Though the effects of these polymorphisms on UCP-2 function are unclear [2], loss-of-function polymorphisms, if not compensated for by increased UCP-2 protein activity, could contribute to glucose intolerance and Type 2 diabetes as a result of lower glucokinase-mediated centrilobular glucose uptake [4] due to decreased thermal stimulation. The gene discussed is UCP2; the disease is Glucose intolerance.