Branched chain amino acids (BCAAs) are essential amino acids involved in regulation of feed intake. The function of BCAAs on the central nervous system has been extensively studied, but effects of BCAAs on secretion of gut satiety hormones and their underlying mechanisms are largely unknown. In this study, we evaluated the distribution of gut hormones and amino acid receptors in the porcine GI tract and found cholecystokinin (CCK) and taste dimeric receptor type 1 member 1/3 (T1R1/T1R3) were predominantly expressed in the jejunum and functionally interrelated. We further evaluated the effects of L-leucine, L-isoleucine, L-valine, and BCAAs on CCK and T1R1/T1R3 expression in porcine jejunum tissue. Our data demonstrated that stimulation of porcine jejunum tissue with 10 mM L-leucine, L-isoleucine or BCAAs mix (L-leucine : L-isoleucine : L-valine = 1 : 0.51 : 0.63) for 2 hours significantly increased mRNA expression and protein abundance of T1R1/T1R3 and secretion of CCK (P < 0.05). However, the L-valine treatment only increased the mRNA and protein abundance of T1R1 and T1R3 (P < 0.05), but not CCK secretion (P > 0.10). L-Leucine-, L-isoleucine- or BCAAs mix-induced CCK secretion was significantly decreased after tissues were pretreated with lactisole, a T1R1/T1R3 inhibitor (P < 0.05). Furthermore, the increased mRNA and protein abundance of T1R1/T1R3 were also largely attenuated by blocking T1R1/T1R3 with lactisole (P < 0.05). L-Leucine, L-isoleucine and BCAAs mix appeared to induce the gut satiety hormone CCK secretion through jejunal T1R1/T1R3. These results indicate over-supplementation with BCAAs in the diet might decrease food intake in swine and humans through gastrointestinal feedback.

Maternal nutrition plays a vital role in fetal development, early development of neonates, and lactation and regulates the lifetime productivity of offspring. During pregnancy, maternal nutrition alters expression of the fetal genome and the development of tissues and organs via fetal programming. After parturition, maternal nutrition continues to regulate growth and development of piglets through maternal milk, which contains carbohydrates, lipids, proteins and oligosaccharides. Thus, deficiencies in maternal nutrition are detrimental to development of piglets, which can lead to inefficient growth and decreased carcass merit. Protein is an important nutritional component for sows, which not only functions in muscle development, but also plays a vital role in embryonic and neonatal development and lactation. Although effects of maternal undernutrition on neonatal development have been widely studied in sows, the function of different maternal dietary protein levels on fetal development, neonatal growth and lactation performance of sows is largely unknown. Determination of the effects and underlying mechanisms of maternal dietary protein levels on development of piglets is vital to the pork industry. Therefore, we summarized recent reports regarding mechanisms of effects of maternal protein levels on regulation of conceptus growth and early postnatal development though uterine fetal programming and lactation in swine.

Chlorogenic acid (CGA) is a natural polyphenol with potent antioxidant and anti-inflammatory activities. However, the exact role of it in regulating intestinal health under oxidative stress is not fully understood. This study aims to investigate the effects of dietary CGA supplementation on the intestinal health of weaned piglets under oxidative stress, and to explore its regulatory mechanism. Twenty-four piglets were randomly divided into two groups and fed either a basal diet (CON) or a basal diet supplemented with 200 mg/kg CGA (CGA). CGA reduced the diarrhea rate, increased the villus height in the jejunum, and decreased the crypt depth in the duodenum, jejunum, and ileum of the weaned piglets (p < 0.05). Moreover, CGA increased the protein abundance of Claudin-1, Occludin, and zonula occludens (ZO)-1 in the jejunum and ileum (p < 0.05). In addition, CGA increased the mRNA expression of pBD2 in the jejunum, and pBD1 and pBD2 in the ileum (p < 0.05). The results of 16S rRNA sequencing showed that CGA altered the ileal microbiota composition and increased the relative abundance of Lactobacillus reuteri and Lactobacillus pontis (p < 0.05). Consistently, the findings suggested that the enhancement of the intestinal barrier in piglets was associated with increased concentrations of T-AOC, IL-22, and sIgA in the serum and T-AOC, T-SOD, and sIgA in the jejunum, as well as T-AOC and CAT in the ileum caused by CGA (p < 0.05). Meanwhile, CGA decreased the concentrations of MDA, IL-1β, IL-6, and TNF-α in the serum and jejunum and IL-1β and IL-6 in the ileum (p < 0.05). Importantly, this study found that CGA alleviated intestinal inflammation and oxidative stress in the piglets by inhibiting the TLR4/NF-κB signaling pathway and activating the Nrf2 signaling pathway. These findings showed that CGA enhances the intestinal health of weaned piglets by inhibiting the TLR4/NF-κB pathway and activating the Nrf2 pathway.

Background: Fat percentage and distribution in pigs are associated with their productive efficiency and meat quality. Dietary branched-chain amino acids (BCAA) regulate fat metabolism in weanling piglets with unknown mechanism. It is reported that N6-methyl-adenosine (m⁶A) is involved in fat metabolism in mice. The current study was designed to investigate the relationship between dietary branched-chain amino acids and fat metabolism through N6-methyl-adenosine (m⁶A) in weanling piglets. Methods: A total of 18 healthy crossbred weaned piglets (Duroc × Landrace × Large White, 10.45 ± 0.41 kg) were divided into 3 treatments and were fed the low BCAA dose diet (L-BCAA), the normal dose BCAA diet (N-BCAA), or the high dose BCAA (H-BCAA) diet for 3 weeks. Results: Our results show that compared with the N-BCAA group, the L-BCAA group had higher concentration of serum leptin (P < 0.05), while the H-BCAA group had lower concentration of serum adiponectin (P < 0.05). Fatty acid synthesis in pigs from the H-BCAA group was lower than those from the N-BCAA group with the down-regulation of lipogenic genes (ACACA, FASN, PPAR-r, SREBP-1c in ventral and dorsal fat, SREBP-1c in liver) and up-regulation of lipolysis genes (HSL, ATGL, CPT-1A, FABP4 in ventral fat, HSL in liver) (P < 0.05). Similarly, fatty acid synthesis in pigs from the L-BCAA group was also lower than those from the N-BCAA group with the decrease of lipogenic genes (ACACA in ventral, ACACA and FASN in dorsal fat, ACACA, FASN, SREBP-1c in liver) and the increase of lipolysis genes (ATGL, CPT-1A CD36, FABP4 in ventral fat and HSL, ATGL, CPT-1A in dorsal fat, CPT-1A) (P < 0.05). Feeding H-BCAA diet significantly reduced total m⁶A levels in ventral and dorsal fat and liver tissues (P < 0.05). The decrease of total m⁶A is associated with down-regulation of METTL3, METTL14 and FTO in dorsal fat and METTL3 and FTO in liver (P < 0.05). Decreased m⁶A modification of ACACA and FASN in ventral and dorsal adipose tissues was observed in pig fed with excessive BCAA. Conclusion: These results suggest that insufficient or excessive BCAA decreased the fat deposition by increasing lipolysis and deceasing lipogenesis in adipose and liver tissues. Dietary excessive BCAA might regulate the process of lipid metabolism partly through the m⁶A RNA methylation.

Glyceryl butyrate attenuated the immune-inflammatory response in piglets challenged with enterotoxigenic Escherichia coli (ETEC) by inhibiting the NF-κB/MAPK pathways and modulating the gut microbiota, and thus improved piglet intestinal health.