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Plasma free fatty acid incorporation into the outer and inner myocardium of unanesthetized dogs
Author(s) -
Steinberg Joel S.,
Gold Martin
Publication year - 1970
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/bf02533202
Subject(s) - fatty acid , clinical chemistry , phospholipid , lipidology , chemistry , biochemistry , membrane
14 C‐Palmitate (16∶0) and 3 H‐oleate (18∶1) were infused into unanesthetized dogs for 90 min. Lipid and isotopic analyses were then performed on the left ventricular outer and inner walls. Average values in μmoles per gram wet weight tissue for both outer wall trigly ceride (TG) (7.0±2.6 (S.E.)) and phospholipid (PL) (17.3±2.4) were higher then the inner wall TG (1.4±0.3) and PL (12.0±2.4). TG fatty acid distribution was similar in the outer and inner myocardium. Thus those factors regulating incorporation of various fatty acids may operate at comparable rates in both heart segments. The same observation and relationship was observed for PL, but the two classes had markedly different fatty acid spectra. The transmural gradients for these classes may be related to relatively hypoxic conditions in the inner wall. Uniform 14 C DPM concentrations were found in both TG and PL of the outer and inner myocardium. A similar distribution pattern was found for 3 H. This may indicate that an individual species of plasma free fatty acid (FFA) undergoes uniform initial incorporation into TG and PL despite the existence of transmural gradients and fatty acid distribution differences. The mean outer and inner wall TG and PL 3 H to 14 C DPM concentration ratio (range of 3.9 to 4.8) was similar to a calculated plasma 3 H‐18∶1 to 14 C‐16∶0 specific activity ratio of 4.23. This indicates that net incorporation of fatty acids into TG and PL over 90 min was proportional to their plasma FFA concentrations, rather than to endogenous tissue lipid concentrations. The lipid gradients and fatty acid spectrum differences observed may thus be caused by recycling and catabolic pathways rather than to direct control of plasma FFA entry into TG and PL.