StudyRepo

Linoleic acid deficiency was induced in mice, and the enzymes responsible for synthesizing fatty acids were measured in the liver. Fatty acid synthesis enzymes were activated 5 to 10-fold in mice on a fat free diet. Saturated fat (coconut oil) was reintroduced to the diet, but did not bring down the enzyme levels. Meanwhile, reintroducing linoleic acid (via corn oil) did, over an 8 day period. This indicates that linoleic acid (or downstream, eg. ARA) deficiency is what activates the fatty acid synthesis enzymes. Only a few days were needed to dramatically deplete the linoleic acid in the mices' livers. Feeding a starved animal with a fat-free diet initiated liver linoleate depletion within 8 hours. Fatty acid synthesis hormones were observed as quickly as 5 days into the fat-free diet. When fatty acid synthesis was activated, increased levels of palmitoleic acid and oleic acid were observed. Stearic, linoleic, and arachidonic acid dropped. Palmitic acid remained about the same. Mead acid (omega-9 PUFA) was endogenously synthesized from oleic acid. Mice maintained on a fat-free or a linoleate-free diet developed fatty livers, which was reversed when linoleic acid was reintroduced to the diet.