In summary, these studies identify FGF19 and FGF1 suppression of HPA axis-mediated lipolysis, resulting in reductions in hepatic acetyl CoA content, PC activity and glycerol turnover, as the major and common mechanism responsible for the insulin-independent effects of FGF19 and FGF1 to acutely reduce hepatic glucose production and hyperglycemia in a rodent model of poorly controlled T1D. The gene discussed is FGF19; the disease is Hyperglycemia.