The present review focuses on the importance of polyunsaturated fatty acid (PUFA) provision for the normal development of the pig neonate. The review describes first the selected fatty acid composition of a range of porcine tissues including nervous tissues, muscle and adipose tissues, reproductive organs and immune-responsive organs and/or cells. The importance of PUFA to the functioning of the immune system of the neonate is considered briefly and is followed by an in-depth consideration of the sources of PUFA for the neonatal pig. The effects of different categories or specific types of fatty acid (i.e. non-essential, linoleic, α-linolenic, long-chain n-6 and n-3 PUFA) on various indices of pig neonatal growth are reviewed. The importance of n-3 PUFA supply to the fetal and early neonatal pig is underlined and evidence is presented for more attention to be given to the amounts available from maternal sources. Based on the material reviewed, recommendations are made on the dietary intake of PUFA in the gestating pig.

The method of Zinn & Owens (1986; Canadian Journal of Animal Science66, 157–166), based on release of purine bases by HClO4 followed by their precipitation with AgNO3, was used to study recovery of purines from lyophilized rumen microbial or Escherichia coli preparations added to matrices such as cellulose, starch and neutral-detergent fibre. The recovery of purines was poor (approximately 50 %). Under the hydrolysis conditions (12 M-HClO4, 90–95° for 1 h) used in the method of Zinn & Owens (1986), the recovery of purines from the rumen microbial preparations added to matrices measured using an HPLC method was 95–102 %, suggesting that the lower recovery of purines in the method of Zinn & Owens (1986) was not due to incomplete hydrolysis of nucleic acids. Using the HPLC method, adenine and allopurinol (an internal standard) were found to be heat-labile as substantial destruction was observed on heating at 121°. On the other hand, another commonly used internal standard, caffeine, was stable at 121°. A complete hydrolysis of nucleic acids from the rumen microbial preparation was observed with 2·5 ml 0·6 M-HClO4 in a total volume of 3 ml (0·5 M-HClO4 during hydrolysis) at 90–95° for 1 h, and under these conditions adenine, guanine, allopurinol and caffeine were stable. Moreover, under these milder hydrolysis conditions, the recovery of purine bases from the rumen microbial or E. coli preparations added to matrices ranged from 92 to 108 % using the method of Zinn & Owens (1986). Based on the results, changes in hydrolysis conditions have been proposed for accurate determination of purine bases using spectrophotometric or HPLC methods.

The effect of previous malnutrition on the metabolic response to surgical hysterectomy was investigated in adult female rats. Malnutrition was achieved by feeding a 20 g protein/kg diet and restricting food intake to 50 % of normal. This dietary regimen was maintained for 3 weeks before surgery and for 4 d after surgery. Unoperated control rats were pair-fed with the hysterectomized rats after surgery. Energy balance was measured by the comparative carcass technique and, in a second experiment, urinary N excretion was measured. Surgery caused energy expenditure to increase by 37 % in ad libitum-fed rats but in malnourished rats it increased by only 22 %. Urinary N excretion rose immediately after surgery. In the ad libitum-fed rats it was on average 85 % greater in hysterectomized rats than controls for the first 3 d after surgery, whereas in the restricted rats it was 74 % greater on the first day and not significantly elevated thereafter. Thus, malnutrition attenuated the metabolic response to surgery but did not abolish it completely.

This paper results from the final phase of the ENDO project (DGXII AIRII-CT94-1095), a European Commission-funded project on non-digestible oligosaccharides (NDO). All participants in the programme met to perform a consensus exercise on the possible functional food properties of NDO. Topics studied during the project (including a workshop on probiotics and prebiotics) and related aspects, for which considerable evidence has been generated recently, were evaluated on the basis of existing published scientific evidence. There was a general consensus that: (1) there is strong evidence for a prebiotic effect of NDO in human subjects. A prebiotic effect was defined as a food-induced increase in numbers and/or activity predominantly of bifidobacteria and lactic acid bacteria in the human large intestine; (2) there is strong evidence for the impact that NDO have on bowel habit; (3) there is promising evidence that consumption of inulin-type fructans may result in increased Ca absorption in man; (4) there are preliminary indications that inulin-type fructans interact with the functioning of lipid metabolism; (5) there is preliminary evidence in experimental animals of a preventive effect against colon cancer. Human nutrition studies are needed to substantiate these findings. It was concluded that the nutritional properties of NDO may prove to be a key issue in nutritional research in the future.

The present study aimed to investigate the prevalence and seasonal variation of hypovitaminosis D (defined as serum 25-hydroxyvitamin D level below 30 nmol/l) among healthy subjects and hospitalized patients living in central Italy. We studied 297 subjects, 131 in February 1997 and 166 in July 1997, subdivided into four groups: (a) young healthy blood donors; (b) healthy postmenopausal women; (c) inpatients with various medical diseases and (d) inpatients engaged in long-term rehabilitation programmes because of various neurological disorders. In all subjects and patients serum levels of 25-hydroxyvitamin D were measured by radioimmunoassay. We found a significant seasonal variation (P < 0·0001) of serum 25-hydroxyvitamin D levels, mean values being higher in summer in all groups, except in patients with a longer hospitalization time (group (d)). In each group, a significantly higher prevalence of hypovitaminosis D was found in winter compared with summer time (P < 0·001), being unexpectedly high in postmenopausal women (winter 32 % and summer 4·5 %); furthermore, in both seasons, inpatients were characterized by the highest incidences of hypovitaminosis, particularly those in group (d) (winter 82·3 % and summer 57·8 %). The results of the present study emphasize the importance of 25-hydroxyvitamin D measurement, and the need to increase vitamin D intake in Italy; foodstuff fortification and supplement use must be considered in order to prevent negative effects of vitamin D deficiency on skeletal integrity.

Serum Cu and caeruloplasmin levels have been suggested to be independent risk factors for CHD operating through oxidative modification of LDL. However, given its function as an acute-phase protein, the question has been raised whether an elevated caeruloplasmin level is not merely an indicator of inflammation. In the current study, we investigated whether serum caeruloplasmin was associated with subsequent myocardial infarction, taking into account indices of inflammation. The study population consisted of 210 cases of first myocardial infarction and controls, frequency-matched on age (5-year categories) and sex, selected from the population-based cohort of the Rotterdam Study. Serum caeruloplasmin levels were significantly elevated in cases of myocardial infarction compared with controls (510 (sd 110) v. 470 (sd 100) mg/1; P = 0·007). Risk of myocardial infarction for the highest compared with the lowest quartile of caeruloplasmin was 2·46 (95 % CI 1·04, 6·00; Ptrend = 0·043) after adjustment for age, sex, BMI, pack-years smoked, serum cholesterol, systolic blood pressure, and income. The relative risk was most evident in current smokers. Adjustment for C-reactive protein and leucocyte count reduced the excess risk by 33 %. This suggests that a substantial part of the observed association between serum caeruloplasmin and CHD may be attributed to inflammation processes rather than to the pro-oxidant activity of caeruloplasmin.

The aim of the present study was to investigate the influence of dietary protein level on the protein anabolic effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I). Female growing rats were fed on either a high- or a low-protein diet with crude protein contents of 222 and 83 g/kg respectively. The diets contained the same amount of metabolizable energy (15·1 MJ/kg) and were given during a 14 d period. During the same time, three groups of rats (n 8) on each diet received subcutaneous infusions of either saline, recombinant human GH (rhGH) or recombinant human IGF-I (rhIGF-I). rhGH and rhIGF-I were given in doses of 360 and 500 μg/d respectively. The low-protein diet alone reduced significantly (P < 0·05) IGF-I concentrations in serum and in tissue taken from the gastrocnemius muscle as well as IGF-I mRNA from the same muscle. The responses to rhGH and rhIGF-I in terms of muscle IGF-I and its mRNA were variable. However, when rhIGF-I was infused into rats on the high-protein diet, significantly elevated levels of IGF-I in muscle tissues could be observed. This was associated with a significantly (P < 0·05) increased N balance, whereas rhGH significantly (P < 0·05) enhanced the N balance in rats on the low-protein diet. Thus, it can be concluded that the level of dietary protein ingested regulates not only the effect of IGF-I on whole-body N economy but also the regulation of IGF-I gene expression in muscles. The exact mechanism by which GH exerts its protein anabolic effect, however, remains to be elucidated.

Weanling rats were offered food ad libitum, or fasted for 18 h, or fasted and refed for times ranging from 5 to 30 min. Five protein kinase C (PKC) isoforms (α, ε, ζ, and μ) were detected in the hindlimb muscles by Western immunoblotting. PKC forms ε and were abundant in plantaris, but not in soleus muscle, and no difference in localization was detected between fed rats and those fasted for 18 h. PKC forms α and μ were affected by fasting and refeeding. PKC-μ was found only in the cytosolic fraction of the plantaris muscle of the fasted animal, but in the fully-fed animals it was also associated with the membrane fraction. The pattern of localization observed in the fully-fed state was restored in the fasted rats by 20 min refeeding. In contrast, PKC-α was not detected in the cytosolic fraction of the plantaris in fasted animals but rapidly reappeared there on refeeding, being restored to 20 % and 80 % of the fed value within 5 and 30 min of refeeding respectively. The timing of these changes was correlated with the increase in serum insulin concentration, which was significantly elevated above the fasted value by 5 min and at subsequent times. These data suggest a possible role for PKC isoforms α and μ in the metabolic changes that occur in skeletal muscle on transition between the fasted and the fed state.

Incorporation of 2·5 g/kg of the anorexigen, simmondsin, in the diet resulted in food intake reduction in both lean and obese Zucker rats; however, the obese rats were much more sensitive to the food intake-reducing activity of simmondsin. In both obese and lean simmondsin-treated Zucker rats, growth was slower than in control rats, but was the same as that in pair-fed animals. The 24 h heat production pattern showed a smaller diurnal variation and a lower mean in obese rats than in lean rats. Food intake reduction, as a result of either simmondsin treatment or pair feeding, caused a decrease in mean heat production. Simmondsin treatment, but not pair feeding, caused a decrease in the diurnal variation of heat production. Plasma total cholesterol levels were increased in both simmondsin-treated and pair-fed obese and lean Zucker rats compared with control animals; this increase was mainly due to an increase in HDL-cholesterol levels. Blood leptin levels in both obese and lean rats decreased with decreased food intake and decreased fat deposition, but in obese rats, simmondsin treatment resulted in an additional decrease in leptin levels. It is concluded that the food intake-reducing effect of simmondsin is more pronounced in obese Zucker rats than in their lean littermates, and except for the simmondsin-specific effects on leptin and total cholesterol values in obese littermates, the effects of simmondsin are related to food intake restriction in obese and lean Zucker rats.