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Chronic dyslipidemia imposed by a high-fat and high-caloric dietary regime leads to debilitating disorders such as obesity, nonalcoholic fatty liver disease (NAFLD), and insulin resistance. As disease rates surge, so does the need for high validity animal models to effectively study the causal relationship between diet and disease progression. The dyslipidemic guinea pig displays a high similarity with the human lipoprotein profile and may in this aspect be superior to other rodent models. This study investigated the effects of 2 long-term Westernized diets (0.35% cholesterol, 18.5% vegetable oil and either 15% or 20% sucrose) compared with isocaloric standard chow in adult guinea pigs. Biochemical markers confirmed dyslipidemia in agreement with dietary regimens; however, both high-fat groups displayed a decreased tissue fat percentage compared with controls. Macroscopic appearance, histopathologic evaluation, and plasma markers of liver function confirmed NAFLD in high-fat groups, supported by liver redox imbalance and markers suggesting hepatic endothelial dysfunction. Plasma markers indicated endothelial dysfunction in response to a high-fat diet, although atherosclerotic lesions were not evident. Evaluation of glucose tolerance showed no indication of insulin resistance. The 5% increase in sucrose between the 2 high-fat diets did not lead to significant differences between groups. In conclusion, we find the dyslipidemic guinea pig to be a valid model of diet imposed dyslipidemia, particularly with regards to hepatic steatosis and endothelial dysfunction. Furthermore, the absence of obesity supports the present study setup as targeting NAFLD in nonobese individuals.
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http://dx.doi.org/10.1016/j.trsl.2015.10.001 | DOI Listing |
Heliyon
December 2024
Institute of Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, Nuremberg General Hospital, Paracelsus Medical University, Prof. Ernst Nathan Str. 1, 90419, Nuremberg, Germany.
Background: Type 2 diabetes mellitus (T2DM) is marked by insulin resistance, low grade chronic inflammation, and endothelial dysfunction. Vitamin K2, especially menaquinone-7 (MK-7), might delay T2DM progression and alleviate its consequences. Hence, this study evaluated the effects of MK-7 on serum and urine markers of diabetes in an animal model of T2DM.
View Article and Find Full Text PDFEndocr Res
December 2024
Department of Biology, College of Science, Salahaddin University-Erbil, Erbil, Kurdistan Region, Iraq.
Background: In patients with diabetes mellitus (DM), vascular endothelial dysfunction (VED) is the main reason for impaired life expectancy. Melatonin (MEL) demonstrates wide-ranging effects across various organs and exhibits pleiotropic characteristics. The current study aims to investigate the modulatory roles of MEL vascular response to angiotensin II (Ang II) and its receptors including angiotensin type 1 receptor (AT-1 R) and angiotensin type 2 receptor (AT-2 R) in isolated thoracic aorta of non-diabetes (non-DM) and diabetes (DM) rats.
View Article and Find Full Text PDFJ Transl Med
December 2024
Institut de Recherche Biomédicale Des Armées (IRBA), 1, Rue du Lieutenant Raoul Batany, 92141, Clamart, France.
Background: Hemorrhagic shock (HS) corresponds to absolute hypovolemia creating an imbalance between oxygen supply and consumption. This causes an impaired hemostasis, a systemic inflammatory response, and microvascular permeability which can lead to multiple organ failure (MOF). There is no specific treatment for the endothelial dysfunction that plays a major role in the evolution towards MOF.
View Article and Find Full Text PDFBackground: TPM3 (tropomyosin 3) is an actin-binding protein in vascular smooth muscle cells, where posttranslational modifications critically regulate its actin affinity, influencing cardiovascular function. Emerging evidence suggests that Khib (2-hydroxyisobutyrylation) plays a significant role in the cardiovascular system. Histone deacetylase 3 (HDAC3) serves as an "eraser" of Khib marks.
View Article and Find Full Text PDFLife Sci
December 2024
Department of Anesthesiology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University & Fujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fujian Provincial Key Laboratory of Critical Medicine, Fujian Provincial Co-constructed Laboratory of "Belt and Road", Fuzhou, Fujian 350001, China. Electronic address:
Aims: Nicotine-exacerbated atherosclerosis significantly increases global mortality. Endothelial cells, which line the interior of blood vessels, are crucial for maintaining vascular function. How nicotine is involved in vascular remodeling in atherosclerosis via modulating endothelial dysfunction remains unknown.
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