Lack of kinin B₁ receptor potentiates leptin action in the liver.

Kinins B1 and B2 receptors (B1R and B2R) are classically associated with inflammation, but our group has recently demonstrated new roles for B1R in metabolism using a knockout model (B1 (-/-)). B1 (-/-) mice display improvement on leptin and insulin sensitivity and is protected from high fat diet (HFD)-induced obesity. Here, we evaluate the hepatic effects of the B1R ablation and its role on hepatic function.

Kinin B1 receptor in adipocytes regulates glucose tolerance and predisposition to obesity.

Background: Kinins participate in the pathophysiology of obesity and type 2 diabetes by mechanisms which are not fully understood. Kinin B(1) receptor knockout mice (B(1) (-/-)) are leaner and exhibit improved insulin sensitivity.

Methodology/principal Findings: Here we show that kinin B(1) receptors in adipocytes play a role in controlling whole body insulin action and glucose homeostasis.

Intracellular proteolysis of kininogen by malaria parasites promotes release of active kinins.

Background: The malaria burden remains a major public health concern, especially in sub-Saharan Africa. The complex biology of Plasmodium, the apicomplexan parasite responsible for this disease, challenges efforts to develop new strategies to control the disease. Proteolysis is a fundamental process in the metabolism of malaria parasites, but roles for proteases in generating vasoactive peptides have not previously been explored.

B1 and B2 kinin receptor participation in hyperproliferative and inflammatory skin processes in mice.

Background: Kinins are released during dermal injury and inflammation and seem to contribute to the pathogenesis of cutaneous diseases.

Objective: Participation of kinins in skin inflammatory process was evaluated using knockout mice and non-peptide kinin receptor antagonists.

Methods: Chronic skin inflammation was induced by multiple applications of TPA in mice ear.

Predisposition to atherosclerosis and aortic aneurysms in mice deficient in kinin B1 receptor and apolipoprotein E.

Kinin B1 receptor is involved in chronic inflammation and expressed in human atherosclerotic lesions. However, its significance for lesion development is unknown. Therefore, we investigated the effect of kinin B1 receptor deletion on the development of atherosclerosis and aortic aneurysms in apolipoprotein E-deficient (ApoE(-/-)) mice.

Kinin B1 receptor deficiency leads to leptin hypersensitivity and resistance to obesity.

Objective: Kinins mediate pathophysiological processes related to hypertension, pain, and inflammation through the activation of two G-protein-coupled receptors, named B(1) and B(2). Although these peptides have been related to glucose homeostasis, their effects on energy balance are still unknown.

Research Design And Methods: Using genetic and pharmacological strategies to abrogate the kinin B(1) receptor in different animal models of obesity, here we present evidence of a novel role for kinins in the regulation of satiety and adiposity.