To combat the stress of weaning, we utilized novel gruel creep feeders to supplement suckling pigs with divergent soluble (n = 6 litters) versus insoluble (n = 6) diets compared with un-supplemented controls (n = 6). Post-weaning, pigs were fed a common phase 1 diet. Average daily weight gains of pigs fed soluble and insoluble creep diets were 53% and 17% greater than control pigs, respectively (p < 0.01). Creep intake was higher (82%) for pigs fed the soluble diet, and the accompanying weight increase was sustained post-weaning (p < 0.02). Villus measures were prematurely altered in soluble-creep-fed pigs (p < 0.01), with decreases in villi length, crypt depth, and villus area pre-weaning. No effects of treatment were detected for VFA concentrations and pH in the cecum. There was an interaction between treatment and age for several pro- and anti-inflammatory cytokines (p < 0.01), where soluble-creep-fed pigs had increased cytokine levels with age, whereas cytokine levels in the insoluble and control groups decreased over time. We conclude that a soluble creep diet fed in a gruel state during the pre-weaning period has a positive impact on weaning weight that is sustained post-weaning, and is accompanied by alterations in the intestinal health of young pigs.

Milk carnitine content decreases quickly with lactation days and is accompanied by PPARα downregulation. This study aimed to investigate the effects of the maternal supplementation of the PPARα agonist, clofibrate, on milk carnitine content and carnitine status in neonates during lactation. Pregnant sows (n = 27) were fed diets containing either 0, 0.25, or 0.5% clofibrate from d107 gestation to d7 of lactation. Carnitines were determined in milk on d1, 3, 5, 7, 10, 14, and 19 post farrowing and in the plasma, intestine, and liver of piglets on d1, 7, 14, and 19. Milk carnitine decreased quadratically with lactation days (p < 0.0001). Hepatic and intestinal carnitines increased with postnatal age (p < 0.05). Correlations between levels were detected between milk and plasma (R² = 0.5, p < 0.0001) and milk and intestine (R² = 0.23; p < 0.05). Clofibrate increased BBH expression (p < 0.05) and tended to increase OCTN2 expression (p = 0.055) in intestine and TMLH in liver (p = 0.059). Hepatic ALD and TMLH increased (p < 0.0005) with postnatal age. However, gene modification had no effect on plasma and mucosa carnitine concentrations. We conclude that changes in carnitines within plasma and mucosa are mostly driven by milk carnitines during postnatal development.