StudyRepo

L.A. veterans were given a high-linoleic diet. Over the course of 4-5 years, the linoleic acid % in their body fat grew asymptotically to approach the linoleic acid % in the diet, minus a few % due to de novo lipogenesis.

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.

One of the study authors, a healthy adult man, went on a "fat-free" diet (<2g fat/day) for 6 months. The diet was created equivalent to one deemed deficient in essential fatty acids in rats, which the rats developed health issues on and eventually got severely sick. The human subject remained well throughout the entire period, and did not even get a common cold. He had no skin issues and did not even get tired of the food. In fact, the subject reported less fatigue and a disappearance of migraines he'd had since childhood. He lost a moderate amount of weight (14lbs) and blood pressure decreased slightly. Arachidonic and linoleic acid were tested in serum before and during the diet. Arachidonic was 3.2% before, and 1.87% during the fat-free diet. Linoleic was 5.7% before and 3.2% during. This study was done in 1933, which explains the very low (for current day) linoleic acid %.

The authors had previously shown that SFAs are preferentially shuttled into oxidation pathways compared to PUFAs. But this was only in an oxidative (catabolic?) state. With this study, they wanted to test the same thing in a state with de novo lipogenesis (DNL) upregulated. To test this, they fed 20 healthy volunteers a high-carbohydrate diet and then gave them either palmitate or linoleate. The two fats were tested 2 weeks apart. During the DNL state, linoleate was preferentially oxidized vs. palmitate.

Liraglutide, a GLP-1 agonist medication, was given to obese and diabetic (type 2) patients. Lipids were analyzed subsequently. In these patients, palmitoleic acid was decreased after taking the medication vs. placebo. This could indicate lower de novo lipogenesis.