A high-fat diet for 28 weeks increased plasma soluble prorenin receptor, nondipping blood pressure, and vascular stiffness in male mice, whereas female mice preserved their phenotype until ovariectomy.
Does a high-fat diet increase plasma soluble prorenin receptor and cause vascular damage in male and female mice?
Plasma sPRR may indicate the status of systemic RAAS activation and the onset of vascular complications during T2DM in a sex-dependent manner.
High-fat diet (HFD) for 28 wk leads to type 2 diabetes mellitus (T2DM) phenotype, concomitant with increased plasma soluble prorenin receptor (sPRR), nondipping blood pressure, and vascular stiffness in male mice. HFD-fed female mice exhibiting a preserved cardiometabolic phenotype until ovariectomy revealed increased plasma sPRR and blood pressure. Plasma sPRR may indicate the status of systemic renin-angiotensin-aldosterone system (RAAS) activation and the onset of vascular complications during T2DM in a sex-dependent manner.
Visniauskas et al. (Fri,) conducted a other in Type 2 diabetes mellitus phenotype and vascular damage. High-fat diet was evaluated on Plasma soluble prorenin receptor (sPRR), blood pressure, and vascular stiffness. A high-fat diet for 28 weeks increased plasma soluble prorenin receptor, nondipping blood pressure, and vascular stiffness in male mice, whereas female mice preserved their phenotype until ovariectomy.
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