AIM: Non-alcoholic steatohepatitis (NASH) increases cardiovascular risk regardless of risk factors in metabolic syndrome. However, the intermediary factors between NASH and vascular disease are still unknown because a suitable animal model has never been established. The stroke-prone (SP) spontaneously hypertensive rat, SHRSP5/Dmcr, simultaneously develops hypertension, acute arterial lipid deposits in mesenteric arteries, and NASH when feed with a high-fat and high-cholesterol (HFC) diet. We investigated whether SHRSP5/Dmcr affected with NASH aggravates the cardiac or vascular dysfunction. METHOD: Wister Kyoto and SHRSP5/Dmcr rats were divided into 4 groups of 5 rats each, and fed with a SP or HFC diet. After 8 weeks of HFC or SP diet feeding, glucose and insulin resistance, echocardiography, blood biochemistry, histopathological staining, and endothelial function in aorta were evaluated. RESULTS: We demonstrate that SHRSP5/Dmcr rats fed with a HFC diet presented with cardiac and vascular dysfunction caused by cardiac fibrosis, endothelial dysfunction, and left ventricular diastolic dysfunction, in association with NASH and hypertension. These cardiac and vascular dysfunctions were aggravated and not associated with the presence of hypertension, glucose metabolism disorder, and/or obesity. CONCLUSIONS: SHRSP5/Dmcr rats may be a suitable animal model for elucidating the organ interaction between NASH and cardiac or vascular dysfunction.
AIM: Non-alcoholic steatohepatitis (NASH) increases cardiovascular risk regardless of risk factors in metabolic syndrome. However, the intermediary factors between NASH and vascular disease are still unknown because a suitable animal model has never been established. Thestroke-prone (SP) spontaneously hypertensiverat, SHRSP5/Dmcr, simultaneously develops hypertension, acute arterial lipid deposits in mesenteric arteries, and NASH when feed with a high-fat and high-cholesterol (HFC) diet. We investigated whether SHRSP5/Dmcr affected with NASH aggravates thecardiac or vascular dysfunction. METHOD: Wister Kyoto and SHRSP5/Dmcrrats were divided into 4 groups of 5 rats each, and fed with a SP or HFC diet. After 8 weeks of HFC or SP diet feeding, glucose and insulin resistance, echocardiography, blood biochemistry, histopathological staining, and endothelial function in aorta were evaluated. RESULTS: We demonstrate that SHRSP5/Dmcrrats fed with a HFC diet presented with cardiac and vascular dysfunction caused by cardiac fibrosis, endothelial dysfunction, and left ventricular diastolic dysfunction, in association with NASH and hypertension. These cardiac and vascular dysfunctions were aggravated and not associated with the presence of hypertension, glucose metabolism disorder, and/or obesity. CONCLUSIONS: SHRSP5/Dmcrrats may be a suitable animal model for elucidating the organ interaction between NASH and cardiac or vascular dysfunction.
Authors: Ebenezer T Oni; Arthur S Agatston; Michael J Blaha; Jonathan Fialkow; Ricardo Cury; Andrei Sposito; Raimund Erbel; Ron Blankstein; Ted Feldman; Mouaz H Al-Mallah; Raul D Santos; Matthew J Budoff; Khurram Nasir Journal: Atherosclerosis Date: 2013-08-09 Impact factor: 5.162
Authors: A Sciacqua; M Perticone; S Miceli; I Laino; E J Tassone; R D Grembiale; F Andreozzi; G Sesti; F Perticone Journal: Nutr Metab Cardiovasc Dis Date: 2010-03-12 Impact factor: 4.222
Authors: Victoria A Nankivell; Joanne T M Tan; Christina A Bursill; Alex Brown; Laura A Wilsdon; Kaitlin R Morrison; Carmel Bilu; Peter J Psaltis; Paul Zimmet; Noga Kronfeld-Schor; Stephen J Nicholls Journal: Sci Rep Date: 2021-05-06 Impact factor: 4.379
Authors: Carolina F F A Costa; Benedita Sampaio-Maia; Ricardo Araujo; Diana S Nascimento; Joana Ferreira-Gomes; Manuel Pestana; Maria J Azevedo; Ines S Alencastre Journal: Nutrients Date: 2022-01-14 Impact factor: 5.717