Health aspects of oxidized dietary fats - Oxidation in Foods and Beverages and Antioxidant Applications - page 162

oxidative stress in every tissue investigated (see Section 1.4.5). In addition, it
has been shown that among many tissues studied, the pancreatic islets are highly
susceptible to antioxidant depletion (Asayama et al., 1986). Furthermore, it is
well documented that the glucose-stimulated insulin-releasing capacity of
pancreatic -cells is impaired by the induction of oxidative stress (Ammon et
al., 1984). This also explains the diabetogenic actions of alloxan and streptozo-
tocin which are mediated by reactive oxygen species (Heikkila et al., 1976;
Sandler and Andersson, 1982). Induction of oxidative stress, therefore, might
also explain that diet-derived hydroperoxides, which are also contained in
heated fats, were shown to contribute to the loss of insulin secretion activity in
pancreatic -cells (Tsujinaka et al., 2005). Tsujinaka et al. (2005) reported that a
diet high in lipid hydroperoxides due to a lack of vitamin E resulted in glucose
intolerance in rats and that this was associated with the development of insulin
resistance and an inability to secrete insulin. In response to the oxidative stress
caused to -cells, activation of nuclear factor-B (NF-B) signaling pathway in
islet cells from hydroperoxide-fed rats was also noticed (Tsujinaka et al., 2005).
NF-B is known to be activated by ROS generated during oxidative stress, and,
thus, activation of NF-B can be used as an indicator of oxidative stress.
As a further mechanism explaining the hypoinsulinemia induced by the
oxidized fat, the authors of the first study raised the hypothesis that alterations in
prostaglandin metabolism might be associated with the hypoinsulinemia (Liao et
al., 2008). This assumption was based on the observation that oxidized fat was
shown to increase prostaglandin E 2 levels in plasma and urine of rats (Huang,
2003), and that transgenic induction of prostaglandin E 2 was reported to cause a
destruction of pancreatic -cells (Oshima et al., 2006).
7.6.7 Effects on inflammation
Several reports in the literature demonstrate that oxidized fats strongly induce
oxidative stress (see Section 1.4.5). Although a link between oxidative stress and
inflammation has been clearly established (Schreck et al. 1991; Sen and Packer,
1996), only one study so far has investigated the effect of oxidized fat on
inflammatory processes (Ringseis et al., 2007c). In that study, two groups of
pigs were fed two different diets containing either fresh fat or oxidized fat
prepared by heating at 200 ëC for 24 h. After 4 weeks on the diets, the pigs were
sacrificed and intestinal epithelial cells were isolated and markers of inflam-
mation (NF-B transactivation and NF-B target gene expression) determined.
NF-B plays a key role in inflammatory diseases due to its ability to bind
specifically to NF-B-response elements in the promoters of key inflammatory
genes (e.g., COX-2, iNOS, TNF, and IL-6) and induce their gene transcription
(Barnes and Karin, 1997).
The results of the pig study (Ringseis et al., 2007c) show that markers of
inflammation in intestinal epithelial cells were not altered by dietary oxidized fat
indicating that oxidized fat does not induce an inflammatory response in the
intestine. These findings were unexpected because in that study an increased