Fig. 3.

Schematic diagram illustrating the role of CYP2E1, Bid-dependent apoptosis, and complement activation in the development of adipose tissue inflammation during chronic ethanol feeding to mice. Chronic ethanol feeding induces the expression of CYP2E1 in adipocytes. CYP2E1 then leads to increased expression of TNFα, which in turn activates BID-dependent apoptosis of adipocytes. C1q, a component of the classical pathway of complement, binds to cell surface markers on apoptotic adipocytes, resulting in complement activation. Complement activation products, interacting with the anaphylatoxin receptors C3a receptor and C5a receptor, further increase cytokine and chemokine production in adipose tissue. The cumulative result of the CYP2E1 Bid-dependent apoptosis C1q-mediated complement activation pathway is the development of adipose tissue inflammation.