ABSTRACT. Although a number of causes of poor fetal growth are known, the involvement of placental transport proteins in the etiology of growth retardation is not undcrstood. The aim of this study was to investigate the activity of the system A amino acid transporter and the Na+/li+ eschanger in vesicles isolated from the microvillous membrane of the syncytiotrophoblast of placentas of appropriate and small for gestational age babies. l'here were no biochemical differences bet~veen the membranes from the two groups of placentas, and there was no difference in the activity of the Na+/I1+ exchanger. The initial rate of uptake of methylaminoisobutyric acid (a nonmetabolizable amino acid analogue) was 63% loner in vesicles from placentas of small for gestational age babies. Kinetic analysis of the system A transporter (utilized by mcthylaminoisobutyric acid) showed that the V,,., in the vesicles from placentas of small for gestational age babies (0.24 f 0.03 nmol/mg protein/30 s, n = 5) was significantly lower than that in vesicles from placentas of appropriate for gestational age babies (0.64 + 0.09 nmol/mg protein/30 s, n = 4, p < 0.001), whereas the Km was not different between the two groups. It is concluded that there is an abnormality of system A amino acid transporter function in placentas of small for gestational age babies. (Pediatr Res 34: 661-665, 1993)

Ongoing challenges in the swine industry, such as reduced access to antibiotics and virus outbreaks (e.g., porcine epidemic diarrhea virus, African swine fever virus), have prompted calls for innovative feed additives to support pig production. Medium-chain fatty acids (MCFAs) and monoglycerides have emerged as a potential option due to key molecular features and versatile functions, including inhibitory activity against viral and bacterial pathogens. In this review, we summarize recent studies examining the potential of MCFAs and monoglycerides as feed additives to improve pig gut health and to mitigate feed pathogens. The molecular properties and biological functions of MCFAs and monoglycerides are first introduced along with an overview of intervention needs at different stages of pig production. The latest progress in testing MCFAs and monoglycerides as feed additives in pig diets is then presented, and their effects on a wide range of production issues, such as growth performance, pathogenic infections, and gut health, are covered. The utilization of MCFAs and monoglycerides together with other feed additives such as organic acids and probiotics is also described, along with advances in molecular encapsulation and delivery strategies. Finally, we discuss how MCFAs and monoglycerides demonstrate potential for feed pathogen mitigation to curb disease transmission. Looking forward, we envision that MCFAs and monoglycerides may become an important class of feed additives in pig production for gut health improvement and feed pathogen mitigation.

The objective of this study was to investigate the effect of increasing degrees of lipid peroxidation on structure and function of the small intestine of nursery pigs. A total of 216 pigs (mean body weight was 6·5 kg) were randomly allotted within weight blocks and sex and fed one of five experimental diets for 35 d (eleven pens per treatment with three to four pigs per pen). Treatments included a control diet without added lipid, and diets supplemented with 6 % soyabean oil that was exposed to heat (80°C) and constant oxygen flow (1 litre/min) for 0, 6, 9 and 12 d. Increasing lipid peroxidation linearly reduced feed intake (P < 0·001) and weight gain (P = 0·024). Apparent faecal digestibility of gross energy (P = 0·001) and fat (P < 0·001) decreased linearly as the degree of peroxidation increased. Absorption of mannitol (linear, P = 0·097) and D-xylose (linear, P = 0·089), measured in serum 2 h post gavage with a solution containing 0·2 g/ml of D-xylose and 0·3 g/ml of mannitol, tended to decrease progressively as the peroxidation level increased. Increasing peroxidation also resulted in increased villi height (linear, P < 0·001) and crypt depth (quadratic, P = 0·005) in the jejunum. Increasing peroxidation increased malondialdehyde concentrations (quadratic, P = 0·035) and reduced the total antioxidant capacity (linear, P = 0·044) in the jejunal mucosa. In conclusion, lipid peroxidation progressively diminished animal performance and modified the function and morphology of the small intestine of nursery pigs. Detrimental effects were related with the disruption of redox environment of the intestinal mucosa.

The role of parathyroid hormone-related protein (PTHrP) in fetal calcium homeostasis and placental calcium transport was examined in mice homozygous for the deletion of the PTHrP gene (PTHrP −/− null; NL) compared to PTHrP +/+ (wild-type; WT) and PTHrP +/− (heterozygous; HZ) littermates. Fetal blood ionized calcium was significantly reduced in NL fetuses compared to WT and HZ groups at 18 days of pregnancy (dp) with abolition of the fetomaternal calcium gradient. In situ placental perfusion of the umbilical circulation at 18 dp was used to measure unidirectional clearance of 45 Ca across the placenta in maternofetal ( Ca K mf ) and fetoplacental ( Ca K fp ) directions; Ca K fp was < 5% of Ca K mf for all genotypes. At 18 dp, Ca K mf across perfused placenta and intact placenta ( Ca K mf(intact) ) were similar and concordant with net calcium accretion rates in vivo.Ca K mf was significantly raised in NL fetuses compared to WT and HZ littermates. Calcium accretion was significantly elevated in NL fetuses by 19 dp. Placental calbindin-D 9K expression in NL fetuses was marginally enhanced (P < 0.07) but expression of TRPV6/ECaC2 and plasma membrane Ca 2+ -ATPase (PMCA) isoforms 1 and 4 were unaltered. We conclude that PTHrP is an important regulator of fetal calcium homeostasis with its predominant effect being on unidirectional maternofetal transfer, probably mediated by modifying placental calbindin-D 9K expression. In situ perfusion of mouse placenta is a robust methodology for allowing detailed dissection of placental transfer mechanisms in genetically modified mice.