Fish oil decreases inflammation and reduces cardiac remodeling in rosiglitazone treated aging mice.

Clinical studies suggest that rosiglitazone (RSG) treatment may increase the incidence of heart failure in diabetic patients. In this study, we examined whether a high corn oil diet with RSG treatment in insulin resistant aging mice exerted metabolic and pro-inflammatory effects that stimulate cardiac dysfunction. We also evaluated whether fish oil attenuated these effects. Female C57BL/6J mice (13 months old) were divided into 5 groups: (1) lean control (LC), (2) corn oil, (3) fish oil, (4) corn oil+RSG and (5) fish oil+RSG. Mice fed a corn oil enriched diet and RSG developed hypertrophy of the left ventricle (LV) and decreased fractional shortening, despite a significant increase in total body lean mass. In contrast, LV hypertrophy was prevented in RSG treated mice fed a fish oil enriched diet. Importantly, hyperglycemia was controlled in both RSG groups. Further, fish oil+RSG decreased LV expression of atrial and brain natriuretic peptides, fibronectin and the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-α, concomitant with increased interleukin-10 and adiponectin levels compared to the corn oil+RSG group. Fish oil+RSG treatment suppressed inflammation, increased serum adiponectin, and improved fractional shortening, attenuating the cardiac remodeling seen in the corn oil+RSG diet fed C57BL/6J insulin resistant aging mice. Our results suggest that RSG treatment has context-dependent effects on cardiac remodeling and serves a negative cardiac role when given with a corn oil enriched diet.

Analytic investigations on protein content in refined seed oils: implications in food allergy.

BACKGROUND: A number of scientific reports have investigated the possible implications of refined seed oils in allergic reactions, resulting in conflicting points of view. Also the total amount of residual proteins after refinement is still a matter of debate. Nevertheless, seed oils are now blamed as possible cause of allergic reactions. OBJECTIVE: To determine the true amount of proteins after oil refinement and to shed new lights on allergenic properties of refined seed oils. METHODS: We optimized a protein extraction procedure on several commercial refined seed oils. Both colorimetric and amino acid analysis were used to measure residual protein content. SDS-PAGE was also used for characterizations of protein band patterns. Sensitized child patients sera were tested by Western blot on PAGE-resolved proteins. RESULTS: Our extraction method proved to be effective and reproducible. Amino acid analysis resulted more accurate in determining the protein content with respect to colorimetric methods, indicating a higher protein content than that previously reported. IgE responsive residual proteins were found in peanut oil extracts. CONCLUSIONS: Our preliminary data suggest that fully refined seed oils should be taken into account in the context of allergic reactions and would benefit of further toxicological studies.

The fatty acid composition of maternal diet affects lung prostaglandin E2 levels and survival from group B streptococcal sepsis in neonatal rat pups.

Dietary fatty acid effects upon the immune system may be mediated in part by effects upon the synthesis of proinflammatory mediators. The effects of maternal dietary fatty acid composition upon lung prostaglandin (PG) E2 levels and survival from group B streptococcal (GBS) infection were investigated in neonatal rat pups. Beginning on d 2 of gestation and throughout lactation, pregnant dams were fed a purified diet whose fat source (22% of energy) was either corn oil or menhaden fish oil. On postnatal d 3, pups were randomly cross-fostered to dams of the same diet group to minimize litter effects; litters were then culled to 10 pups per dam. On postnatal d 7, pups were either injected with 1 x 10(7.5) GBS organisms or were killed for determination of lung tissue levels of PGE2 and lung and erythrocyte fatty acid composition. Arachidonic acid and PGE2 levels were significantly higher in the lungs of pups in the corn oil group compared with the fish oil group. Forty-nine percent of pups in the corn oil group survived the GBS challenge compared with 79% of pups in the fish oil group (P = 0.0005). These data suggest that the fatty acid composition of pre- and/or postnatal diet affects the neonatal response to immune challenge, which may be due in part to effects upon the synthesis of pro-inflammatory mediators.

Dietary fish oil alters specific and inflammatory immune responses in chicks.

Two experiments were designed to determine the effects of dietary (n-3) fatty acids and grain source on the growth-suppressive effects of the inflammatory response and indices of specific immunity. In Experiment 1, chicks were fed diets containing 0.5, 1, or 2 g/100 g of either corn oil or fish oil. In Experiment 2, chicks were fed diets containing up to 2 g/100 g of either fish oil, linseed oil or corn oil as the source of dietary fat, in either cereal grain- or corn-based diets. In each experiment, subsets of chicks within each dietary treatment were either vaccinated with infectious bronchitis virus (IBV) vaccine, injected with Salmonella typhimurium lipopolysaccharide (LPS), heat-killed Staphylococcus aureus, or remained noninjected. Increasing dietary fish oil, but not corn oil increased body weight and lessened the growth-suppressing effect of heat-killed S. aureus or S. typhimurium LPS. Increasing the concentration of dietary fish oil decreased febrile response, circulating hemopexin and metallothionein concentrations. Dietary fish oil resulted in decreased release relative to dietary corn oil of interleukin-1 by peritoneal macrophages. Although IBV titers were not significantly affected by dietary oil treatment, phytohemagglutination-induced wattle swelling was greater among chicks fed fish oil. In Experiment 2, the modulating effects of fish oil on the immune system were dependent on the type of grain used in the diet, with fish oil/cereal diets resulting in greater cell-mediated immunity and lower indices of inflammation than fish oil/corn diets. Inclusion of increasing amounts of fish oil in the diet improved performance, decreased indices of the inflammatory response and either improved or did not change indices of the specific immune response of growing chicks.

Melanoma lung metastases and cytolytic effector cells in mice fed antioxidant-balanced corn oil or fish oil diets.

(C57BL/6 x DBA/2)F1 mice were fed antioxidant-matched fish oil (FO) or corn oil (CO) diets for weeks, were challenged with B16.F10 melanoma cells, and lung metastases were enumerated 17 days later. Mice fed FO had fewer lung tumors than mice fed CO. This dietary effect persisted in mice injected with monoclonal antibodies which depleted natural killer cells, CD8+ T cells or CD4+ T cells. Generation of specific anti-B16.F10 cytotoxic cells in vitro by splenocytes from immunized mice was greater in mice fed FO. Even though host resistance to lung metastases by B16.F10 cells is mediated in large part by natural killer cells, CO and/or FO may have affected cells not tested here or tumor cells themselves.

Dietary fish-oil supplementation in experimental gram-negative infection and in cerebral malaria in mice.

Dietary fish-oil supplementation interferes with eicosanoid production and appears to decrease production of interleukin-1 (IL-1) and tumor necrosis factor (TNF). The effect of fish oil was investigated in an intramuscular Klebsiella pneumoniae infection in Swiss mice and in cerebral malaria induced by Plasmodium berghei in C57B1/6 mice. After a low inoculum of K. pneumoniae, 90% of fish oil-fed mice survived; survival in control mice fed equal amounts of corn or palm oil or normal chow was 30%, 40%, and 0, respectively. Cerebral malaria occurred in only 23% of fish oil-fed mice; in the controls, cerebral malaria developed in 61%, 81%, and 78%, respectively. Contrary to what was expected, lipopolysaccharide-induced ex vivo production of IL-1 alpha and TNF alpha by peritoneal cells was significantly enhanced in fish oil-fed mice compared with controls. Indomethacin treatment did not alter the outcome in these two infections, thus arguing against reduced prostaglandin synthesis as an explanation for the increase in resistance to infection.