These findings suggest that activation of the inflammatory programme in obesity induces expression of IKK-ε/TBK1 in both adipocytes and preadipocytes of subcutaneous fat, initiating a process of catecholamine resistance that reduces energy expenditure, but also suppresses the catecholamine-induced increase in adipose IL-6 expression, thereby contributing to elevated hepatic glucose production in obesity. The gene discussed is TBK1; the disease is obesity due to melanocortin 4 receptor deficiency.