Nutrition has marked influences on gene expression and an understanding of the interaction between nutrients and gene expression is important in order to provide a basis for determining the nutritional requirements on an individual basis. The effects of nutrition can be exerted at many stages between transcription of the genetic sequence and production of a functional protein. This review focuses on the role of post-transcriptional control, particularly mRNA stability, translation and localization, in the interactions of nutrients with gene expression. The effects of both macronutrients and micronutrients on regulation of gene expression by post-transcriptional mechanisms are presented and the post-transcriptional regulation of specific genes of nutritional relevance (glucose transporters, transferrin, selenoenzymes, metallothionein, lipoproteins) is described in detail. The function of the regulatory signals in the untranslated regions of the mRNA is highlighted in relation to control of mRNA stability, translation and localization and the importance of these mRNA regions to regulation by nutrients is illustrated by reference to specific examples. The localization of mRNA by signals in the untranslated regions and its function in the spatial organization of protein synthesis is described; the potential of such mechanisms to play a key part in nutrient channelling and metabolic compartmentation is discussed. It is concluded that nutrients can influence gene expression through control of the regulatory signals in these untranslated regions and that the post-transcriptional regulation of gene expression by these mechanisms may influence nutritional requirements. It is emphasized that in studies of nutritional control of gene expression it is important not to focus only on regulation through gene promoters but also to consider the possibility of post-transcriptional control.

Twenty-four middle-aged healthy men were given a low-fat high-carbohydrate (5.5 g fat; L), or a moderately-fatty, (25.7 g fat; M) breakfast of similar energy contents for 28 d. Other meals were under less control. An oral glucose tolerance test (OGTT) was given at 09.00 hours on day 1 before treatment allocation and at 13.30 hours on day 29. There were no significant treatment differences in fasting serum values, either on day 1 or at the termination of treatments on day 29. The following was observed on day 29: (1) the M breakfast led to higher OGTT C-peptide responses and higher areas under the curves (AUC) of OGTT serum glucose and insulin responses compared with the OGTT responses to the L breakfast (P < 0.05); (2) treatment M failed to prevent OGTT glycosuria, eliminated with treatment L; (3) serum non-esterified fatty acid (NEFA) AUC was 59% lower with treatment L than with treatment M, between 09.00 and 13.20 hours (P <0.0001), and lower with treatment L than with treatment M during the OGTT (P = 0.005); (4) serum triacylglycerol (TAG) concentrations were similar for both treatments, especially during the morning, but their origins were different during the afternoon OGTT when the Svedberg flotation unit 20–400 lipid fraction was higher with treatment L than with treatment M (P = 0.016); plasma apolipoprotein B-48 level with treatment M was not significantly greater than that with treatment L (P = 0.086); (5) plasma tissue plasminogen-activator activity increased after breakfast with treatment L (P = 0.0008), but not with treatment M (P = 0.80). Waist:hip circumference was positively correlated with serum insulin and glucose AUC and with fasting LDL-cholesterol. Waist:hip circumference and serum TAG and insulin AUC were correlated with factors of thrombus formation; and the OGTT NEFA and glucose AUC were correlated. A small difference in fat intake at breakfast has a large influence on circulating diurnal NEFA concentration, which it is concluded influences adversely glucose tolerance up to 6 h later.

Resistant starch (RS) has been defined as the sum of starch and starch-degradation products that reach the human large intestine (Champ, 1994), and it is now regarded as a sub-fraction of starch with a positive impact on colonic welfare and lipid metabolism. An early estimate of the RS intake in Europe gave an average value of approximately 4 g/d (Dyssler & Hoffem, 1994a). However, since no information is available for Italy, the aim of the present study was to estimate the intake of RS in the Italian diet by direct analysis of RS in a range of typical foods representing the main sources of starch intake in the country. The selection of representative foods and of food consumption data were based on published results of the National Food Consumption Study conducted during the 1980s by the National Institute of Nutrition on 10 000 households, using weighed-food records plus inventory methodologies (Saba et al. 1990; Turrini et al. 1991). Three main groups of foods were considered: cereals (pasta, rice, bread and bread products, and pastries), potatoes, legumes. Different commercial brands for each sample were purchased, according to the known presence on the market. Samples were prepared ‘as eaten’ and submitted to simulated chewing, followed by total and resistant starch determination using the enzymic procedure published as a result of the EC Concerted Action EURESTA (Champ, 1992). From these results, the estimated average intake of RS in Italy was found to be 8.5 g/d, with regional differences (from 7.2 g/d in the north-west to 9.2 g/d in the south) mainly due to the different consumption of some typical Italian starchy food (bread, pasta, legumes).

The energy value of NSP has been expressed as their metabolizable energy (ME) content. The aim of the present study was to determine whether differences in ME and net energy (NE) contents were similar for insoluble and soluble NSP. Nine healthy young men were offered three diets according to a Latin-square design (3 × 3) with three repetitions: diet C (control), diet B (control + 50 g sugarbeet fibre/d) and diet I (control + 50 g commercial inulin/d). After a 16 d adaptation period to NSP isolate, food intake was controlled (duplicate meal method) and faeces and urine were collected for 8 d. A period of 60 h was devoted to measurement of energy expenditure (EE) by whole-body indirect calorimetry. NSP-isolate ingestion induced significant increases in the number of defecations and stool weight resulting from increases in water, DM and microbial mass excretion. After deduction of microbial N, differences in faecal N excretion between diets were not significantly different. Urinary N excretion was slightly decreased by sugarbeet fibre or commercial inulin ingestion but the N balances for the diets were not significantly different. Diet energy, N and lipid apparent digestibilities decreased by only 1–2 %. Commercial inulin was entirely fermented and fermentability of sugarbeet fibre averaged 0.886 (sd 0.117). Sugarbeet fibre and commercial inulin ME values averaged 10.7 (sd 1.2) and 13.0(sd 2.3) kJ/g DM respectively. NSP-isolate ingestion caused significant (sugarbeet) and nonsignificant (inulin) increases in daily EE. The maintenance NE contents of sugarbeet fibre and inulin averaged 5.0 (sd 5.0) and 11.9 (sd 1.3)kJ/g DM respectively. Differences in maintenance NE contents of NSP isolates were much greater than differences in ME values.

To study the relationship between lycopene intake and plasma concentration, ten healthy female subjects were given one or more portions of tomato purée or fresh raw tomato containing 16.5mg total lycopene (all-trans + cis forms). In Expt 1 subjects (n 9) were randomly assigned the single portions of the two tomato products and blood samples were collected to follow the change in plasma carotenoid concentrations within the first 12 h and on each of the following 5 d (104 h). In Expt 2 subjects (n 10) were divided into two groups of five each receiving daily dietary portions of tomato purée or fresh raw tomato containing 16.5mg total lycopene for 7 d. Fasting blood samples were collected daily. In Expt 1 the plasma total lycopene (all-trans + cis forms) concentration, after the single portions of tomato purée and raw tomato, varied significantly over time, with a first peak reached after 6 h, a further increase after 12 h and a slow decrease until 104 h. In Expt 2, when the tomato products were given daily, there was a day-by-day increase in the plasma total lycopene concentration, and through the following week of a diet without tomato there was a gradual decrease. However, values did not return to basal concentrations. Plasma total lycopene concentration was higher after the tomato purée intake than after the raw tomato in both the first (F (1,8) 7.597; P < 0.025) and the second experiments (F (1,8) 12.193; P < 0.01) demonstrating a significant effect of food matrix on absorption.

The physiological importance and mechanism of the postprandial fall in plasma Zn concentration is not well understood. In order to gain further information on this apparent redistribution of plasma Zn, a stable isotope, 70Zn, was used to study the effect of a breakfast meal on plasma Zn kinetics. Nine women participated in two trials, a fasting trial and a breakfast-meal trial; five of the women participated in a third trial in which the energy content of the breakfast meal was doubled. At each trial, 0.1mg of 70Zn was infused intravenously, and the plasma disappearance of the isotope was analysed using a two-compartment model of Zn kinetics. Plasma Zn concentration fell significantly following the two trials in which the subjects were given meals, reaching low points that were 13 and 19 %, respectively, below concentrations at comparable times during the fasting trial. Kinetic analysis revealed that after the doubled breakfast meal there was a significant fall (P < 0.007) in the size of the most rapidly turning over Zn pool (pool (a)) from 2.90 (se 0.13)mg in the fasting state to 2.47 (se 0.14) mg postprandially. The fractional turnover rate of pool (a) to other extravascular Zn pools, i.e. outside the two-compartment system, was also significantly elevated after the doubled breakfast meal (P < 0.05). These results suggest that the decline in plasma Zn concentration following a meal is due to a redistribution of Zn from the plasma to other more slowly turning over extravascular pools that may be involved in the assimilation and metabolism of fuels following food intake.

The effect of acute (4.5 h) infusions into the mesenteric vein of an amino acid (AA) mixture, which simulated the composition of rumen microbial protein, on net transfers of NH3, urea and total AA across the portal-drained viscera (PDV) and liver in the ovine has been examined. Four wether sheep were surgically prepared with vascular catheters across the PDV and liver (Lobley et al. 1995) and were offered a basal diet of 1000 g grass pellets/d (approximately 1.4 × energy maintenance). Each animal was infused at weekly intervals with one of four dilutions of the AA mixture. These dilutions provided 0.44, 0.88, 1.32 and 1.84mmol AA-N/min infused, the lowest of which approximately doubled the net absorption of AA-N from the basal diet. Animals were treated with heparin to allow continuous collection of blood by peristaltic pump for 2 h preceding, and between 0.5–2.5 and 2.5–4.5 h after, the start of the AA infusions. Blood flow in the hepatic artery increased (100 v. 208 g/min; P = 0.002) in response to AA infusion, while hepatic portal venous flow decreased (2090 v. 1854 g/min; P = 0.006). The AA infusion also stimulated O2 uptake by the PDV (P < 0.001) and liver (P = 0.016). Absorption across the PDV and hepatic removal of NH3 were unchanged between basal and amino acid infusion conditions. Urea-N removal across the PDV was unaltered, but hepatic production increased (P < 0.001) with level of AA infusion. During infusions, net appearance of AA across the PDV was below the theoretical level. This may have been due to inhibition of AA uptake from the small intestine, and/or increased removal by the digestive tract of AA from the systemic circulation associated with greater arterial concentrations. Hepatic extraction of AA increased with level of infusion, both for total AA and those included in the infusate. Total hepatic urea-N production tended towards a maximum (estimated as 2 μmol N/g liver wet weight per min). The AA removed by the liver and not used for ureagenesis remained similar (170 μmol AA-N/min) between basal and AA infusions. This was presumed available for anabolic purposes (mainly synthesis of export proteins). The proportion of net AA-N appearance (absorption plus infused) across the PDV removed by the liver declined from 0.71 to 0.53 between basal and AA infusions. In contrast to findings from cattle (Wray-Cahen et al. 1997), increased AA infusion did not alter the net removal of glutamine across the liver. This may reflect differences between the studies in NH3: AA-N absorbed. Further differences between the cattle study and the current findings may relate to the different physiological state (pregnancy v. growth), which may alter the partition of AA between anabolic and catabolic fates.

External digesta markers (Yb-labelled diets and Co-EDTA) were given orally as a pulse dose to four pairs of Rasa Aragonesa twin ewe lambs, fed on either chopped or ground and pelleted lucerne hay, in order to estimate slow (k1) and fast (k2) rates of passage of liquid and solid phase from faecal marker excretion curves. After the faecal sampling period daily doses of the same markers were infused continuously for 5 d and the animals slaughtered. Concentrations of markers in the different compartments of the gut were determined and used to calculate mean retention times. The results showed that the rumen and the large intestine were the two main mixing compartments of the gut, accounting for more than 95% of total mean retention time. Rates of passage estimated from faecal marker excretion did not accurately represent marker kinetics in the compartments of the gut derived from slaughter data. Accuracy in the estimation of fractional outflow rate from rumen (kR) by k1 was higher for low values of kR whereas k2consistently overestimated large intestine outflow rate (kLI), especially for high values of kR. The relationship between outflow rates from the main two mixing compartments was important in influencing the accuracy of prediction of faecal estimates.

Responses to supplemental dietary l-carnitine of broilers fed on diets with different levels of metabolizable energy (ME) were investigated using growth performance and some carcass measurements. Three isonitrogenous diets containing 13.5, 12.8 or 12.2 MJ ME/kg were formulated, with or without supplemental l-carnitine (50mg/kg) and fed ad libitum from 18 to 53 d of age. Supplemental l-carnitine increased body-weight gain (BWG) and improved feed conversion (FC) during the first 2 weeks of study. FC was also improved during the fourth week of the experiment. Weights of breast yield and thigh meat yield were significantly increased, whereas quantity and percentage of abdominal fat were reduced by supplemental l-carnitine. A significant interaction between supplemental dietary l-carnitine and dietary energy level was noted for BWG and FC during the second week of study.

The effect of vitamin A on chicken intestinal mucosal morphology and functionality was tested in relation to severe and mild vitamin A deficiency and vitamin A repletion. Compared with rats and mice, chickens have a very quick response to a deficient dietary intake. Severe vitamin A deficiency altered the small intestine of chickens at both the biochemical and the morphological levels. It caused the loss of mucosal protein, reduced villus height and crypt depth and diminished activities of disaccharidases, transpeptidase and alkaline phosphate (EC 3.1.3.1). The ratios RNA-.DNA, RNA:protein and protein:DNA, and the DNA concentrations in 1 g intestinal tissue, together with morphological measurements, provided knowledge about the pattern of lesion. The results indicated that (1) lack of vitamin A influenced cellular hyperplasia as it caused an increase in DNA content and in the number of enterocytes per villus; (2) lack of vitamin A influenced cellular hypertrophy as it decreased the protein:DNA ratio. There was no difference in mucosal enzyme activity between the two deficient groups. The repletion group exhibited a remarkable increase in mucosal enzyme activity only 4 d after switching to the control diet. The evidence presented in our paper suggests that the low vitamin A supply interferes with the normal activity of chicken intestinal mucosa as it influences the processes of proliferation and maturation of enterocytes.