In order to study the mechanism by which increasing unsaturation of dietary fat lowers HDL-cholesterol levels, we studied various measures of HDL metabolism in hamsters fed with fats with different degrees of saturation. Hamsters were fed on a cholesterol-enriched (1 g/kg) semipurified diet containing 200 g/kg of maize oil, olive oil, or palm oil for 9 weeks. Increasing saturation of dietary fat resulted in increasing concentrations of total plasma cholesterol (4·29 (SD 0·51), 5·30 (sd 0·67) and 5·58 (sd 0·76) mmol/l respectively, n 12) and HDL-cholesterol (3·31 (sd 0·50), 3·91 (sd 0·12) and 3·97 (sd 0·43) mmol/l) and these concentrations were significantly higher (P < 0·05) in the palm-oil and olive-oil-fed hamsters compared with the maize-oil group. Total plasma triacylglycerol levels also increased with increasing fat saturation (1·01 (sd 0·59), 1·56 (sd 0·65) and 2·75 (sd 1·03) mmol/l) and were significantly higher (P < 0·05) in the palm-oil group compared with the olive-oil and maize-oil-fed hamsters. The three diets did not have differential effects on plasma activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). Levels of phospholipid transfer protein (PLTP) tended to be higher with increasing fat saturation but this effect was not significant. The capacity of liver membranes to bind human HDL3 was significantly higher (P < 0·05) in the hamsters fed with maize oil (810 (sd 100) ng HDL3 protein/mg membrane protein, n 4) compared with those fed on palm oil (655 (sd 56) ng/mg), whereas the olive-oil group had intermediate values (674 (sd 26) ng/mg). The affinity of HDL3 for the binding sites was not affected by the type of dietary fat. Hepatic lipase (EC 3.1.1.3) activity, measured in liver homogenates, increased with increasing fat saturation. We conclude that dietary maize oil, when compared with either olive oil or palm oil, may lower HDL-cholesterol concentrations by enhancing HDL binding to liver membranes.

Methionine (Met) is usually the first limiting amino acid for sheep and supplements of Met may increase production of wool and meat. The wool response may be due to an increased supply of cysteine (Cys) from transsulfuration (TS) of Met. Met is catabolized through homocysteine to form Cys when the S from Met is transferred to serine (Ser). We hypothesized that providing additional Met would create a deficiency of Ser and that by simultaneously providing Met and Ser, TS and wool growth could be increased more than by providing Met alone. The effects of i.v. infusions of Met and Ser to young Merino lambs on TS, fractional synthesis rate (FSR) of protein in skin, follicle mRNA and wool growth were examined. Following 4 d of constant i.v. infusion of 3 g Met/d, or 10 g Ser/d or both, the isotope tracers: L-[3-13C]CYS, l-[ring-d5]phenylalanine (Phe) and l-[2,3,3-d3]Ser were infused over 8 h to allow for measurements of irreversible loss rate (ILR), and TS in whole body and skin. Skin biopsies were taken for measurement of FSR. Wool growth rate was measured using autoradiography. An infusion of Met significantly (P < 0·05) improved wool growth rate and increased skin FSR, Cys supply from TS and enhanced levels of follicle mRNA (from the K2.10 intermediate filament gene and three gene families encoding keratin associated proteins KAP1, KAP4 and KAP12). The extra Met lowered Ser ILR. The infusion of Ser doubled Ser ILR in the body and increased skin FSR calculated using the Cys tracer in plasma (P < 0·05). However, there were no significant (P > 0·05) changes in TS, skin FSR calculated using the Phe and Ser tracers, follicle mRNA or wool growth rate as a result of Ser infusion. While there were trends towards increased TS and FSR with Ser infusion, the overall lack of significant changes indicates a high capacity for the de novo synthesis of Ser.

Central obesity is a powerful predictor for disease. By utilizing salivary cortisol measurements throughout the day, it has now been possible to show on a population basis that perceived stress-related cortisol secretion frequently is elevated in this condition. This is followed by insulin resistance, central accumulation of body fat, dyslipidaemia and hypertension (the metabolic syndrome). Socio-economic and psychosocial handicaps are probably central inducers of hyperactivity of the hypothalamic–pituitary adrenal (HPA) axis. Alcohol, smoking and traits of psychiatric disease are also involved. In a minor part of the population a dysregulated, depressed function of the HPA axis is present, associated with low secretion of sex steroid and growth hormones, and increased activity of the sympathetic nervous system. This condition is followed by consistent abnormalities indicating the metabolic syndrome. Such ‘burned-out’ function of the HPA axis has previously been seen in subjects exposed to environmental stress of long duration. The feedback control of the HPA axis by central glucocorticoid receptors (GR) seems inefficient, associated with a polymorphism in the 5′ end of the GR gene locus. Homozygotes constitute about 14 % of Swedish men (women to be examined). Such men have a poorly controlled cortisol secretion, abdominal obesity, insulin resistance and hypertension. Furthermore, polymorphisms have been identified in the regulatory domain of the GR gene that are associated with elevated cortisol secretion; polymorphisms in dopamine and leptin receptor genes are associated with sympathetic nervous system activity, with elevated and low blood pressure, respectively. These results suggest a complex neuroendocrine background to the metabolic syndrome, where the kinetics of the regulation of the HPA axis play a central role.

There is new evidence that a good folate status may play a critical role in the prevention of neural-tube defects and in lowering elevated homocysteine concentrations. This adequate folate status may be achieved through folic acid dietary supplementation. Folate is a water-soluble vitamin with a low potential toxicity. However, the possible consequences of long-term high-dose folic acid supplementation are unknown, especially those related to the methionine cycle, where folate participates as a substrate. With the aim of evaluating such possible effects, four groups of Wistar rats were classified on the basis of physiological status (virgin v. pregnant) and the experimental diet administered (folic-acid-supplemented, 40 mg/kg diet v. control, 2 mg folic acid/kg diet). Animals were fed on the diets for 3 weeks. Results showed that gestation outcome was adequate in both groups regardless of the dietary supplementation. However, there were reductions (P < 0·001) in body weight and vertex-coccyx length in fetuses from supplemented dams v. control animals. Folic acid administration also induced a higher (P < 0·01) S-adenosylmethionine : S-adenosylhomocysteine value due to increased S-adenosylmethionine synthesis (P < 0·01). However, hepatic DNA methylation and serum methionine concentrations remained unchanged. Serum homocysteine levels were reduced in supplemented dams (P < 0·05). Finally, pregnancy caused lower serum folate, vitamin B6 and vitamin B12 levels (P < 0·05). Folic acid administration prevented the effect of pregnancy and raised folate levels in dams, but did not change levels of vitamins B12 and B6. These new findings are discussed on the basis of potential benefits and risks of dietary folic acid supplementation.

A study was conducted with conventional and germ-free broiler chicks to obtain more information on the role of the intestinal microflora in the anti-nutritive effects of NSP in broiler chicks. As the NSP source, highly methylated citrus pectin (HMC) was used at a dose level of 30 g/kg in a maize-based diet. The diets fed to the germ-free chicks were γ-irradiated, whereas those fed to the conventional chicks were not. Feeding the HMC diet to conventional birds depressed weight gain and food utilization (P < 0·05), whereas in germ-free birds only weight gain was reduced (P < 0·05). Feeding the HMC diet to conventional birds reduced digestibilities of energy and starch at the end of the jejunum. Ileal digestibilities of starch and energy were not strongly affected when birds were fed on the HMC-containing diet. Faecal digestibilities of organic matter, crude fat, starch and amino acids, N retention and metabolizable energy were reduced when conventional chicks were fed on the HMC diet. Feeding the HMC diet to germ-free birds hardly affected faecal digestibility of nutrients and N retention, whereas metabolizable energy was increased. Feeding the HMC diet to conventional or germ-free birds increased the viscosity of the digesta in the small intestine. This increase in digesta viscosity was more pronounced in conventional than in germ-free birds. The pH of ileal digesta was reduced when HMC was added to the diet of conventional chicks, but not in germ-free chicks. Feeding the HMC diet to conventional birds markedly affected morphology of the gut wall, whereas in germ-free chicks very little effect was found on gut morphology. Based on the results of the present study, it is concluded that the gastrointestinal microflora mediates the magnitude of the anti-nutritive effects of HMC in broiler chicks. However, the exact role of the microflora in chicks in the magnitude of the anti-nutritional effects of HMC could not be derived from the present study, since the results might have been influenced by γ-irradiation of the diets fed to the germ-free chicks.

The plasma glucose–insulin relationships and thyroid status were investigated in two lines of adult cockerels divergently selected for high (R+) or low (R-) residual food consumption (RFC). For a given body weight, R+ birds had a 74 % higher food intake than R- birds. Plasma glucose concentrations were significantly lower in the R+ line compared with the R- when fasted, whereas R+ birds exhibited a significantly lower plasma insulin concentration than R- birds either in fed or fasted state. After an overnight fast, R+ birds also exhibited a higher sensitivity to exogenous insulin in view of its more pronounced hypoglycaemic effect. After an oral glucose load, the glucose disposal of R+ cockerels was faster despite lower glucose-induced plasma insulin concentration. Whilst plasma triacylglycerol concentrations were lower in the R+ line when fed, plasma non-esterified fatty acid concentrations were higher in fasted R+ than R- cockerels (684 v. 522 μmol/l). Higher plasma triiodothyronine concentrations were observed in fed R+ compared with R- birds (3·0 v. 2·1 nmol/l respectively). The higher plasma concentrations of triiodothyronine associated with lower concentrations of insulin could account for the leanness and the elevated diet-induced thermogenesis previously observed in the R+ line.

Four ruminally and duodenally cannulated multiparous Finnish Ayrshire cows were fed on diets consisting of grass silage (0·6 kg/kg DM) and one of four concentrates: barley, barley + urea, barley + rapeseed meal and barley + rapeseed cake. The objective of the present study was to compare omasal canal and duodenal digesta flows. Values for digesta flow into the omasal canal and duodenum were determined using a triple-marker method based on Co-EDTA, Yb-acetate and indigestible neutral-detergent fibre (NDF) markers. Microbial non-NH3 N (NAN) flow was assessed by purine flow. Microbial samples to determine the bacterial purine: N ratio were harvested from the rumen, omasum and duodenum. Organic matter flow was significantly lower into the omasum than the duodenum, indicating an endogenous organic matter secretion into the abomasum. In contrast, NDF and acid-detergent fibre flows were significantly higher into the omasum indicating digestion of fibre in the omasum. Microbial NAN flows were significantly different (P < 0·001) when estimates were based on bacterial samples harvested from different sites. Differences in total NAN, microbial NAN and dietary NAN flows entering the omasal canal and duodenum were non-significant. The results indicated that the omasal sampling technique provides a promising alternative to the duodenal sampling technique to investigate forestomach digestion in dairy cows and offers an alternative means to study rumen N metabolism.

This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the n-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. The data discussed indicate that dietary PUFA function as fuel partitioners in that they direct glucose toward glycogen storage, and direct fatty acids away from triglyceride synthesis and assimilation and toward fatty acid oxidation. In addition, the n-3 family of PUFA appear to have the unique ability to enhance thermogenesis and thereby reduce the efficiency of body fat deposition. PUFA exert their effects on lipid metabolism and thermogenesis by up-regulating the transcription of the mitochondrial uncoupling protein-3, and inducing genes encoding proteins involved in fatty acid oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA oxidase) while simultaneously down-regulating the transcription of genes encoding proteins involved in lipid synthesis (e.g. fatty acid synthase). The potential transcriptional mechanism and the transcription factors affected by PUFA are discussed. Moreover, the data are interpreted in the context of the role that PUFA may play as dietary factors in the development of obesity and insulin resistance. Collectively the results of these studies suggest that the metabolic functions governed by PUFA should be considered as part of the criteria utilized in defining the dietary needs for n-6 and n-3 PUFA, and in establishing the optimum dietary ratio for n-6 : n-3 fatty acids.

There have been many attempts to characterize day-to-day variation in nutrient intake. This variation has a fixed component, associated with particular days of the week, and a random component. Both components were studied for a range of nutrients, using 4 d weighed diary data from a large, nationally representative survey of people aged 65 years or over. Since day-to-day variation may distort the characterization of the population distribution of habitual nutrient intakes, especially when diets are studied over only a small number of days, a statistical method was developed to correct for this distortion. Results suggested that population distributions of habitual nutrient intake could be accurately constructed from 4 d weighed diary data and that the method might be successfully applied to studies based on as little as 2 d of observation. The method is particularly valuable for correcting estimates of extreme nutrient intakes for biases induced by uneven representation of days of the week and by within-person variation.

Cholesterol precipitation from supersaturated bile is the earliest and determinant step in the formation of cholesterol gallstones, which is thought to be diet-dependent. Bile composition, appearance and growth of cholesterol crystals were studied in fresh gall-bladder biles from pigs adapted to four different protein-containing diets over 3 weeks: 160 g dietary protein/kg as casein (C16; n 6), or as soyabean-protein concentrate (S16; n 6), or a mixture of both protein sources (casein–soyabean protein, 70 : 30, w/w) (CS16;n 6), or 320 g of the mixed protein/kg (CS32; n 6). Moreover, all four diets contained 3 g cholesterol/kg and 50 g β-cyclodextrin/kg as modifiers of bile composition towards cholesterol pro-crystallization. Cholesterol precipitation was most active after the high-protein diet, CS32, and the casein diet, C16, and lowest after the soyabean-protein diet, S16. It was intermediate after the mixed diet, CS16, but still much lower than in the former two groups. These diet-induced variations were suggested to be mediated through modifications in the biliary profile of bile acids, whereas all other biliary constituents studied were essentially unchanged. The fasting level of plasma cholesterol was lowest in both 160 g protein/kg diets containing soyabean protein (S16 and CS16), highest for the high-protein diet CS32, and intermediate for the C16 diet. These results should encourage clinical studies on the effect of soyabean protein, or other vegetable proteins, for primary or recurrence prevention of cholelithiasis at its earliest stage.

Intrauterine growth retardation associated with maternal undernutrition is proposed to play a significant role in the aetiology of hypertension and CHD. Animal experiments suggest that the kidney, which is extremely vulnerable to the adverse effects of growth-retarding factors, may play an important role in the prenatal programming of hypertension. Maintenance of renal haemodynamic functions following structural impairment in fetal life is proposed to require adaptations which raise systemic blood pressure and promote a more rapid progression to renal failure. Rats were fed on diets containing 180 g casein/kg (control) or 90 g casein/kg (low protein) during pregnancy. The offspring were studied in terms of blood pressure, creatinine clearance, blood urea N, plasma and urinary albumin, renal morphometry and metabolic activity at 4, 12 and 20 weeks of age. Blood pressure was elevated at all ages in the low-protein-exposed offspring, relative to control rats. Rats (4 weeks old) exposed to the low-protein diet had smaller kidneys which were shorter and wider than those of control animals. Creatinine clearance was significantly reduced in 4-week-old rats exposed to the low-protein diet. Renal morphometry and creatinine clearance at older ages were not influenced by prenatal diet. Blood urea N, urinary output and urinary albumin excretion were, however, significantly greater in low-protein-exposed rats than in control rats at 20 weeks of age. These findings are suggestive of a progressive deterioration of renal function in hypertensive rats exposed to mild maternal protein restriction during fetal life. This is consistent with the hypothesis that adaptations to maintain renal haemodynamic functions following impairment of fetal nephrogenesis result in an accelerated progression towards glomerulosclerosis and increased intrarenal pressures mediated by rising vascular resistance.

The hypothesis that olive-oil consumption alters plasma sphingomyelin concentrations and hepatic sphingomyelin metabolism was tested. Rats were fed on purified, high-cholesterol diets with either coconut fat or olive-oil (180 g/kg). In accordance with previous work, olive-oil v. coconut-fat consumption significantly elevated hepatic and total plasma cholesterol concentrations. During the course of the experiment, the concentration of plasma sphingomyelin rose in the coconut-fat group and remained constant in the olive-oil group. When compared with the coconut-fat-fed group, the plasma sphingomyelin levels were significantly lower in the olive-oil-fed group after 14 and 21 d of treatment. Dietary olive oil raised the amounts of cholesterol and sphingomyelin in the VLDL density region, and this change was associated with a reduction in the cholesterol and sphingomyelin contents of the LDL and HDL density ranges. Olive-oil consumption reduced the activity of serine palmitoyltransferase, while the activities of phosphatidylcholine:ceramide cholinephosphotransferase and phosphatidylethanolamine:ceramide ethanolaminephosphotransferase were left unchanged. Dietary olive oil also enhanced the activity of acidic sphingomyelinase, but not that of neutral sphingomyelinase. The present data indicate that dietary olive oil v. coconut fat has opposite effects on total plasma cholesterol and sphingomyelin concentrations. The lower plasma sphingomyelin levels observed in olive-oil-fed, as compared with coconut-fat-fed rats, may be explained by a simultaneous elevation and reduction in sphingomyelin catabolism and synthesis respectively, as based on the measured enzyme activities.

The consumption of fat-enriched diets may alter the uptake and metabolism of chylomicron remnant cholesterol by the liver. To test this hypothesis, [3H]cholesterol-labelled chylomicron remnants derived from different dietary fats were studied in perfused livers both from rats fed on diets enriched in the corresponding fats and from rats fed on a low-fat diet. Livers from rats fed on each of the fat-enriched diets removed similar amounts (34–40 %) of the [3H]cholesterol-labelled remnants added, whereas livers from rats fed on the low-fat diet removed significantly more labelled fish-oil and butter-fat remnants than olive-, maize- or palm-oil remnants. Significantly more remnant [3H]cholesterol was secreted into the perfusate HDL by livers from rats fed on the olive-oil, fish-oil and butter-fat diets when compared with those from rats fed on the low-fat diet or the maize-oil diet. Furthermore, the excretion of remnant [3H]cholesterol via the bile acid was increased by the olive-, maize-, palm- or fish-oil diets, and decreased by the butter-fat diet when compared with the low-fat diet, although the [3H]bile acid excreted remained less on saturated fat diets. This investigation shows that the hepatic uptake and subsequent metabolism of cholesterol from chylomicron remnants is influenced by the type of fat in the diet as well as the fatty acid composition of the particles themselves, and may help to explain some of the hyper- and hypocholesterolaemic effects of saturated and unsaturated fatty acids.

An experiment was conducted to investigate the compartmental mean residence time, (CMRT) of feed residues in segments of gastrointestinal digesta of mature Holstein steers. The objective was to evaluate assumptions that feed residues flow through ruminal digesta as sequential mixing pools having age-dependent (GN) and age-independent (G1) distributed residence times respectively (GN → G1 flow). The basal diet was a semi-tropical hay containing 98 g crude protein and 503 g apparently digestible DM per kg DM. The hay was consumed and feed residues of different size and/or previous digestion from the hay were inserted into the reticulo-rumen (rumen) and abomasum. Marker profiles appearing at the duodenum and faeces were fitted to various compartment models to estimate CMRT. Post-abomasal CMRT did not differ among solutes or feed residues of different size and previous digestion and constituted only 5·8 % of the CMRT for the entire gastrointestinal tract. Markers initially applied to orally or ruminally dosed feed residues exhibited profiles in duodenal digesta and faeces conforming to GN → G1 flow. Previously undigested, masticated feed residues inserted into the dorsal rumen digesta had longer ruminal CMRT in the GN pool but not the G1 pool than did similarly inserted faecal small particles or normally ingested hay. These results support model assumptions of GN → G1 flow within rumen digesta. The results support mechanisms proposed for the GN pool as the ‘lag-rumination pool’ and the G1 pool as the ‘mass action turnover pool’. If further validated, rumen CMRT in cattle could be estimated from marker profiles in more easily obtained faeces to estimate ruminal CMRT required for feed evaluation systems.

The aim of the present study was to assess how high doses of dietary vitamin K influence the intestinal profile of K-vitamins in vitamin K-deficient rats, and whether the induced changes are reflected in the hepatic vitamin K store. Vitamin K-deficient rats were fed for 10 d on diets containing different forms of vitamin K, and it was determined how these diets affected the vitamin K concentration at various sites of the instestine, serum, and the liver. It was found that the absorption of phylloquinone from standard food is not more than 10 %, while the absorption of pharmacological doses of oil-solubilized phylloquinone and menaquinone-4 was also far from complete (18 and 55 % respectively). High intakes of phylloquinone suppress the colonic production of all higher menaquinones. High menaquinone-4 intake induces very high menaquinone-8 concentrations, both in the colonic contents as well as in the liver. These data suggest that menaquinone-4 may be converted into menaquinone-8 (but not into other menaquinones) via a metabolic pathway which has not been reported previously.

Two rapeseed (Brassica napus) meals, RM1 and RM2, with two levels of glucosinolates (GLS; 5 and 41 μmol/g DM respectively) were incorporated at the levels of 300 and 500 g/kg of the diets of juvenile rainbow trout (Oncorhynchus mykiss) in replacement of fish meal, and compared with a fish-meal-based diet. A decrease in the digestibility of the DM, protein, gross energy and P was observed with high-rapeseed meal (RM) incorporation. In trout fed on RM-based diets, growth performance was reduced even after only 3 weeks of feeding. Feed efficiency was adversely affected by RM and GLS intake. Protein and energy retention coefficients were significantly lower in fish fed on the diet containing the higher level of GLS. P retention was significantly lower with all the RM-based diets than with the fish-meal diet. Irrespective of the degree of growth inhibition, fish fed on RM-based diets exhibited similar typical features of hypothyroid condition due to GLS intake, expressed by lower plasma levels of triiodothyronine and especially thyroxine and a hyperactivity of the thyroid follicles. This hypothyroidal condition led to a strong adjustment of the deiodinase activities in the liver, the kidney and the brain. A significant increase of the outer ring deiodinase activities (deiodinases type I and II respectively) and a decrease of the inner ring deiodinase activity (deiodinase type III) were observed. It is concluded that the observed growth depression could be attributed to the concomitant presence of GLS, depressing the thyroid function, and of other antinutritional factors affecting digestibility and the metabolic utilization of dietary nutrients and energy.

Obesity, especially visceral adiposity, is a major determinant of the development of type 2 diabetes. Both visceral adiposity and insulin resistance are strongly related to cardiovascular risk factors in diabetic and non-diabetic subjects. One of the areas where the correlation between visceral fat (upper body adiposity) and cardiovascular risk is most apparent is the prediabetic state. We have recently shown that only prediabetic subjects (those who later develop type 2 diabetes) who are insulin resistant and with upper body adiposity have increased triglycerides, decreased HDL cholesterol and high blood pressure.

There is a lack of agreement on index of Cu status and reliable and sensitive biomarkers are still required. The purpose of this present work was to assess in rats the sensitivity of diamine oxidase (DAO) activity, a recently proposed biomarker, to modifications in dietary Cu intake in comparison with other plasma biomarkers of Cu status. We also evaluated the effect of Cu dietary level on Cu and Zn intestinal absorption. Results showed that plasma Cu and plasma caeruloplasmin were significantly decreased at day 8 compared with the control group (7·4 mg Cu/kg diet) while DAO activity was significantly decreased at day 12 of the deficient diet (0·61 mg Cu/kg diet). Cu supplementation (35 mg Cu/kg diet) had no effect on any of the studied biomarkers of Cu status. In Cu-deficient rats plasma Cu and DAO activities were normalized 4 d after return to the control diet while caeruloplasmin was normalized later, at day 11. Apparent absorption values (%) of total Cu or 65Cu isotope were significantly increased in the Cu-deficient rats compared with the other groups and similar in the control and the Cu-supplemented groups. The urinary excretion of total Cu or 65Cu isotope were increased in the Cu-supplemented group compared with the other two groups. Both apparent absorption and urinary excretion of total Zn or 67Zn isotope remained unchanged in the three experimental groups. In conclusion, DAO activity seemed to be less sensitive to Cu deficiency than plasma Cu or caeruloplasmin concentrations. The present study also showed a significant increase in Cu intestinal absorption with dietary Cu restriction but no decrease with Cu supplementation in the rat.

The mass transfers of O2, glucose, NH3, urea and amino acids across the portal-drained viscera (PDV) and the liver were quantified, by arterio–venous techniques, during the last 4 h of a 100 h infusion of 0 (basal), 150 or 400 μmol NH4HCO3/min into the mesenteric vein of three sheep given 800 g grass pellets/d and arranged in a 3 × 3 Latin-square design. Urea irreversible loss rate (ILR) was also determined by continuous infusion of [14C]urea over the last 52 h of each experimental period. PDV and liver movements of glucose, O2 and amino acids were unaltered by NH4HCO3 administration, although there was an increase in PDV absorption of non-essential amino acids (P = 0·037) and a trend for higher liver O2 consumption and portal appearance of total amino acid-N, glucogenic and non-essential amino acids at the highest level of infusion. PDV extraction of urea-N (P = 0·015) and liver removal of NH3 (P < 0·001), release of urea-N (P = 0·002) and urea ILR (P = 0·001) were all increased by NH4HCO3 infusion. Hepatic urea-N release (y) and NH3 extraction(x) were linearly related (R2 0·89), with the slope of the regression not different from unity, both for estimations based on liver mass transfers (1·16; SE 0·144; PB ≠ 1 = 0·31) AND [14C]UREA (0·97; se 0·123; Pb ≠ 1 = 0·84). The study indicates that a sustained 1·5 or 2·4-fold increase in the basal NH3 supply to the liver did not impair glucose or amino acid supply to non-splanchnic tissues; nor were additional N inputs to the ornithine cycle necessary to convert excess NH3 to urea. Half of the extra NH3 removed by the liver was, apparently, utilized by periportal glutamate dehydrogenase and aspartate aminotransferase for sequential glutamate and aspartate synthesis and converted to urea as the 2-amino moiety of aspartate.

The purpose of this study was to differentiate between the effects of the amount and the type of dietary lipids on the expression of the retinoic acid receptor (RAR), but also the peroxisome proliferator-activated receptor (PPAR) and the receptor of the 9-cis retinoic acid (retinoid X receptor (RXR)) in rat liver. Six groups of eight rats (5-weeks old) were fed during 4 weeks on the following diets: control 50 g vegetable oil/kg, high-fat diet 250 g vegetable oil/kg. These oils were either coconut oil (rich in saturated fatty acids) or olive oil (rich in monounsaturated fatty acids) or safflower oil (rich in polyunsaturated fatty acids, mainly as n-6). The three high-fat diets induced a significant decrease of the maximal binding capacity of RAR and of the abundance of RARβ mRNA. Simultaneously, an increased expression of PPARα mRNA was observed while no significant difference on abundance of RXRα mRNA was observed. The mechanisms involved are probably multiple, but one hypothesis is that a modification of the equilibrium between the nuclear receptors, resulting from an increased expression of PPAR, induces a decreased expression of RAR in rat liver.