Food Lipids: Chemistry, Nutrition, and Biotechnology

addition, these functions must be monitored by the cell in order for there to be a
regulatory adaptation. How a cell senses its acyl composition is not understood. To
date, the best data on adaptive acyl regulation in mammalian cells involve the essential
fatty acid deficiency response. Cells deficient in arachidonic acid or its precursor
n-6 fatty acids convert de novo-produced oleic acid to n-9 eicosatrienoic
(mead) acid by the action of the �5 and �6 desaturases. The conversion mechanism
is identical to that of the production of C20 n-6 and n-3 fatty acids. The unusual
desaturation of oleic acid is commonly believed to be the result of a cell’s attempt
to replace arachidonic acid in the membrane with a similarly unsaturated species.
This is an example of a cross-family compensation and provides further evidence
for the lack of an association between n designation and function. The regulation of
mead acid production is intriguing in that it is not found in animals fed sufficient
dietary n-6 fatty acids. This may be the consequence of a differential activity of the
�6 desaturase on linoleic and oleic acids.
Given that each fatty acid is unique in terms of its chemistry and potentially
its function, one interesting question concerning PUFA metabolism is, can animals
recognize n designation? If not, how big of a role do dietary PUFAs play in physiology?
How can animals regulate the production of important acyl compounds in
the face of changing dietary n-3/n-6 ratios, given that animals have a redundant
system of desaturation for both n families? Changing n-3/n-6 PUFA ratios appears
to have significant effects on much pathology in humans, including cardiovascular
disease, immune function, and cancer. Because dietary acyl compositions vary tremendously
throughout the world and over time, key questions must be answered
concerning the regulatory factors and signals associated with the production of fatty
acid and their metabolic products.
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