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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
Author(s) -
Baker N.,
Mead J.,
Kannan R.
Publication year - 1981
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02534901
Subject(s) - lipogenesis , lipidology , clinical chemistry , adipose tissue , corn oil , medicine , endocrinology , chemistry , polyunsaturated fatty acid , food science , fatty acid , biology , biochemistry
We have reexamined an earlier rat study in which the authors concluded that 60 min after [U‐ 14 C]‐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‐ 14 C data with radioactivity found in liver and in adipose tissue in 60 min. Without using Triton WR 1339, mathematical analysis of plasma TGFA‐ 14 C following the glucose test‐meal leads one to the same conclusion: 97% of 14 C‐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‐ 14 C from liver to adipose tissue.