Increased dietary intake of α-linolenic acid (ALA) may be desirable to enrich tissue eicosapentaenoic acid (EPA; 20:5n-3) but competition between n-3 and n-6 fatty acids for enzymes involved in elongation and subsequent acylation will determine the relative proportions of phospholipid fatty acids. The aim of the present study was to examine the effects of altering the dietary ALA: linoleic acid (LA) ratio on rat platelet EPA and arachidonic acid (AA; 20:4n-6) concentrations. Sprague Dawley rats were fed on diets containing 30% total energy as fat with approximately 10% each of saturated, monounsaturated and polyunsaturated fatty acids with one of the following ALA:LA values; 1:7, l:4, l:1 or 1.3:1 (nine rats per group). After 4 weeks, blood was withdrawn from the abdominal aorta and platelet fatty acids analysed. The proportion of EPA was greater at the 1:1 and 1·3:1 ratios compared with the 1:7 and 1:4 (P < 0·05), and a decrease in AA was observed (P < 0·05) at the higher ratios. It was established that the platelet EPA:AA value increased (P < 0·05) as the dietary ALA:LA value increased

Tibial traits were investigated for turkey poults fed on soyabean-meal-based semi-purified diets high in phytate P (2·2 g/kg) with added phytase and inorganic P. Dietary treatments were: (1) 2·7 g non-phytate P (nP)/kg; (2) diet 1 + 1000 U phytase/kg diet; (3) 36 g nP/kg; (4) diet 3+800 U phytase; (5) 4·5 g nP/kg; (6) diet 5+600 U phytase; (7) 6·0 g nP/kg. Added phytase and nP increased (P < 0·006) tibial dry matter, ash weight and content, body-weight gain, feed intake and gain:feed. The Mg and Zn concentrations in the tibial ash were also increased (P < 0·001 and P < 0·09 respectively) by added phytase or nP; tibial P and Ca concentrations tended to be increased. Hypertrophy zone width of the tibial proximal end decreased (P < 0·001), while proliferating zone width, tibial length, and widths at the long and short axes increased (P < 0·003) as phytase and nP were added. The addition of phytase also tended to enlarge the cartilaginous zone width, which was linearly increased (P < 0·05) by added nP. Disorganization scores of the hypertrophy zone and trabecular bone were low, approaching normal (P < 0·05), for turkey poults fed on diets with phytase supplementation, and tibial abnormality scores were linearly decreased (P < 0·001) as nP levels increased (zero score is considered normal). Adding phytase and nP improved the orderliness of development, mineralization and arrangement of cartilage and bone cells, and alleviated the effects of P deficiency on the histological and gross structure of the tibias. Tibial shear stress increased (P < 0·04) as phytase and nP were added. In summary, similar improvements in bone characteristics were achieved for turkey poults fed on a P-deficient diet supplemented with either phytase or nP.

Epidemiological studies in humans show that size in early life is related to blood cholesterol concentrations in adult life, raising the hypothesis that early nutrition programs later lipid metabolism, affecting risk for later vascular disease. Here, we tested the hypothesis that nutrition during pregnancy or lactation in the rat programs lipid metabolism in the offspring, studied in adult life (mean 6 months). Rats (n 35) from normally-fed dams (controls) were compared with (1) rats (n 22) from dams protein-restricted in pregnancy and lactation; (2) rats (n 9) born to normally-fed mothers crossed to protein- restricted lactating dams and (3) those (n 9) born of protein-restricted dams and crossed to normally-fed lactating animals. In these latter three groups the offspring showed long-term reduction in plasma cholesterol, HDL-cholesterol and triacylglycerol concentrations compared with controls. The effects were predominantly in males. These findings suggest that in the rat the sensitive period for nutritional programming of cholesterol and triacylglycerol metabolism is both pre- and postnatal (pre-weaning) and that rats may be ‘indirectly’ programmed by altering the maternal nutritional milieu during gestation or lactation. whilst it has been hypothesized that early human undernutrition programs risk for vascular disease, one aspect of undernutrition, low maternal protein intake, in this rat model programmed lower plasma cholesterol and triacylglycerol concentrations.

Supersaturation of bile with cholesterol is a prerequisite of the development of gallstones. With the intention to study the integrated response of enzymes regulating hepatic cholesterol metabolism during gallstone formation we used an established model for the induction of cholesterol gallstone disease in mice. Ten mice were fed on a lithogenic diet containing 10 g cholesterol/kg and 5 g cholic acid/kg for 8 weeks and were compared with ten mice fed on a standard pellet diet. Cholesterol crystals or gallstones developed in 90% of gallbladders in treated mice. The lithogenic diet had an inhibitory effect on the rate-limiting enzyme of cholesterol biosynthesis, hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (EC 1.1.1.88) activity, 39·6 (SEM 2·8) v. 171·0 (SEM 47·3) pmol/min per mg protein. Cholesterol 7α-hydroxylase (EC 1.14.13.17) activity, regulating bile acid synthesis, was decreased by 80%, and this was assumed to be due to cholic acid in the diet. The cholesterol-enriched diet also induced a tenfold increase in cholesterol esterification rate in the liver, i.e. acyl-CoA: cholesterol acyl transferase (ACAT; EC 2.3.1.26) activity. The total, as well as esterified, cholesterol contents of liver homogenates were significantly higher in cholesterol- and cholic acid-treated mice and correlated well with the ACAT activity (rs 0·72 (P < 0·005), and rs 0·68 (P < 0·01) respectively). A significantly higher ACAT activity was obtained in mice given cholesterol and cholic acid even when the enzyme was saturated with exogenous cholesterol, thus indicating an increased amount of the enzyme. The formation of gallstones is dependent on a delicate balance between lithogenic factors (increased absorption of cholesterol and reduced secretion of bile acids) and defence mechanisms (decreased synthesis and increased esterification of cholesterol). In the specific animal model studied here the two defence mechanisms cannot compensate for the increased absorption of cholesterol and the reduced synthesis of bile acids.

The present study examined the effects of Se, vitamin E and combined Se and vitamin E deficiencies in rats on plasma lipid, Lipoprotein and apolipoprotein (apo) concentrations. Deficiencies were induced by feeding rats the respective diets for 6 weeks. The study shows that Se deficiency results in increased concentrations of plasma cholesterol and apo E. Both could be explained by an increase in the HDL1 fraction. Vitamin E deficiency alone had no significant effect on plasma lipid, lipoprotein and apo concentrations. Se deficiency in combination with vitamin E deficiency leads to an increase in plasma LDL and apo B concentrations. These results point to the need for further investigations on the mechanism by which Se deficiency affects lipoprotein metabolism.

Differences in the nutritive value of four grades of stackburned yellow maize, obtained from a single storage unit in Mozambique, were examined. Samples were analysed for chemical composition, and subjected to the following in vitro assays for estimating digestibility: total dietary fibre and pancreatin for non-ruminants, and gas production using sheep rumen fluid for ruminant livestock. Samples were also fed to broiler chicks at 600 g/kg diet in a growth trial. There were no significant differences in crude protein contents of the maize samples, but there was evidence for the development of Maillard reaction products. Detectable amino acids were lower in discoloured maize, with decreases of 52% in lysine, 35% in arginine, and 15% in glycine concentration in the most severely discoloured sample compared with control. Total starch, reducing sugar, acid-detergent fibre a d amylase-neutral-detergent fibre values increased, while total non-reducing sugar content decreased with increased discolouration. Total dietary fibre and pancreatin assays indicated a lowering in digestibility of maize with increasing discolouration. Weight gain of chicks (P=0·0228), efficiency of feed utilization (P=0·0009) and the metabolizable energy value of diets decreased (P<0·0001) with increasing stackburn discolouration. There were no significant effects on N retention of diets. In vitro fermentation using sheep rumen fluid showed a linear decrease in gas production with increasing maize discolouration, indicating a reduction in rumen degradability with stackburn

Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching.The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg α-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:ln-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5, 25 or 125 mg α-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg α-tocopherol/kg.In l-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the orderdietary linolenic >linoleic >oleic acid. In liver, also, the effect of α-tocopherol supplementation on phospholipid fatty acids was most pronounced. Theunsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the α-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.

Young growing rats weighing approximately 83g were fed on diets containing kidney bean (Phaseolus vulgaris) lectin (phytohaemagglutinin, PHA) in the range of 0–0.45g/kg body weight for 10d to ascertain whether there was a minimum dose below which the lectin had no significant effect on body and skeletal muscle weights in comparison with pair-fed lectin-free controls. Averaged over all experiments, PHA doses of less than 10 mg/d (0.12 g/kg body weight) reduced body dry weight by 1.14 (SE 0.25) g when compared with controls. Between 10 and 27 mg/d (0.12−0.32 g/kg body weight) a further reduction of 0–64 (SE 0.21)g occurred, suggesting a slight but steady decline of body dry weight with increasing dose. However, above 27 mg/d the depression of growth and changes in body composition accelerated. The difference between the proportional losses of skeletal muscle and body weight was not significant at doses of PHA below 10 mg/d (0.12 g/kg body weight) but the ratio of these losses rose to 1.5–2.0 at doses above this. The proportional decrease in lipid weight exceeded that of both body and skeletal muscle weights at all lectin doses, suggesting that lipid catabolism was the first target of the PHA effect. Plasma insulin level was depressed at the PHA dose of 0.02 g/kg body weight at which growth depression and muscle atrophy were minimal but, contrary to expectations, plasma glucose levels remained stable over the whole PHA dose range. It appears that despite a PHA-induced lowering of blood insulin, glucose catabolism is elevated by an unknown, possibly hormonal, compensatory mechanism. Thus, because low insulin levels facilitate the mobilization and catabolism of lipids, it may be possible to use low doses of PHA to reduce hyperglycaemia and body fat.

The present study was designed to test the hypothesis that increasing short-chain fatty acid (SCFA)production in the large bowel increases gut epithelial proliferation rate (EPR). Two experiments were carried out in which rats were fed on bread (wholemeal or white)-based diets containing graded amounts of cooked haricot (Phaseofus vulgaris) beans; the latter are a rich source of fermentable carbohydrates. Consumption of beans was associated with several-fold increases in SCFA production with the greatest relative increase being for butyrate. Despite the very large increase in SCFA production, there was no evidence that this had any effect on EPR in the duodenum. Where the basal diet contained wholemeal bread (Expt 1) there was no effect of enhanced SCFA supply on EPR in either the caecum or colon, but with the white bread-based diet (Expt 2) adding beans produced increments in both SCFA supply and EPR in the caecum. Evidence that SCFA are responsible for enhanced EPR above normal levels is not convincing. In those instances where enhanced SCFA supply is associated with increased EPR, the increase may be (1) from a hypoproliferative state towards normal, (2) a transient phenomenon accompanying tissue hypertrophy or (3) a homeostatic response to increased cell loss by cell sloughing or apoptosis. It is not likely that there is any direct link with risk of colon cancer

Previous control studies carried out in children showed that respiratory infection alters riboflavin metabolism and leads to excessive urinary losses of the vitamin. In order to understand the nature of biochemical changes in riboflavin metabolism during respiratory infection, a study was carried out using the mouse as the experimental model, and Klebsiella pneumonjue as the infective organism. Mice were fed on either a low(0·5 mg/kg)- or high(13·3 mg/kg)-riboflavin semi-synthetic diet. Infection resulted in a 5–6-fold higher excretion of riboflavin in the urine of mice fed on the low-riboflavin diet. Higher erythrocyte FAD levels and lower liver FAD levels were also observed during infection. Of the four enzymes involved in the synthesis and breakdownof the flavin coenzymes studied, the activity of hepatic flavokinase (ATP: riboflavin 5'-phosphotransferase; EC 2.7.1.26) was significantly lower, and that of FAD synthetase (ATP: FMN adenylyltransferase; EC 2.7.7.2) was higher during riboflavin restriction and infection. The activity of FMN (acid) phosphatase (EC 3.1.3.2) was unchanged, whereas FAD (nucleotide) pyrophosphatase (EC 3.6.1.9) activity was significantly higher both with the low-riboflavin diet and during infection. Thyroid hormone is known to modulate flavokinase activity and, hence, thyroid status was assessed. Plasma triiodothyronine (T3) levels were not affected, but thyroxine levels were lower in the mice fed on the low-riboflavin diet. However, plasma T3 was significantly lower during infection, suggesting a mechanistic role for the hormone in the reduction of flavokinase activity.

The mechanism underlying the reduced Cu status in rats fed on a high-sulphide diet was investigated. Male rats aged 6 weeks were fed ad libitum on purified diets containing either 0 or 500 mg S2-/kg and demineralized water for a period of 2 weeks. The high-sulphide diet had no effect on feed intake, body-weight gain or weight of liver and kidney bat significantly reduced Cu concentrations in plasma and kidney. Biliary Cu excretion was decreased significantly in rats fed on the high-sulphide diet. Apparent Cu absorption (Cu intake -faecal Cu) and true Cu absorption (Cu intake - (faecal Cu - biliary Cu)) were significantly lowered after sulphide feeding for 2 weeks. Rats fed on the high-sulphide diet excreted less Cu in urine than did the controls. We conclude that high sulphide intake reduces Cu status in rats through inhibition of Cu absorption which is reflected by a decrease in biliary Cu excretion as a secondary feature

Effects of feeding soluble dietary fibre on apparent Ca absorption and the contribution of the caecum to Ca absorption were examined in five-sixths nephrectomized (NPX)and normal rats with or without caecectomy in four experiments. It is known that Ca absorption is lowered by renal failure. In the first experiment the amounts of femur Ca increased linearly with increasing dietary Ca up to 3·0 g Ca/kg diet in intact rats. Partial nephrectomy decreased apparent Ca absorption in rats fed on diets containing 30 and 4·5 g Ca/kg diet. In the NPX groups, Ca absorption in rats fed on the diet containing guar-gum hydrolysate (GGH; 50 g/kg diet; 3·0 g Ca/kg diet) was significantly higher than that in rats fed on a fibre-free diet, and the increase in Ca absorption with GGH feeding was completely abolished by caecectomy. Also, ingestion of GGH increased Ca absorption in normal rats, but not in normal, caecectomized rats. Mg absorption was also increased with GGH feeding and was decreased with caecaectomyin NPX and normal rats. In experiments which used caecectomized rats, coprophagy wasprevented with an anal cup to avoid re-ingestion of faecal Ca. We conclude that ingestion of the soluble dietary fibre, GGH, increased apparent Ca absorption in NPX and non-NPX rats, and the caecum was responsible for these increases in Ca absorption.

We questioned whether polyamines coming from the diet or produced by intestinal microflora or by intracellular metabolism influence intestinal functions. Therefore, we compared pathogen-free rats and germ-free rats receiving a diet with low polyamine content and either treated or not treated with difluoromethylornithine (DFMO) and/or methylglyoxal bis (guanylhydrazone) (MGBG). Wet weight, protein content, DNA content, sucrase (EC3.2.1.48), maltase (EC 3.2.1.20) and lactase (EC 3.2.1.23) specific activities, amounts of putrescine, spennidine and spemine were measured in the mucosa of the proximal and distal intestine. Body weight was also determined. Rats without microflora had a higher specific activity of maltase and higher amounts of spermidine and spermine but lower lactase specific activity than pathogen-free animals; the low-polyamine diet given to gem-free rats had little effect on the functional variables measured (decrease of maltase and lactase specific activities) and did not modify the amounts of polyamines. DFMO and/or MGBG administered to germ-free rats receiving a low-polyamine diet induced modifications of most of the variables studied. Body weight and wet weight of proximal and distal intestine decreased, disaccharidase specific activities decreased, and amounts of polyamines changed according to the inhibitor used. Thus, our results showed that the deprivation of polyamine supply from microflora or from the diet failed, under our experimental conditions, to affect the intestinal properties analysed but exogenous and endogenous polyamine restriction altered general properties of the organism as well as intestinal functions.

The present study investigated the effect of the acute-phase ‘injury’ response, induced by subcutaneous injection of turpentine, on the hydration and protein content of organs and tissues of normally nourished rats receiving a diet containing 200g protein/kg, and of protein-malnourished rats receiving a diet containing 30 g protein/kg. The measurements were carried out 48 h after turpentine injection, and were compared with both saline-injected animals, and pair-fed control animals. Circulating α2-macroglobulin was also measured as an index of the acute-phase-protein response. In normally nourished rats turpentine injection caused a significant increase in the mean masses of the liver, kidney and lung (7–35% compared with saline-injected animals, and 20–44% compared with pair-fed controls), and a small reduction in the mass of extra-abdominal and extrathoracic tissues (‘carcass’). In general the protein content of tissues changed in a similar way (for liver, kidney and lung a 16–33% increase compared with saline-injected animals, and 32–49% compared with pair-fed controls). Protein deficiency produced a significant attenuation in the response to turpentine. The change in the mass and protein content of several tissues was reduced (for lung, liver and kidney, the increase in protein content was only 5–15%), and the effects on anorexia (1 v. 41% reduction infood intake) and the α2,-macroglobulin response (1·28 v. 4·28 g/l; P< 0·001) were also reduced. It is concluded that the injury response spares most central thoracic and abdominal organs, but this effect as well as the anorexia and acute-phase-protein response to injury are attenuated by protein deficiency.

Fifty-four male and forty-five female 7-week-old rats, Wistar strain, average weights 190 g and 140 g respectively, were randomized by weight into three groups of eighteen rats each (males) and three groups of fifteen rats each (females) and fed on a semi-purified diet containing (per kg) 2 (low), 5 (normal) or 20 g (high) Ca as CaCO3, for 2 weeks. Each group was then further randomized into three groups of six rats each (males) and five rats each (females) and given a meal (10 g of the same diet) containing either 2,5 or 20 g Ca as 47CaCO3. 47Ca was determined in quantitative daily collections of faeces over 7 d and fractional absorption of 47Ca estimated by extrapolating the linear portion (days 3–7) of the plot of log 47Ca retention Y. time back to the time of isotope administration. Absorption of meal Ca was higher in males than in females and was affected similarly in males and females by previous dietary Ca intake and meal Ca content. Fractional absorption of meal Ca decreased with increasing previous dietary Ca intake and with increasing meal Ca content, and the combined effect of these two variables caused fractional Ca absorption to vary from 11–89 %. Absolute absorption of meal Ca decreased with increasing previous dietary Ca intake and increased with increasing meal Ca content. The influence on Ca absorption of variations in meal Ca content (load effect) was greater than that of variations in previous dietary Ca intake (adaptive effect). These results show that previous dietary Ca intake and meal Ca content are both major determinants of Ca absorption from meals in intact rats fed in the normal way and that the rat responds to these factors in a manner similar to that reported for humans. This study provides further evidence of similarities between rats and humans in dietary Ca absorption.

It has increasingly been suggested that the short-chain fatty acids (SCFA) acetic, propionic and butyric acids, derived from colonic fermentation of dietary fibre and other indigestible carbohydrates, exert different physiological effects. Formation of propionic acid is discussed in terms of beneficial effects on glucose and cholesterol metabolism. The aim of the present study was to evaluate possible metabolic effects of propionic acid and to differentiate between effects mediated in the upper gastrointestinal tract and those mediated in the hind-gut. For this purpose, obese hyperinsulinaemic (fa/fa) rats were studied during a 19 d test period. Sodium propionate was either fed orally through the diet (1 g/d), or infused rectally (0·15 g/d) to animals given diets high in cholesterol (20 g/kg) and saturated fat (130g/kg). At the end of the test period total liver cholesterol pools were 20% lower (P < 0·01) in rats given dietary or rectally infused propionate (481 and 484 mg respectively) compared with the control group (614 mg). This was due to lower liver weights (P < 0·05) in propionate-treated animals, 15·5 and 15·3 g, v. 18·2 g in the control group, and no differences were noted in hepatic cholesterol concentrations. The urinary glucose excretion was measured during days 15–19 and was found to be lower (P < 0·05) in rats fed with propionate (23 mg) compared with the control group or the group infused rectally (39 and 38 mg respectively). In addition, fasting plasma glucose concentrations decreased significantly (P < 0·05) over the test period. It is concluded that orally supplied propionate affects both glucose and cholesterol metabolism as judged from lowered urinary glucose excretion, fasting blood glucose and liver cholesterol pools. On the other hand, propionate administered to the hind-gut at a physiologically relevant level reduces the hepatic cholesterol pool.

The properties of nuclear receptors belonging to the superfamily of receptors acting as transcription factors are modulated by nutritional and hormonal conditions. We showed recently that retinoic acid (RA) restored to normal the expression of receptors attenuated by hypothyroidism. The present study was designed to find out whether dietary vitamin A (as retinol) had the same effect. Propylthiouracil in drinking water induced both hypothyroidism and a vitamin A-deficient status in rats. The maximum binding capacity (Cmax) of triiodothyronine nuclear receptors (TR) was unchanged, while that of nuclear RA receptors (RAR) and nuclear glucocorticoid hormone receptors (GRn) was reduced in the liver of these hypothyroid rats. The reduced Cmax of RAR stemmed from a lower level of RAR mRNA, while the reduced Cmax of GRn was assumed to be due to reduced translocation of the receptor from the cytosol to the nucleus. Feeding the hypothyroid rats with a vitamin A-rich diet did not restore the Cmax of either RAR or GRn to normal. The lack of effect of dietary retinol on RAR expression may be attributed to either genomic (unoccupied TR block the expression of RAR genes) and/or extragenomic (hypothyroidism decreases the availability of retinol and/or its metabolism to RA) mechanisms. Triiodothyronine is thought to favour the translocation of glucocorticoid hormone receptors from cytosol to nucleus. These findings provide more information on the relationship between vitamin A and hormonal status, showing that a vitamin A-rich diet is without apparent effect on the expression of nuclear receptors in hypothyroid rats.