Our primary hypotheses were that (1) blockade of β1- and β2-AR signaling by propranolol would attenuate the dietary fat absorption and the high fat-calorie-diet-induced development of obesity and (2) such an effect would be associated with changes in PNLIP expression in pancreatic acinar cells. The gene discussed is PNLIP; the disease is obesity due to melanocortin 4 receptor deficiency.