230" target="_blank"><i class="ai ai-orcid size-16" ></i></a></sup>
464                                                
465                                                                            <sup><a class="inline-block" href="#aff2" >2</a></sup>                                                                    </li>
466                                                    </ul>
467            
468                                                    <p class="margin-bottom-3 ltr" id="aff1">
469                                                                    <sup>1</sup>
470                                                                Dept. of Physiology, Biochemistry, and Pharmacology, College of Veterinary Medicine, University of Mosul                            </p>
471                                                    <p class="margin-bottom-3 ltr" id="aff2">
472                                                                    <sup>2</sup>
473                                                                Alkendey                            </p>
474                                    
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491                    
492                    
493                        <div class="margin-bottom-3 ltr" id="ar_doi"><i class="ai ai-doi size-25 text-orange"></i> <span dir="ltr">
493<a href="https://doi.org/10.33899/ijvs.2025.159710.4269">10.33899/ijvs.2025.159710.4269</a></span></div>
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529                                    <p class="padding-0" style="margin:12px -2px 0 -2px"><strong>Abstract</strong></p>
530                    <p class="justify_txt ltr">Diabetes is the predominant metabolic condition in humans and animals, particularly in pets; it frequently coexists with many other metabolic abnormalities involving carbohydrates, proteins, and lipids. This study was conducted to investigate the correlation between experimentally generated diabetes and dyslipidemia concerning the gene expression of low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), apolipoprotein-E (APOE), and lipoprotein lipase (LPL) in adipose tissue. Sixty-four adult male albino rats were divided into four groups: the first group (control group), receiving a standard diet, while the second group became the dyslipidemia group, which was fed accordingly high-fat diet (HFD), the third group was the diabetes and dyslipidemia group or mixed group fed HFD. Taking a single dosage of 50 mg/kg of streptozotocin (STZ) intraperitoneally, the fourth group became the diabetic group. fed a standard diet and using a single-dose of 50 mg/kg STZ. Results demonstrated that diabetes and dyslipidemia cause significant changes in lipid profile, insulin resistance, and body weight parameters. Dyslipidemia exhibited a significant elevation in total cholesterol and triglycerides relative to the control group. STZ caused a notable elevation in glucose levels and a reduction in insulin levels, those changes resulted in upregulation or downregulation in gene expression of LPL, LDLR, APOB, and APOE. LPL gene expression is downregulated except in the diabetes group, which is slightly upregulated. LDLR gene expression significantly increased in dyslipidemia. It could be concluded that the coexistence of diabetes and dyslipidemia worsens most biochemical markers and gene expression, appearing to be more synergistically harmful than either condition alone.</p>
531                                
532                
533                <div class="kw">
534                  
535                                            <p class="padding-0" style="margin:12px -2px 0 -2px"><strong>Keywords</strong></p>
536                        
537                        <ul class="block list-inline list-inline-seprator margin-bottom-6 ltr">
538                                                            <li class="padding-3">
539                                    <a href="./?_action=article&amp;kw=49438&amp;_kw=Diabetes" >Diabetes</a>
540                                </li>
541                                                            <li class="padding-3">
542                                    <a href="./?_action=article&amp;kw=31467&amp;_kw=Dyslipidemia" >Dyslipidemia</a>
543                                </li>
544                                                            <li class="padding-3">
545                                    <a href="./?_action=article&amp;kw=69267&amp;_kw=Gene+Expression" >Gene Expression</a>
546                                </li>
547                                                            <li class="padding-3">
548                                    <a href="./?_action=article&amp;kw=302924&amp;_kw=LDLR" >LDLR</a>
549                                </li>
550                                                            <li class="padding-3">
551                                    <a href="./?_action=article&amp;kw=308103&amp;_kw=LPL" >LPL</a>
552                                </li>
553                                                    </ul>
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756                                                	<h6 style="margin-top:0px;"><a href="./issue_15428_15644.html">Volume 40, Issue 3 - Issue Serial Number 3</a><br/>July 2026<div id="sp_ar_pages">Page <span dir="ltr">449-456</span></div></h6>
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937                            <p>Mahmood, H.,  & Mustafa, N. (2026). Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats. <em>
937Iraqi Journal of Veterinary Sciences</em>, <em>40</em>(3), 449-456. doi: 10.33899/ijvs.2025.159710.4269</p>
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954                            <p>Harikar Salih Mahmood; Nashaat Ghalib Mustafa. "Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats". <em>Iraqi Journal of Veterinary Sciences</em>, 40, 3, 2026, 449-456. doi: 10.33899/ijvs.2025.159710.4269</p>
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971                            <p>Mahmood, H., Mustafa, N. (2026). 'Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats', <em>Iraqi Journal of Veterinary Sciences</em>, 40(3), pp. 449-456. doi: 10.33899/ijvs.2025.159710.4269</p>
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988                            <p>Mahmood, H., Mustafa, N. Gene Expression of LDLR, APOB, APOE, and LPL in Experimentally Induced Diabetes and Dyslipidemia in Rats. <em>Iraqi Journal of Veterinary Sciences</em>, 2026; 40(3): 449-456. doi: 10.33899/ijvs.2025.159710.4269</p>
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