Fig. 7.

Proposed model for resistin-mediated metabolic differences. Increased resistin levels cause central leptin resistance. This reduces sympathetic outflow from the brain and particularly affects BAT, which also experiences reduced BAT marker expression in a tissue-autonomous fashion in the transgenic state. Functionally impaired BAT is responsible for the delayed triacylglycerol clearance, impaired insulin sensitivity and, in the case of the Ldlr^−/− background, more rapid atherosclerotic plaque formation