The present study was designed to determine the interrelationships between sex, weaning age, and weaning weight on aspects of physiological and gastrointestinal development in pigs. Forty-eight Large White × Landrace pigs were used in a factorial arrangement with the respective factors being: age at weaning (14 or 28 days), weight at weaning (heavy or light), sex (boar or gilt), and time after weaning (1, 7, and 14 days). At weaning, 48 pigs were removed from the sow: 16 pigs were then fasted for 24 h before euthanasia for determination of organ weights, gut histology, and enzymology, and 32 pigs were offered a high quality pelleted weaner diet ad libitum for subsequent assessment of organ weights, histology, and enzymology at 7 and 14 d after weaning. On Day 6 and 13 after weaning, 2 pigs from each group had their feed removed, and 24 h later were euthanased and similar measurements were taken. In general, the data highlighted the overall gastrointestinal underdevelopment of pigs weaned at 2 weeks of age and of pigs weaned light-for-age at either 2 or 4 weeks. Heavier body organs, gastrointestinal organs, and accessory digestive organs observed after weaning, except for the spleen, presumably reflected the increase in substrates available for cellular growth as feed intake increased after weaning, and the development of organs required to process this feed. Interestingly, the relative weights (% of liveweight) of the stomach and small intestine and, to a lesser extent, the caecum and colon, were greater in the light, 14-day-old weaned pigs, but these differences diminished with increasing time after weaning. Consistent effects due to age, weight, and sex were not observed for villous height and crypt depth, or for the specific activities of the brush-border and pancreatic enzymes measured. However, increases (P < 0.001) in the activities of maltase (P�<�0.001), glucoamylase (P < 0.001), and sucrase (P = 0.020) (all expressed per gram of mucosa), and that of trypsin (per gram of pancreas), occurred by 14 days after weaning. This most likely reflected the inducible nature of these enzymes in response to the increasing intake of substrates provided in the diet. In contrast, the specific activity of lactase declined (P = 0.012) in the first 14 days after weaning. These data suggest that pigs weaned at 2 weeks of age and pigs weaned light-for-age at either 2 or 4 weeks have a less developed gastrointestinal tract, and that its development after weaning might proceed differently to that of pigs weaned older and heavier.

1. The contribution to acidification of the stomach contents of pigs by hydrochloric acid secretion or by lactic acid produced by fermentation was studied in fifteen suckling pigs from six litters born and reared either in a ‘conventional’ environment or in an isolated ‘clean’ environment. Sequential samples of stomach contents obtained during periods of up to 24 h were analysed for their chloride and lactic acid contents, pH and total titratable acidity. These values gave a measure of organic and inorganic acids respectively.2. Six pigs from two litters born and reared in a ‘clean’ environment had acid secretion in the stomach at 2 d of age, and the concentrations of lactic acid in stomach contents remained low (0-40 mmol/1) throughout the suckling period.3. Eight pigs from three litters born and reared in a ‘conventional’ environment, and a ninth pig born in this environment but moved to the ‘clean’ environment at 24 h of age, had lactic acid in concentrations of up to 250 mmol/l in stomach contents within the 1st week of life. The pattern of lactic acid production (and hence the acidity of stomach contents) was governed by the frequency of suckling.4. Both between- and within-litter variation in the age of onset of HCl secretion was evident in the group reared in a ‘conventional’ environment, and when HCl secretion did occur it was usually accompanied by a reduction in lactic acid production.5. It is concluded: (I) that the environment at birth is important in determining the fermentative ability of the stomach flora; (2) that if lactic acid is produced in large amounts in the stomach, it may partly or completely inhibit acidification by HCl.

1. The development of gastric secretory capacity of hydrochloric acid and pepsin (EC 3. 4. 23. 1) was studied in thirty-eight Large White x Landrace pigs from the litters of six sows (three pairs of two), 9–38 d of age. The pigs of each pair of sows were born within 24 h of each other. The pigs of a litter were paired according to sex and size and cross-fostered, i.e. one pig from each pair was allocated to each sow.2. One litter from each pair was reared entirely by the sow (milk-fed, MF) whereas the other litter was reared by the sow for 21 d, but was allowed access to solid food (210 g crude protein (nitrogen x 6.25)/kg) at 12 d and was entirely dependent on solid food after 21 d (creep-fed, CF).3. Following a 14–18 h fast, pigs were anaesthetized (Halothane–sodium pentobarbitone) and their stomachs perfused a a constant rate with Ringer solution. Gastric secretion was stimulated by intravenous infusion of betazole hydrochloride (Histalog) at 3 mg/kg per h for 2 h. Hydrochloric acid and pepsin were measured in the perfusate which was collected at 15-min intervals.4. There were significant positive correlations between stomach weight and body-weight for both MF and CF pigs. The slope of the regression line for CF pigs was significantly greater than that for MF pigs (P < 0.01).5. There were significant positive correlations between maximal acid output and stomach weight for both MF and CF pigs.6. There were significant positive correlations between maximal pepsin output and stomach weight for both MF and CF pigs. The slope of the regression line for CF pigs was significantly different from that for MF pigs (P < 0.01). There were also significant positive correlations between maximal pepsin output per unit stomach weight and stomach weight for both MF and CF pigs.7. The pattern of development of pepsin secretory capacity in both CF and MF pigs was different from that for acid secretion. Maximal outputs of acid per unit stomach weight for MF and CF pigs remained relatively constant. Maximal outputs of pepsin per unit stomach weight and per unit body-weight increased with age for both MF and CF pigs.8. The results indicate that pigs given access to solid food before weaning and weaned on to solid food have heavier stomachs and greater acid and pepsin secretory capacity than pigs fed entirely on sows' milk.

The present study aimed to determine whether lysine and/or methionine are absorbed in nutritionally significant amounts from the proximal colon of milk-formula-fed piglets (15-32 d old; 24-7.4 kg liveweight). Piglets, surgically prepared with simple catheters which allowed infusion into the proximal colon, were randomly allocated to one of two milk-formula diets which were either 40% deficient in lysine (L -diet) or 60 % deficient in methionine and 40 % deficient in cysteine (S -diet), yet balanced for all other amino acids. The piglets were individually bottle-fed the milk-formula diets seven times daily at 2 h intervals between 08.00 and 20.00 hours. Physiological saline (9 g NaCI/I) or an isotonic solution containing the deficient amino acid was infused via the catheter at each feeding. The experimental procedure followed a cross-over design. Total daily excretions of urinary urea and total N were determined. There were no significant differences (P > 0.05) in urinary N metabolite excretion for piglets infused with amino acids compared with those infused with saline. Lysine and methionine do not appear to be absorbed in nutritionally significant amounts from the proximal colon of the milk-fed piglet.

The present study was designed to determine the interrelationships between sex, weaning age, and weaning weight on subsequent growth performance. Ninety-six Large White × Landrace pigs were used in a 2 × 2 × 2 factorial experiment with the respective factors being: age at weaning (14 or 28 days), weight at weaning (heavy or light), and sex (boar or gilt). Eighty pigs were offered a high quality pelleted weaner diet ad libitum while the remaining 16 pigs (2 pigs from each treatment group) were removed from the sow and fasted for 24 h before being euthanased for determination of gut histology and enzymology. The remaining pigs were weaned into individual pens and given an ad libitum diet containing 15.5 MJ DE/kg and 0.95 g available lysine/MJ DE. On Day 6 and 13 after weaning, 2 pigs from each group at each time had their feed removed and, 24 h later, were euthanased. From 3 weeks post-weaning, the remaining pigs were group-penned with contemporary pigs and fed commercial rations until slaughter at 23 weeks of age. In the first week after weaning, the heavy pigs and those weaned at 28 days ate more feed and grew faster, and gilts ate more and grew faster than boars over the same time. Pigs that were heavier at weaning were also heavier at every subsequent age. At slaughter, heavy boars weighed more than heavy gilts (110.5 v. 103.7 kg, P = 0.027), whereas this was not the case for light boars and gilts (94.1 v. 94.4 kg, P = 0.96). Whereas there were no effects of sex or weight at weaning on P2 backfat depth, pigs weaned at 14 days had more backfat at 23 weeks than pigs weaned at 28 days (13.1 v. 10.9 mm, P = 0.009). In conclusion, these data clearly indicate that the greatest determinants of immediate post-weaning performance under the present conditions were the age and weight of the pigs at weaning. However, the key determinant of lifetime growth rate appeared to be weight of pigs at weaning or, by inference, birth. Although age at weaning had no effect on lifetime growth rate, early-weaned pigs were fatter at slaughter.

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Gastric acid secretion, gastrin-releasing peptide (GRP)-stimulated gastrin secretion and concentrations of somatostatin in gastric tissues were studied in sucking pigs (n = 48). In addition, gastrin concentrations in plasma and antral tissue were measured in fetal and sucking pigs (n = 66) from 22 days before birth (93 days gestation) to 36 days of age. From 3 days of age littermate pairs were treated twice a day with either saline (n = 20) or adrenocorticotropin [ACTH (1–24); n = 20]. Pentagastrin-stimulated acid secretion per unit stomach weight was 39 ± 7 μmol H⁺/g/h at 0–1 day, increased to 194 ± 15 μmol H⁺/g/h at 5–7 days and plateaued. Antral gastrin concentration was 0.14 nmol/g 10 days before birth and increased to 2.7 nmol/g at 5 weeks of age. Plasma gastrin was 25 ± 2 pmol/l at 22 days before birth, increased to 102 ± 14 pmol/l at birth and decreased during the postnatal period. Somatostatin concentrations were higher in antral than fundic tissues (p < 0.05) and remained constant during the postnatal period. Increased levels of glucocorticoids in plasma following ACTH treatment had no effect on the studied parameters except that it reduced basal (p < 0.07) and GRP-stimulated (p < 0.05) plasma gastrin concentrations at 6–7 days of age. Development of acid secretion and its gastric regulatory peptides in the pig is different from that in the rat in that it occurs at an earlier age and does not appear to be greatly influenced by elevated glucocorticoid levels from 3 days after birth.

Experiments were performed on conscious dogs with chronic pouches of the antrum, the duodenal bulb or the ileum, which were perfused with solutions of varying pH. Gastrin and somatostatin levels were measured in the perfusates. When the pouches were perfused with 0.15 M NaCl only small amounts of gastrin and somatostatin (1 pmol/min) were released into the lumen of the antrum and of the duodenal bulb. By lowering pH of the perfusion fluid a pH dependent release of somatostatin was induced into the lumen of the antrum and the duodenal bulb. Perfusion with 0.1 M HCl caused a large output of somatostatin (6--60 pmol/min) into the pouches. The upper pH limit for stimulation of the intraantral or intrabulbar somatostatin release appeared to be approximately pH 3--4. Somatostatin was also released into ileal perfusates at intraluminal pHs below 3--4. Lowering of pH in the antral pouches caused an increased intraluminal gastrin release, which was quantitatively less impressive than that of somatostatin. Occasionally also the gastrin release into the duodenal bulb increased during perfusion with 0.1 M HCl, whereas no such release was induced by acidification of the lumen of the ileum. It is suggested that the inhibition of gastrin release observed at low intraantral pH is mediated by a local effect of somatostatin, since this peptide is released in a pH dependent manner in the antropyloric region. It is also suggested that acidification of any region of the gastrointestinal tract will stimulate the release of peptides from all endocrine cells of the open type, probably by an unspecific effect on the membrane. Thus both gastrin and somatostatin are released by acidification of the antrum, but in the presence of high local levels of somatostatin, the release of gastrin is substantially inhibited.