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TALKING POINT
(Bishop, M. J. and Rawlings, C. J., eds), IRL
Press at OUP (in press)
MARK BORODOVSKY
School of Biology, Georgia Institute of
Technology, Atlanta, GA 30332-0230, USA.
EUGENE V. KOONIN AND
KENNETH E. RUDD
National Center for Biotechnology Information,
National Library of Medicine, National
Institutes of Health, Bethesda, MD 20894, USA.
HEPATIC FATrY ACID metabolism has
been studied largely through the use of
in vitro preparations, such as isolated
hepatocytes and the isolated perfused
liver. Despite proving extremely useful
for studying the effects of individual
hormones and the role of specific post-
receptor events, such preparations
have serious drawbacks. For example,
isolated hepatocytes lose the cell po-
larity and zonation that exist within the
intact liver, while in the perfused liver,
parameters such as perfusate flow rate,
pressure and efficiency Of oxygenation
all determine the balance of fatty acid
metabolism i. As with many in vitro sys-
tems, perhaps the most serious draw-
backs arise through our inability to
mimic the infinite combinations of sub-
strate, hormonal and neuroendocrine
inputs that exist in vivo. Consequently,
several controversies have arisen over
which system (perfused liver or isolated
hepatocytes) most closely resembles
the situation in vivo.
It was to overcome such problems,
specifically with respect to the intra-
hepatic partitioning of fatty acids
between their different metabolic fates
in the liver, that a method was devised 2
to label hepatic fatty acids selectively
in vivo. Its development has allowed
the noninvasive study of fatty acid par-
titioning during metabolic transitions
characterized by rapid changes in liver
metabolism 3,4.
Selective labelling of hepaticfatty acids
in vivo
The major obstacle to the study of
liver-specific fatty acid m.,~,~,abolism in
V. A. Zammit and A. M. B. Molr are at the
Departmentof Biochemistryand Molecular
Biology, HannahResearchInstitute, Ayr,UK
KA6 5HL
Monitoring the partitioning of
hepatic fatty acids in vivo:
keeping track of control
Victor A. Zammit and Alison M. B. Moir
Noninvasive labelling of hepatic fatty acids in conscious, unrestrained rats
shows how liver lipid metabolism responds acutely to physiological pertur-
bations, such as the starved-to-refed transition. The speed with which the
liver switches from fatty acid oxidation to esterification varies widely
according to the requirement of the animal for continued synthesis of glu-
cose 6-phosphate from three-carbon precursors. Ingestion of a meal also
provides a strong signal for the diversion of fatty acids away from triacyl-
glycerol synthesis and secretion, but insulin may only play an indirect role
in this effect.
vivo is the fact that most tissues can
metabolize free fatty acids (FFA) di-
rectly. Consequently, only a minor
portion of any dose of labelled FFA in-
jected into an animal ends up in the
liver. Moreover, this occurs over a con-
siderable length of time, such that se-
cretion and re-uptake of labelled products
of liver metabolism make quantitative
studies impossible over a physiologi-
cally relevant timescale. Any method
that aims to deliver fatty acids selec-
tively to the liver and pulse-label its
fatty acid pool(s) has to do so very
rapidly and in vast preference to the
pool(s) in any other tissue, such that
the metabolic products that reach the
circulation are known to be of hepatic
origin. The method devised to achieve
this is to 'encapsulate' the labelled
fatty acyl moiety within particles that
interact rapidly and specifically with
hepatocytes, and from which the label
does not escape into the circulation and
is not abstracted by other tissues. These
conditions are met through the use
of cholesteryl esters of fatty acids
(labelled in their acyl moiety) incorpor-
ated within the hydrophobic core of
apolipoprotein C (apoC)-depleted very
low density lipoprotein (VLDL)- and
chylomicron-remnants. The particles
are subsequently injected intravenously
into rats chronically implanted with a
jugular cannula. Our studies 5 show that
cholesteryl esters in these particles are
taken up preferentially by the liver
before the irreversible uptake of the
lipoprotein particles themselves. This
effect is presumed to be due to the
transfer of cholesteryl ester directly
into hepatocytes during the multiple
© 1994, Elsevier Science Ltd 0968-0004/94/$07.00 3~l.3