Nutrition
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Significant impairments of several aspects of immunity have been described in acute and chronic nutritional deficiencies; however, there have been few studies on antigen-presenting cells during starvation. We examined the antigen-presenting capacities of mouse dendritic cells (DCs) from lymphoid organ (spleen DCs) and non-lymphoid tissue (liver DCs) during starvation. The total numbers of spleen DCs and liver DCs were significantly fewer in starved mice than in control mice. ⋯ In particular, liver DCs from starved mice were unable to induce interferon-gamma. Liver DCs from starved mice were unable to induce proliferation of antigen-specific memory lymphocytes. These data indicated that one major cause of impairment of immunologic responses during starvation may be mediated through DCs.
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Although soy foods have been consumed for more than 1000 y, it is only in the past 20 y that they have made inroads into Western diets. We investigated the effect of dietary supplementation with natto extracts produced from fermented soybeans on intimal thickening of arteries after vessel endothelial denudation. Natto extracts include nattokinase, a potent fibrinolytic enzyme having four times greater fibrinolytic activity than plasmin. ⋯ Dietary natto extract supplementation suppressed intimal thickening (0.06 +/- 0.01; P < 0.05) compared with the control group. Natto extracts shortened euglobulin clot lysis time, suggesting that their thrombolytic activities were enhanced. These findings suggest that natto extracts, because of their thrombolytic activity, suppress intimal thickening after vascular injury as a result of the inhibition of mural thrombi formation.
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In a previous study, we showed that prior oral feeding of oils rich in omega-3 eicosapentaenoic acid and docosahexaenoic acid and omega-6 gamma-linolenic acid and arachidonic acid prevent the development of alloxan-induced diabetes mellitus in experimental animals. We also observed that 99% pure omega-6 fatty acids gamma-linolenic acid and arachidonic acid protect against chemically induced diabetes mellitus. ⋯ Prior oral supplementation with alpha-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid prevented alloxan-induced diabetes mellitus. alpha-Linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid not only attenuated chemical-induced diabetes mellitus but also restored the anti-oxidant status to normal range in various tissues. These results suggested that omega-3 fatty acids can abrogate chemically induced diabetes in experimental animals and attenuate the oxidant stress that occurs in diabetes mellitus.