The present study compared the effect of dietary conjugated linolenic acid (CLNA) on body fat and serum and liver lipid levels with that of CLA in rats. FFA rich in linoleic acid, a-linolenic acid, CLA, or CLNA were used as experimental fats. Male Sprague-Dawley rats (4 wk old) were fed purified diets containing 1% of one of these experimental fats. After 4 wk of feeding, adipose tissue weights, serum and liver lipid concentrations, serum tumor necrosis factor (TNF)-alpha and leptin levels, and hepatic beta-oxidation activities were measured. Compared with linoleic acid, CLA and, more potently, CLNA were found to reduce perirenal adipose tissue weight. The same trend was observed in the weight of epididymal adipose tissue. CLNA, but not CLA, was found to significantly increase serum and liver TG concentrations. Serum FFA concentration was also increased in the CLNA group more than in the other groups. The activity of beta-oxidation in liver mitochondria and peroxisomes was significantly higher in the CLNA group than in the other groups. Thus, the amount of liver TG exceeded the ability of hepatic beta-oxidation. Significant positive correlation was found between the adipose tissue weights and serum leptin levels in all animals (vs. perirenal: r = 0.557, P < 0.001; vs. epididymal: r = 0.405, P < 0.05). A less significant correlation was found between adipose tissue weights and serum TNF-alpha level (vs. perirenal: r = 0.069, P > 0.1; vs. epididymal: r = 0.382, P < 0.05). Although the mechanism for the specific effect of CLNA is not clear at present, these findings indicate that in rats CLNA modulated the body fat and TG metabolism differently from CLA.

The effect of the interaction of CLA and type of dietary protein on lipid metabolism was studied in male rats by feeding diets containing casein (CAS) or soy protein (SOY) as dietary protein and either linoleic acid (LA, a control FA) or graded levels of CLA at 0, 0.1, 0.5, and 1.0% for 28 d. CLA reduced the weight of perirenal adipose tissue in a dose-dependent manner, but the magnitude of the reduction was greater when rats were fed SOY. Feeding SOY resulted in a significant reduction of the concentrations of serum total and HDL cholesterol, TG, glucose, and insulin irrespective of dietary CLA. The concentration of serum leptin tended to be lower on the SOY diet free of CLA than in the corresponding CAS diet, but it fell with an increasing dietary level of CLA in the CAS groups. In contrast, serum leptin tended to increase when CLA was added to SOY diets. The concentration of serum adiponectin was higher in the CAS than in the SOY groups, and it tended to increase in response to dietary CLA levels in the CAS-fed rats, whereas CLA showed no effect in SOY-fed rats. The activity of liver mitochondrial carnitine palmitoyltransferase was higher in the SOY than in the CAS groups, but it tended to increase with an increasing dietary level of CLA in both protein groups. Although the body fat-reducing activity of CLA was more effective when the protein source was SOY, rats fed CAS appeared to be more susceptible to CLA than in those fed SOY with respect to cytokines examined. These results suggest that the type of dietary protein may modify the antiobesity activity of CLA.

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Summary To study the effects of different types of stressors on intestinal immune function, the lymphocyte subsets and associated immunoglobulin production in stressed rats were observed. Physical (electric foot shock) or psychological (non foot-shock) stress respectively were induced using a communication box. Rats were exposed to stress for 2 h per day, and the treatment was maintained for 14 consecutive days. Lymphocytes were isolated from the mesenteric lymph node (MLN) and spleen using Lympholyte-Rat. There was no change the lymphocyte subsets in MLN or spleen in either group. Foot-shock stress increased immunoglobulin secretions in MLN lymphocytes. These results demonstrated that intestinal immune functions were adaptively regulated under conditions of moderate stress.

A large-scale, biocompatible, and low-cost procedure for peptide fractionation based on the amphoteric nature of peptide is developed. A sample cell (120 x 100 x 50 mm) with four joint tubes (17 mm i.d. and 20 mm in length) on the front and back was prepared. On the end of the joint tubes, a nylon screen (100 mesh)-supported agarose gel layer was formed. Five or nine of the sample cells were connected. A tryptic digest of casein (2.0-3.6 L) was applied to the sample cells. At each end of the sample cell apparatus, an additional cell filled with 0.1 M H(3)PO(4) or NaOH was connected and used as anode and cathode compartments, respectively. Reproducible fractionation of peptide could be achieved by collecting fractions with specific pH values when voltage reached a plateau by applying direct current at constant power. Running time necessary for fractionation of peptide was inversely proportional to electric power and directly proportional to sample volume.

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Although epidemiological studies on the relationship between dietary fat and the incidence of breast cancer do not necessarily show a firm positive correlation (1-3), dietary fat plays a crucial role in the pathogenesis of breast cancer in animal models (4-6). In general, polyunsaturated fatty acid (PUFA) in relation to saturated or monounsaturated fatty acids are more promotive in chemical carcinogenesis and the growth of transplanted cancer cells in rodents (4-6). PUFA of the n-6 family, in particular linoleic acid is probably the responsible fatty acid for tumor promotion, while n-3 PUFA works anti-carcinogenic in experimental animals. Despite numerous data on the effect of dietary fat type on animal carcinogenesis, no reports are available regarding the influence of the structure of dietary fat on this process. Currently, diacylglycerol (DAG) attracted attention with respect to its body fat reducing potential as compared with triacylglycerol (TAG) having the same fatty acid composition (7-10), though the precise mechanism underlying this effect remains to be resolved (10, 11). Since the energy density of diets is a factor influencing the incidence of several cancers in