Excessive alcohol intake induces white adipocyte death and macrophage infiltration, which trigger lipolysis via the elevation of epinephrine and norepinephrine. Alcohol and dysfunctional white adipocytes can also promote lipolysis by induction of insulin resistance and elevation of FGF21. WAT lipolysis subsequently elevates the circulating FFA levels, thereby inducing hepatic FFA influx, lipotoxicity, steatosis, hepatocyte death, and liver inflammation. As opposed to the detrimental effect on WAT, alcohol consumption switches on defensive mechanisms in BAT against ALD development. UCP1-mediated FFA oxidation and thermogenesis are activated by alcohol, which reduces the circulating FFA pool and attenuates FFA-induced hepatocyte death as well as hepatic fat accumulation. Alcohol intake elevates the expression of adiponectin in BAT, which reduces the burden of ALD at multiple levels by suppressing hepatic fat accumulation, hepatocyte death, and liver inflammation. CPT1, carnitine palmitoyltransferase I.