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Pathways of acetyl CoA production for lipogenesis from acetoacetate, β‐hydroxybutyrate, pyruvate and glucose in neonatal rat lung
Author(s) -
Sheehan Patricia M.,
Yeh YuYan
Publication year - 1984
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/bf02534499
Subject(s) - lipogenesis , fatty acid synthesis , atp citrate lyase , acetyl coa , biochemistry , ketone bodies , fatty acid , lipid metabolism , lyase , glycolysis , medicine , biology , thiolase , clinical chemistry , endocrinology , chemistry , metabolism , enzyme , citrate synthase , dehydrogenase
The rate of fatty acid synthesis from acetoacetate (AcAc) is 2–3 times greater than from glucose in developing rat lung. To determine the reason for this difference, we investigated the pathways of lipogenesis from [3‐ 14 C] AcAc, [3‐ 14 C]β‐hydroxybutyrate (βOHB), [U‐ 14 C] glucose or [2‐ 14 C] pyruvate in minced lung tissue of 3‐ to 4‐day‐old rats. The addition of (−)hydroxycitrate, an inhibitor of ATP‐citrate lyase, inhibited fatty acid synthesis from glucose, pyruvate, and βOHB by 88%, 70% and 60%, respectively, but had no effect on that from AcAc. Benzene 1,2,3‐tricarboxylate, an inhibitor of tricarboxylate translocase, inhibited fatty acid synthesis from all substrates by at least 50%. Incubation with aminooxyacetate, an inhibitor of aspartate aminotransferase, has no effect on lipid synthesis from glucose, pyruvate or AcAc, but increased lipid synthesis from βOHB. Results indicate that for lipid synthesis in the neonatal lung, acetyl CoA from AcAc is derived predominantly from a cytoplasmic pathway involving AcAcCoA synthetase and AcAcCoA thiolase, whereas citrate is the major route of acetyl group transfer from glucose. Lipogenesis from βOHB involves both the cytoplasmic and citrate pathways.