This study was conducted to clarify whether preferential fat intake by adult rats could be linked to fat-feeding of rats during the growth period using high-fat diet-1 (HFD-1) and high-fat diet-2 (HFD-2) with added cellulose to maintain the same energy concentration as a low-fat diet (LFD). Three groups of 4-week-old male Fischer 344 rats were fed either LFD (LFD group), HFD-1 (HFD-1 group) or HFD-2 (HFD-2 group). After 8 weeks, the LFD group was further divided into two groups. One of the LFD groups and the HFD-1 group were placed on a self-selection regimen of LFD and HFD-1 (pair I), and the other LFD group and the HFD-2 group were placed on a self-selection regimen of LFD and HFD-2 (pair I) for 4 weeks. No significant difference in calorie intake or body weight was observed among the groups throughout the experimental period. When rats were placed on a self-selection regimen, the ratio of HFD-1 dietary intake for rats fed LFD and HFD-1 in pair I was 80% and 55%, respectively, and that of HFD-2 intake for rats fed LFD and HFD-2 in pair I was 20% and 27%, respectively. These findings indicate that (1) HFD-1 has food properties preferable to those of HFD-2, (2) in HFD-1, fat-feeding during the growth period affects the food choice of adult rats, (3) HFD-2 guards against fat overfeeding.

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We investigated the effects of boiling and steaming by steam convection oven (SC) on the taste and isoflavone derivative content of soybeans. In this study, boiling in an ordinary stainless steel pan (pan-boil), boiling by SC (SC-boil), and steaming by SC (SC-steam) were used. During presoaking for 16h at 4°C, the isoflavones were mostly retained in the soybeans. Although the pan-boil and SC-boil methods gave similar results (70% retention of the original isoflavone content in soybeans with 30% leaching into the cooking water), SC-steam resulted in nearly 100% retention of isoflavones in the soybeans, preferred method based on overall palatability of the cooked soybeans by sensory evaluation. More than 80% of total isoflavones in soybeans were categorized into 4 kinds of isoflavone derivatives: 6″-o-malonyldaidzin, 6″-o- malonylgenistin, daidzin, and genistin. Aglycone was slightly increased while malonyl glucoside changed to β-glucoside during cooking by both the SC-boil and SC-steam methods.

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Soybean oil is ranked as one of the most allergenic soy foods. However, theoretical and circumstantial evidence suggests that the total protein content of edible soybean oil is clearly lower than the threshold level for inducing an allergic reaction. The reason for this discrepancy was therefore studied, and the findings suggested that the previously suggested possibilities that soybean oil contains either allergen proteins or hydroperoxides in sufficient amounts to cause or promote allergic reactions, or the abundance of linoleic acid in the oil as a cause, can all be dismissed. It seems likely that previous experiences with soybean oil produced in the past when the refining technology was unskilled have been unconsciously handed down. Therefore it is concluded that from a common sense viewpoint, soybean oil can no longer be regarded as a hazardous food, although care may be necessary with regard to the allergenicity of soybean lecithin preparations, because of its protein content and various uses.

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Studies in mice that are deficient in AMP-activated protein kinase (AMPK) have indicated that exercise-mediated reduction of fat mass requires activation of skeletal muscle AMPK. AMPK is a sensor of energy in cells and acts by increasing fat and glucose oxidation when energy production is required. Repeated exercise increases GLUT4, whereas a sedentary lifestyle decreases in GLUT4, in skeletal muscle. GLUT4 in the plasma membrane is responsible for glucose intake in skeletal muscle, and the increase in GLUT4 resulting from regular exercise is considered to be a major reason why regular exercise prevents diabetes mellitus. In serial studies of deleted GLUT4 minigene transgenic mice, exercise-responsive elements in the 5′-flanking sequence of the GLUT4 gene were located. Habitual fish consumption prevents myocardial infarction. Fish oil feeding activates PPARα, a transcription factor, that promotes β-oxidation of fatty acid, decreases the activity of SREBP-1c, a sterol regulatory element binding protein, and thus decreases lipogenesis. Both fish oil and fasting decrease SREBP-1c activity, but their mechanisms differ. Fibrate, an activator of PPARα, can prevent myocardial infarction, suggesting that the prevention of myocardial infarction by fish intake might be mediated by activation of PPARα. Regular exercise and fish intake affect the energy metabolism of the whole body, and help to prevent lifestyle-related disease. To develop new drugs and a strategy for prevention of lifestyle-related disease for individuals having different genetic backgrounds, it is necessary to understand how exercise and fish can prevent lifestyle-related disease.

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Fat-soluble hormones, including food-derived vitamins A and D, regulate complex programs of gene expression via the nuclear receptor family of transcription factors. Recent studies, including some done by our group, have led to the identification of cofactor protein molecules that appear to play important roles in mediating transcription by members of the nuclear receptor family. We have shown that CREB binding protein (CBP) is able to function as a nuclear receptor cofactor, and integrate various types of cellular signaling. Moreover, we have investigated the biological roles of cofactor proteins, focusing on skeletal muscle and adipose tissue, which are important for maintaining energy balance in the human body. We showed that a nuclear receptor cofactor, PGC-1β, can bind to, and activate orphan estrogen receptor-related receptors (ERRs). Transgenic mice overexpressing PGC-1β show increased energy expenditure, and are resistant to obesity induced by a high-fat diet or by genetic abnormality. Furthermore, we showed that another cofactor, FOXO1, negatively regulates skeletal muscle mass and type I fiber gene expression, leading to impaired skeletal muscle function. Activation of FOXO1 appears to be involved in the pathogenesis of muscle atrophy. These results provide insight into the molecular basis of lifestyle-related diseases such as obesity and diabetes mellitus, and the possibility of new treatments.

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