PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

Sodium nitroprusside Endothelial Dysfunction
DOI: 10.1016/j.atherosclerosis.2021.08.006 Publication Date: 2021-08-05T11:11:54Z
ABSTRACT
Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one bed to another.In this study, MetS was induced by a high-fat, high-sucrose diet, after 28 weeks, aorta renal arteries were removed used for isometric recording of tension organ baths, protein expression Western blot, histological analysis assess the presence atherosclerosis.MetS mild hypertension, pre-diabetes, central obesity dyslipidaemia. Our results indicated that did not change contractile response either or artery. Conversely, vasodilation affected both different way. The showed dysfunction, including lower acetylcholine sodium nitroprusside, while artery presented preserved relaxation an increased sensitivity nitroprusside. We find oxidative stress MetS, but we found significant decrease PPARγ, phospho-Akt (p-Akt) phospho-eNOS (p-eNOS) expression. On other hand, Akt p-Akt overexpressed. No evidence atherosclerosis MetS.MetS affects function differently depending on vessel. In aorta, it decreases PPARγ/Akt/eNOS pathway, artery, increases PPARγ/Akt signalling pathway without decreasing vasodilation.
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