The hypothesis was tested that dietary lactose v. glucose stimulates Mg absorption in rats because lactose lowers pH of the ileal lumen, which improves Mg solubility which in turn enhances Mg availability for transport across the ileal epithelium. For comparison, the effects of lactulose were studied because it shares with lactose the characteristic of being poorly digestible. Replacement of glucose by lactose (100 g/Kg) significantly stimulated apparent absorption of Mg. Apart from Mg absorption, lactulose also significantly enhanced absorption of Ca and phosphate. Lactose v. glucose lowered the pH of the ileal lumen from 7.5 to 7.2, whereas lactulose significantly reduced it to 7.0. In in vitro incubations a decrease in pH within the range of fluctuation in vivo was found to cause an improved solubility of Mg, and to a lesser extent also of Ca and phosphate. The smaller fall of ileal pH induced by feeding lactose instead of lactulose may explain why lactose improved Mg absorption only. For all individual rats combined there were negative relationships between ileal pH and apparent absorption of minerals, the relationship being strongest for Mg. Neither lactose nor lactulose was found to raise ileal solubility of minerals, which could relate to the possibility that the time of sampling was not appropriate. It is suggested that lactose-induced stimulation of Mg absorption in rats is caused by a lowering of ileal pH.

A diet rich in fish oil results in proarrhythmia compared to a control diet during regional ischemia in pigs. Myocardial excitability is reduced in the fish oil and sunflower oil group during the early phase of arrhythmogenesis. In the late phase of arrhythmogenesis, excitability is more reduced in the control group than in the fish oil and sunflower oil group.

The effects of dietary calcium (Ca) concentration and calcium: phosphorus (Ca:P) ratio on mineral balance and nephrocalcinosis were studied in female rats. In the first experiment there were two dietary Ca concentrations (0.25 and 0.50%, wt/wt) at two different Ca:P ratios (0.6 and 1.3). In the second experiment the diets were formulated to contain 0.40% P and either 0.13, 0.25, 0.50 or 0.75% Ca. The diets contained 0.03% magnesium (Mg). The fecal outputs of Ca, P and Mg were lower (P less than 0.01) after feeding low Ca diets than after feeding high Ca diets. Urinary excretion of P decreased with increasing dietary Ca and increased with increasing P intake. In rats fed the 0.25% Ca diets whole-body retentions of Ca and P were lower than in the rats fed 0.50% Ca. Both increases in dietary Ca from 0.13 to 0.50% and P from 0.20 to 0.40% elevated Ca and P content of kidneys as well as the degree of nephrocalcinosis. However, after feeding the highest Ca concentration (0.75%) nephrocalcinosis was essentially absent while kidney concentrations of Ca and P were relatively low. When compared with 0.50% Ca in the diet, 0.75% Ca increased group mean whole-body retention of Ca but lowered that of P. In individual rats the degree of nephrocalcinosis and the concentrations of minerals in kidney were positively correlated.

The question was addressed whether dietary phosphorus-induced nephrocalcinosis in rats is associated with impaired kidney function. Weanling female rats were fed purified diets containing either 0.4 or 0.6% (wt/wt) phosphorus for 28 d. The diet containing 0.6% phosphorus produced marked kidney calcification, as determined both by chemical analysis of kidney calcium and histological examination in kidney sections. Histological examination did not show calcification in stomach, lung, heart or thoracic aorta, which are predisposition sites of metastatic calcification in secondary renal hyperparathyroidism. In rats fed the 0.6% phosphorus diet, phosphorus retention and urinary excretion were greater compared with rats fed the 0.4% phosphorus diet. The following indicators of kidney function were examined: water intake, urinary volume, urine and plasma osmolality, urine and plasma creatinine, urine and plasma urea, urea and creatinine clearance and urinary albumin excretion. Of these indicators, only urinary albumin excretion was significantly increased in rats fed the nephrocalcinogenic diet. In a further experiment, the increase of urinary albumin was reproduced. After pooling the results of the two experiments, in individual rats fed the 0.6% phosphorus diet, the concentration of kidney calcium was found to be positively related with kidney weight expressed relative to body weight (r = 0.82, n = 22) and with albumin excretion in urine (r = 0.79, n = 28). The increased weight of calcinotic kidneys was mainly due to both calcium deposition and tubular hyperplasia. It is concluded that dietary phosphorus-induced nephrocalcinosis is associated with impaired kidney function in rats.

The objective of this study was to compare the effects of conjugated linoleic acid (CLA) as triacylglycerols (TAG) or free fatty acids (FFA) on body composition and energy balance in mice. We fed four groups of 5-wk-old Balb-C mice (n = 9) semipurified diets containing either CLA (0.5 g CLA/100 g of diet) or high oleic sunflower oil (HOSF) in the form of FFA or TAG for 42 d. Body composition was determined and the energy in the carcasses, excreta and food was measured in a bomb calorimeter. The amount of body fat was 4.72 +/- 0.95 g (17.9 +/- 2.8%) in the HOSF-FFA group, 2.36 +/- 0.29 g (9.4 +/- 1.0%) in the CLA-FFA mice (mean +/- SD, P < 0.05), 4.76 +/- 0.74 g (18.2 +/- 2.2%) in the HOSF-TAG group and 2.32 +/- 0.38 g (9.3 +/- 1.1%) in the CLA-TAG mice (P < 0.05). The percentage of energy intake that was stored in the body was 3.5 +/- 1.2% in the HOSF-FFA group, 0.6 +/- 0.3% in the CLA-FFA group (P < 0.05), 3.5 +/- 1.1% in the HOSF-TAG group and 0.5 +/- 0.4 in the CLA-TAG mice (P < 0.05). Conversely, the percentage of energy intake that was expended as heat was 89.4 +/- 1.2% in the HOSF-FFA group, 92.4 +/- 0.8% in the CLA-FFA mice (P < 0.05), 89.47 +/- 1.23% in the HOSF-TAG group and 92.2 +/- 0.4% in the CLA-TAG group (P < 0.05). Thus, CLA in the form of FFA or TAG had similar effects on body composition and energy balance.

No abstract

In a cross-over trial, five healthy dogs were fed a dry food without or with 1% (w/w) oligofructose to assess any oligofructose-induced effects on the faecal bacterial profile, nitrogen excretion and mineral absorption. The diets were given for a period of 3 weeks. Oligofructose feeding significantly raised the number of Bifidobacteria, Streptococci and Clostridia in faeces. The numbers of faecal anaerobic and aerobic bacteria were raised after ingestion of oligofructose. The faecal pH was unchanged. There was no effect of oligofructose feeding on the route of nitrogen excretion which was associated with a lack of effect on faecal ammonium and urinary urea excretion. It is suggested that the absence or presence of an effect of oligofructose on urinary and faecal nitrogen excretion depends on the background composition of the diet, in particular the content of non-digestible, fermentable carbohydrates. In the diets used, the content of non-digestible, fermentable carbohydrates was not measured. Both apparent magnesium and calcium absorption were significantly raised by oligofructose feeding, but phosphorus absorption was unaffected. The data presented may contribute to the qualification of the use of oligofructose in dog foods.

In the present study the effects of some C 18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C 18 : 0 , C 18 : 1 cis or C 18 : 1 trans isomers as the variables. In accordance with previous work, oleic acid in the diet caused an increase in cholesterol concentration in the liver and in the lipoprotein fraction of density (d; kg/l) , 1·006. Oleic acid also reduced the triacylglycerol:cholesterol value in this fraction. Surprisingly, the C 18 : 1 trans isomers diet induced a decrease in the amount of cholesterol in total plasma as well as in the 1·019 , d , 1·063 lipoprotein fraction. Both oleic acid and C 18 : 1 trans isomers increased the concentration of triacylglycerols in the liver. The two C 18 : 1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C 18 : 1 trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid-and C 18 : 1 trans isomers-fed rats, when compared with the rats fed stearic acid. No diet effects were seen for the activities of acetyl-CoA carboxylase, fatty acid synthase, diacylglycerol acyltransferase, citrate synthase and phosphofructokinase. The results are interpreted in that oleic acid raised liver triacylglycerol by reducing the secretion of it with the d , 1·006 lipoprotein fraction whereas the C 18 : 1 trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.