Receptor for advanced glycation end products regulates adipocyte hypertrophy and insulin sensitivity in mice: involvement of Toll-like receptor 2.

Receptor for advanced glycation end products (RAGE) has been shown to be involved in adiposity as well as atherosclerosis even in nondiabetic conditions. In this study, we examined mechanisms underlying how RAGE regulates adiposity and insulin sensitivity. RAGE overexpression in 3T3-L1 preadipocytes using adenoviral gene transfer accelerated adipocyte hypertrophy, whereas inhibitions of RAGE by small interfering RNA significantly decrease adipocyte hypertrophy.

Receptor for advanced glycation end-products (RAGE) regulation of adiposity and adiponectin is associated with atherogenesis in apoE-deficient mouse.

Objective: Receptor for advanced glycation end-products (RAGE) has been shown to be involved in cardiovascular diseases. We examined the involvement of RAGE in atherosclerosis under non-diabetic status, and its relation to the effect on adiposity.

Methods: Apolipoprotein E (apoE)(-/-)RAGE(+/+) or apoE(-/-)RAGE(-/-) mice were fed with an atherogenic diet or the standard chow diet.

Regions of arterial stenosis and clinical factors determining transcutaneous oxygen tension in patients with peripheral arterial disease.

Aims: Despite the clinical usefulness of transcutaneous oxygen tension (TcPO(2)) to assess the severity of limb ischemia, the factors determining TcPO(2) in patients with peripheral arterial disease (PAD) have not been fully clarified. We therefore examined the regions of arterial stenosis and clinical factors affecting lower-extremity TcPO(2).

Methods: Resting TcPO(2) (REST-TcPO(2)) and postexercise TcPO(2) (Ex-TcPO(2)) in the calf region and the dorsalis pedis were measured simultaneously in 66 patients (132 limbs) with clinically suspected PAD, in whom angiography was also performed.