Schreyer and coworkers reported that in contrast to apoe-/- mice that remained lean, Ldlr-deficient (ldlr-/-) mice fed a diabetogenic high-fat high-sucrose diet (35.5% fat mainly from lard and 36.6% carbohydrate mainly from sucrose) became more obese than wild-type mice and developed severe hypertriglyceridemia and hyperleptinemia[52]. The gene discussed is APOE; the disease is hypertriglyceridemia.