AJP - Gastrointestinal and Liver Physiology, Vol 267, Issue 6 1028-G1034, Copyright © 1994 by American Physiological Society
Evidence that hepatic triglycerides provide acylglycerides for synthesis of bile phosphatidylcholines
G. M. Patton, J. M. Fasulo and S. J. Robins
Lipid Metabolism Laboratory, Veterans Affairs Medical Center, Boston 02130.
To determine the biochemical origin of bile phosphatidylcholines (PCs), rat
liver perfusions with 16:1 fatty acid (FA) and [3H]glycerol were performed
to generate novel radiolabeled bile and liver PCs and their hepatic
glyceride precursors. Results showed total equilibration of bile and liver
16:1-16:1 PC when the specific activity of precursor glycerol-3-phosphate
was kept constant. However, when the specific activity of
glycerol-3-phosphate decreased during the labeling period and during a
prolonged chase period with 17:1 FA and nonradiolabeled glycerol, the
specific activity of bile 16:1-16:1 PC was appreciably higher than this
same PC in the liver and during the chase period was even higher than its
hepatic 16:1-16:1 acylglycerol precursors, phosphatidic acid and
diglyceride. During the chase period with 17:1 FA, new radiolabeled
16:1-17:1 PC was formed, and again the specific activity of this PC in bile
was greater than this PC and 16:1-17:1 phosphatidic acid and diglyceride in
the liver. Only the specific activity of liver 16:1-16:1-(FA) triglyceride
equaled or was high enough to support the formation of new bile 16:1-16:1
PC. These studies indicate that bile PCs do not directly derive from
preexisting hepatic PCs or by de novo synthesis through phosphatidic acids
and diglycerides, but likely originate by remodeling from a pool of hepatic
triglycerides.
