Paradoxical conservation of cardiac and renal arachidonate content in essential fatty acid deficiency.

摘要: The effects of essential fatty acid (EFA) deprivation on the arachidonate content and phospholipid composition different tissues are quite diverse. When C57B1 mice were placed a fat-free diet, hepatic liquids readily depleted arachidonate. In contrast, renal cortex tenaciously retained arachidonate, whereas surprisingly heart showed doubling its This increase in cardiac was due to four-fold arachidonylphosphatidylethanolamine (PE). preservation PE, phosphatidylserine, phosphatidylcholine. Only phosphatidylinositol or cortex. Using an vivo labeling technique, it shown that liver incorporated most [1-14C]arachidonate initially following intraperitoneal injection. Over 11 days, as levels labeled fell liver, EFA-deficient accumulated selectively PE (8-fold greater than control), phosphatidylcholine (2-3-fold control). uptake be specific for over 20:3(n-9). Despite conservation seen with EFA deficiency, prostaglandin production by isolated perfused kidney markedly decreased relative control response agonist stimulation angiotensin II, although equivalent nonspecific ischemia. These data suggest serves supply other both contain mechanisms accumulate certain phospholipids. However, phosphatidylinositol, which is uniquely appears principal source receptor-mediated agonists.