Health aspects of oxidized dietary fats - Oxidation in Foods and Beverages and Antioxidant Applications - page 164

exert a different effect on inflammatory gene transcription during states of acute
intestinal inflammation, e.g. in animal models of experimental colitis.
Whether the impairment of the antioxidant defense system by oxidized fat is
of significance for the integrity of the intestinal epithelium (barrier function) has
to be investigated in future studies. It has been suggested that a progressive fall
in enzymatic and nonenzymatic antioxidants as observed in the present study
precedes the occurrence of damage to intestinal cell constituents (Bernotti et al.,
2003). Since the intestinal epithelial cells are primarily responsible for the
antioxidant defense of the epithelium against luminal oxidants (Grisham et al.,
1990), it is likely that in the presence of stronger irritants, such as toxins or
pathogens, the already impaired defense mechanisms of the intestinal epithelial
cells in response to oxidized fat are not sufficient to cope with this additional
challenge nor to preserve cellular integrity and homeostasis of the intestinal
epithelium.

7.7 Future trends
Although oxidized fats are widely considered to be detrimental on health,
feeding experiments in rats, mice and pigs have also demonstrated several
beneficial effects of oxidized fat such as lowering of blood lipids and prevention
of ethanol-induced fatty liver development. The reduction of blood and liver
lipids by oxidized fat might be of particular significance for human health,
because elevated plasma concentrations of both cholesterol and triacylglycerols
are known risk factors for cardiovascular disorders such as atherosclerosis, and
atherosclerosis is the principle cause of coronary heart disease and stroke, both
being responsible for more than 40% of all deaths in Europe and the US. Thus,
future studies employing animal models of experimental atherosclerosis have to
demonstrate whether oxidized fat might be useful in the prevention from

atherosclerosis.
The finding that dietary oxidized fat prevents from ethanol-induced fatty liver
development in rats might be also of great interest for health prevention in
humans. Chronic alcohol abuse is the most common reason for the development
of fatty liver in humans. Since fat accumulation in the liver makes this organ
more prone to injury by various agents such as drugs and toxins (Bhagwandeen
et al., 1987), which are involved in the pathogenesis of alcoholic hepatitis and
fibrosis (Yang et al., 1997; Diehl et al., 2001), approaches to prevent or even
treat fatty liver are of great importance. However, whether oxidized fat is indeed
a suitable nutritional approach for the prevention of alcoholic fatty liver
development in humans remains to be established, because humans, unlike rats
and mice, have a lower expression of PPAR in the liver and show a weaker
response to treatment with PPAR agonists (Cheon et al., 2005). Nevertheless,
as PPAR agonists retain a triacylglycerol-lowering effect also in non-
proliferating species (Holden and Tugwood, 1999), it is not unlikely that
oxidized fat counteracts the development of an alcoholic fatty liver in humans.