Biology Reference
In-Depth Information
co-workers who could detect no significant difference between 16:0-18:1
D
9c
PC and
16:0-18:1
D
9t
PC at the aqueous interface
[39]
, but did observe a difference between the two
PCs within the bilayer hydrophobic interior
[40]
. They concluded that the trans-PC was
more similar to the disaturated DMPC control than to the cis- PC. A similar conclusion
was obtained from a diet study of serum lipoprotein levels
[41]
. The effect of dietary trans
elaidic acid was more similar to saturated stearic acid than to cis oleic acid. In addition there
has been a plethora of membrane enzymes and receptors whose activity has been shown to
decrease with TFAs
[42]
.
Although it is now clear that TFAs are incorporated into membrane phospholipids where
they affect many membrane properties, questions still abound. Are TFAs mistakenly
identified as a saturated fatty acid and placed in the sn-1 chain of a phospholipid, or are
they recognized as an unsaturated fatty acid and placed in the sn-2 position? Either option
seems possible. Emken et al.
[43]
reported that in human erythrocytes and platelets, three
times more elaidic acid than oleic acid accumulates in the sn-1 position of PCs. Since elaidic
acid resembles a saturated fatty acid, its accumulation into the sn-1 position is not
surprising and would likely have only a minimal effect on normal membrane structure
and function
[44]
. Supporting this, Larque et al.
[36]
reported that as dietary TFA levels
rise in liver microsomes and mitochondria, saturated fatty acid levels drop. Being a natural
food product, elaidic acid in low amounts is probably not responsible for human heart
problems. Instead, it is the enormous number of positional and geometric isomers found
in partially hydrogenated oils that are likely responsible for causing heart disease. When
incorporated into membrane phospholipids, TFAs must replace existing saturated or
natural cis unsaturated acyl chains.
It is more likely that addition of polyunsaturated TFAs to the sn-2 position of phospho-
lipids alters membrane structure and function far more than incorporation of elaidic acid
in the sn-1 position
[45]
. For example, if dietary TFAs replace natural DHA in the sn-2
position of brain membrane phospholipids, it is likely that electrical activity of neurons
and hence brain function will be affected. However, other completely different possibilities
also exist. For example, it is possible that only one of the multitude of TFA isomers, existing
at miniscule levels, is doing 99
รพ
percent of the harm. Identifying such a unique trans isomer
will be a difficult endeavor.
2. Docosahexaenoic Acid (DHA)
Docosahexaenoic acid (DHA) (22:6(n-3), see Chapters 4 and 10) is the longest (22 carbons)
and most unsaturated (6 cis double bonds) fatty acid commonly found in mammalian
membranes
[46]
. In recent years DHA (and other omega-3 fatty acids) has received a great
deal of attention due to its reputed involvement in alleviating a wide variety of human afflic-
tions
[47]
(listed in
Tabl e 15. 2
,
[48]
). This list, which spans the entire gambit of human disor-
ders, can be roughly divided into six non-exclusive categories; heart disease, cancer,
immune problems, neuronal functions, aging and 'other' hard to categorize problems such
as migraine headaches, malaria, and sperm fertility. Historically the primary source of DHA
in the human diet has been oily, coldwater fish. In fact, the initial link of fish oils to a human
health problem (ischemic heart disease in Greenland Eskimos) originated in the pioneering
work of Bang and Dyerberg from the 1970s
[49]
. DHA supplementation is currently in vogue.
