Why the study?
Resistin is implicated in adipose tissue dysfunction and modulated by PPARγ, but its role alongside PPARγ in the development of CVS disease required investigation.
Does PPARγ agonist administration improve lipid profile, inflammatory status, and aortic histopathology in rat models of obesity and atherosclerosis?
Does PPARγ agonist administration improve lipid profile, inflammatory status, and aortic histopathology in rat models of obesity and atherosclerosis?
In a rat model, PPARγ agonist administration improved inflammatory status, dyslipidemia, and aortic histopathological changes associated with obesity and atherosclerosis.
Obesity and atherosclerosis are inflammatory states involving variable metabolic signals. The adipokine resistin is implicated in adipose tissue dysfunction and is modulated by PPARγ. In this study, resistin and PPARγ role is investigated in the development of CVS disease. Forty-eight Adult male albino rats were divided into control, obesity and atherosclerotic groups; each group is divided into two subgroups; with and without PPARγ agonist administration for 8 weeks. To assess pathological changes; lipid profile, inflammatory mediator, serum resistin level and resistin expression in adipose tissue were measured. Aorta is histopathologically evaluated. It was found that resistin expression is significantly correlated with lipid profile and inflammatory status in obesity and atherosclerotic groups, and PPARγ agonist administration significantly improves inflammatory status and dyslipidemic profile across studied groups (p < .05). Aortic wall shows histopathological evidence of atherosclerosis in obesity group which is more evident in atherosclerotic group, and milder changes upon receiving PPARγ agonist.
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Sabry et al. (2019) studied this question.
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