Hepatic contribution to newly made fatty acids in adipose tissue in rats and inhibition of hepatic and extrahepatic lipogenesis from glucose by dietary corn oil.

We have reexamined an earlier rat study in which the authors concluded that 60 min after [U-14C]-glucose injection half of labeled fatty acids found in adipose tissue had been made in liver and then transported to the adipose tissue. We have shown that even under conditions in which the lipogenic role of the liver is optimized (fed-refed rats on a fat-free, high-carbohydrate diet), almost none of the labeled fatty acids found in adipose tissue of rats 60 min after they were fed a labeled glucose test meal was derived from the liver. This conclusion was based experimentally on (a) the use of the blocking agent Triton WR 1339 to measure the total labeled triglyceride fatty acids (TGFA) synthesized and secreted by the liver in 60 min and (b) comparison of plasma TGFA-14C data with radioactivity found in liver and in adipose tissue in 60 min. Without using Triton WR 1339, mathematical, analysis of plasma TFGA-14C following the glucose test-meal leads one to the same conclusion: 97% of 14C-labeled fatty acids found in adipose tissue at 60 min was made in situ. Additional studies in rats established that the source of error in the earlier studies was an incorrect assumption that dietary corn oil could inhibit hepatic lipogenesis from glucose C without inhibiting fatty acid synthesis in adipose tissue. In our studies, 10% corn oil inhibited equally both hepatic and adipose tissue fatty acid synthesis from glucose C under conditions that precluded any significant transport of labeled TGFA-14C from liver to adipose tissue.