Rats were fed cholesterol-free purified diets containing casein, rice (RP), potato (PP) or soybean (SP) proteins having different amounts of methionine (25.9, 21.3, 16.2 and 10.9 g methionine/kg, respectively). Each protein was fed at 250 g/kg diet for 14 d. Growth rates of rats were the same in all groups. Serum total cholesterol concentrations were lower in rats fed SP, PP and RP than in those fed casein. Fecal bile acid plus neutral steroid excretion was significantly higher in rats fed the RP, PP and SP diets compared with those fed casein. There was a significant negative correlation between serum cholesterol concentration and fecal total steroid excretion (r = -0.490, P = 0.01). However, a stronger positive correlation was observed between serum cholesterol concentration and dietary methionine concentration (r = 0.674, P = 0.0003) or methionine:glycine ratios (r = 0.656, P = 0.0005). In a separate experiment in rats fed diets containing amino acid mixtures simulating the RP, PP and SP diets, serum total cholesterol concentrations were lower than in rats fed simulated casein. Fecal total steroid excretion was the same in all groups. A strong correlation was found between serum cholesterol concentration and dietary methionine concentration (r = 0.743, P = 0.0002) or the methionine:glycine ratio (r = 0.685, P = 0.0009) in rats fed the amino acid mixtures. Finally, we examined the hypocholesterolemic effects of 250 g SP or casein/kg diet with or without supplementation with 0.3 g/100 g sodium taurocholate (TC). Supplementation with TC did not alter the hypocholesterolemic effect of SP. These results support the view that RP, PP and SP lower serum cholesterol concentration in a similar manner.

The relation between blood taurine (2-aminoethanesulfonic acid) concentrations and obesity was investigated. Taurine is supplied to the body by dietary ingestion as well as by de novo synthesis; it is anabolized by cysteine dioxygenase (CDO), which is abundantly expressed in liver and white adipose tissue. Overexpression of CDO in 3T3-L1 preadipocytes caused a decrease in the level of cysteine (precursor of taurine) and an increase in the level of taurine in the culture medium, suggesting that CDO is involved in biosynthesis and secretion of taurine in white adipose tissue. In high-fat diet-induced and/or genetically obese mice, a decrease in the blood taurine concentration was observed along with a decrease in CDO expression in adipose tissue but not in liver. Dietary taurine supplementation prevented high-fat diet-induced obesity with increased resting energy expenditure. Thus, taurine deficiency observed in association with obesity may create a vicious circle promoting obesity. Dietary taurine supplementation interrupts this vicious circle and may prevent obesity.

The objective of this study was to examine the physiologic importance of undigested protein on cecal fermentation in rats fed a low (LAS) and high (HAS) amylose cornstarch. In Experiment 1, rats were fed diets containing LAS (655 g/kg diet) with one of four protein sources: casein, rice (RP), potato (PP) or soybean protein (SP) at 250 g/kg diet for 15 d. Apparent digestibilities of casein, RP, SP and PP were 96, 94, 93 and 92%, respectively. In rats fed the LAS diet with casein, acetate, propionate and succinate were the major cecal organic acids. The succinate pools in rats fed RP or SP were significantly lower than in those fed casein, whereas butyrate did not differ. Butyrate was significantly higher in rats fed PP, but succinate was the same as in rats fed casein. In Experiment 2, rats were fed diets containing HAS (200 g/kg diet) with one of the four protein sources at 250 g/kg diet for 10 d. HAS was substituted for the same amount of LAS. In rats fed the HAS diet, succinate was the major acid in rats fed casein; in rats fed RP or PP, however, the pools of this acid were significantly lower than in those fed casein, whereas butyrate was significantly higher in rats fed RP or PP. Fecal starch excretion was significantly lower in rats fed RP or PP than in those fed casein. In Experiment 3, rats were fed the casein-HAS diet with graded levels of PP (0, 10, 30, 50, 100 and 250 g/kg diet) for 14 d. The PP was substituted for the same amount of casein. Cecal butyrate was low in rats fed up to 100 g of PP/kg diet and then rose with 250 g of PP/kg diet. In Experiment 4, ileorectostomized rats were used and fed the same diets described in Experiment 3 for 9 d. The ileal starch/nitrogen ratio declined with increasing dietary PP, due solely to greater nitrogen excretion, whereas starch excretion was unaffected. In Experiment 5, rats were fed the casein-HAS diet with or without 60 g of artificial resistant protein/kg diet for 10 d. The resistant protein (apparent digestibility, 63%) was substituted for the same amount of casein. Rats fed the casein-HAS diet with resistant protein had significantly greater cecal butyrate and lower succinate than those fed the casein-HAS diet. These data show that large bowel fermentation of starch is altered by dietary protein. They support the hypothesis that nondigested protein, namely, resistant protein, may control fermentation efficiency as well as the fermentation profile of HAS, possibly as a result of a change in microflora through the change in the ratio of starch to nitrogen in the cecum.

No abstract

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. However, when 1 g CLA/100 g diet was given to mice in a low fat diet (4 g fat/100 g diet), they showed a marked decrease in fat mass, but demonstrated symptoms of lipoatrophic diabetes, i.e., marked hepatomegaly and insulin resistance. In this study, to determine whether the decrease in adipose tissue was responsible for these adverse effects, mice were fed different doses of CLA and dietary fat. In Experiment 1, mice were fed different doses of CLA (0, 0.1 and 1 g CLA/100 g diet) in a fixed 4 g fat/100 g diet; in those fed 0.1 g CLA, subcutaneous white adipose tissue (WAT) weight was 48% lower than in mice fed 0 g CLA. The mice fed 0.1 g CLA did not exhibit hepatomegaly and insulin resistance. In Experiment 2, mice were fed for 5 mo different amounts of dietary fat (4, 13 and 34 g fat/100 g diet) in 0 or 1 g CLA/100 g diet; in mice fed 1 g CLA with 34 g fat, retroperitoneal and subcutaneous WAT weights were 76 and 79% lower, respectively, than those of mice fed 0 g CLA with 34 g fat. Mice fed 1 g CLA in the diet with 34 g fat had normal plasma insulin concentrations and a 45% greater liver weight. These data suggested that the percentage of CLA in dietary fat might be a determinant of CLA-mediated lipodystrophy.