Blockade of kinin B1 receptor reverses plasma fatty acids composition changes and body and tissue fat gain in a rat model of insulin resistance

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Kinin B1 receptor (B1R) contributes to insulin resistance through a mechanism involving oxidative stress. This study examined the effect of B1R blockade on the changes in plasma fatty acids composition, body and tissue fat mass and adipose tissue inflammation that influence insulin resistance.


Sprague–Dawley rats were fed with 10% D-glucose or tap water (Control) for 13 weeks and during the last week, rats were administered the B1R antagonist SSR240612 (10 mg/kg/day, gavage) or vehicle. The following parameters were assessed: plasma fatty acids (by gas chromatography), body composition (by EchoMRI), metabolic hormone levels (by radioimmunoassay), expression of B1R and inflammatory markers in adipose tissue (by Western blot and qRT-PCR).


Glucose feeding significantly increased plasma levels of glucose, insulin, leptin, palmitoleic acid (16:1n-7), oleic acid (18:1n-9), Δ6 and Δ9 desaturases while linoleic acid (18:2n-6), arachidonic acid (20:4n-6) and Δ5 desaturase were decreased. SSR240612 reduced plasma levels of insulin, glucose, the homeostasis model assessment index of insulin resistance, palmitoleic acid and n-7 family. Alterations of Δ5, Δ6 and Δ9 desaturases were normalized by SSR240612. The B1R antagonist also reversed the enhancing effect of glucose feeding on whole body and epididymal fat mass and on the expression of macrophage CD68, interleukin-1β, tumour necrosis factor-α and inducible nitric oxide synthase in retroperitoneal adipose tissue. B1R protein and mRNA were not detected in retroperitoneal adipose tissue.


Insulin resistance in glucose-fed rats is associated with low state inflammation in adipose tissue and plasma fatty acids changes which are reversed by B1R blockade. These beneficial effects may contribute to insulin sensitivity improvement and the prevention of obesity.

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