Abstract
Dietary polyunsaturated fatty acids （PUFAs） are essential nutrients required for maintaining membrane structure and producing lipid mediators that support metabolic homeostasis. Because mammals cannot synthesize n-6 and n-3 PUFAs endogenously, adequate dietary intake is indispensable for normal growth and physiological function. When dietary PUFA intake is insufficient, the body undergoes compensatory metabolic remodeling and synthesizes alternative fatty acids thatre normally absent under physiological conditions. A representative example is Mead acid （20:3n-9），an n-9 PUFA produced specifically during essential fatty acid deficiency. We have identified the biosynthetic pathway of Mead acid and established
experimental systems that enable regulation of its production under PUFA-deficient conditions. In addition, we have developed a novel PUFA-deficient animal model and are conducting detailed phenotypic analyses associated with PUFA deficiency. In this review, we summarize PUFA deficiency–induced metabolic remodeling and discuss the molecular mechanisms underlying disease development, particularly hepatic steatosis.
