Maternal diets during pregnancy and lactation are key determinants that regulate the development of metabolic syndrome (MetS) in offspring. l-malic acid (MA) was previously reported to improve antioxidant capacity and aerobic metabolism. However, the effects of maternal MA consumption on the metabolic features of offspring remain largely unexplored. Herein, through pig models consuming MA-enriched diets during late pregnancy and lactation, we found that maternal MA consumption potentiated the anti-inflammatory and antioxidant capacity of sows, thereby improving their reproductive performance and the growth performance of piglets. Maternal MA consumption also induced a transition of slow-twitch to fast-twitch fibers in the early life of offspring. Along with muscle growth and fiber-type transition, insulin sensitivity and glucose metabolism, including aerobic metabolism and glycolysis, were improved in the skeletal muscle of offspring. An untargeted metabolomic analysis further revealed the contribution of modified amino acid metabolism to the improved aerobic metabolism. Mechanistically, maternal MA consumption remodeled colonic microbiota of their offspring. Briefly, the abundance of Colidextribacter, Romboutsia, and Family_XIII_AD3011_group increased, which were positively associated with the antioxidant capacity and glucose metabolism of skeletal muscles. A decreased abundance of Prevotella, Blautia, Prevotellaceae_NK3B31_group, and Collinsella was also detected, which were involved in less insulin sensitivity. Notably, milk metabolites, such as ascorbic acid (AA) and granisetron (GS), were found as key effectors regulating the gut microbiota composition of piglets. The properties of AA and GS in alleviating insulin resistance, inflammation, and oxidative stress were further verified through mice treated with high-fat diets. Overall, this study revealed that maternal MA consumption could modulate the inflammatory response, antioxidant capacity, and glucose metabolism by regulating the gut microbiota of offspring through the vertical transmission of milk metabolites. These findings suggest the potential of MA in the prevention and treatment of MetS in early life.

Proinflammatory cytokines play a key role in the pathophysiology of muscle atrophy. In addition, n3 polyunsaturated fatty acids (PUFAs) exert an inhi

The quality of pork determines consumers' purchase intention, which directly affects the economic value of pork. Minimizing the proportion of inferior pork and producing high quality pork are the ultimate goals of the pig industry. Muscle energy metabolism, serving as a regulative hub in organism energy expenditure and storage as a fat deposit, is compatible with myofiber type composition, affecting meat color, intramuscular fat content, tenderness, pH values and drip loss. Increasing data illustrate that dietary nutrients and bioactive ingredients affect muscle energy metabolism, white adipose browning and fat distribution, and myofiber type composition in humans, and rodents. Recently, some studies have shown that modulating muscle energy metabolism and lipid accumulation through nutritional approaches could effectively improve meat quality. This article reviews the progress and development in this field, and specifically discusses the impacts of dietary supply of amino acids, lipids, and gut microbiota as well as maternal nutrition on skeletal muscle energy metabolism, lipid accumulation and meat quality of pigs, so as to provide comprehensive overview with respect to effective avenues for improving meat quality.

Pork produced by outdoor-reared pigs raised mostly on alfalfa pastures attracts increasing population of consumer from most of the world. In China, pigs were raised with alfalfa-containing diets to seek for good quality pork. However, the influence of dietary alfalfa involving high level of insoluble dietary fiber (IDF) on pig intestinal luminal microbiota composition remains unclear. The objective of this study was to investigate the effects of alfalfa on luminal microbiota and short chain fatty acids (SCFA) production, and gene expressions involved in SCFA sensing, transporting and absorbing in pig caecal mucosa. Twenty-four growing pigs were randomly allotted to four diets containing 0%, 5%, 10% and 15% alfalfa meal for a 28-d experiment. Ingestion of alfalfa meal-contained diets significantly increased the ratio of body weight gain to feed consumption. Illumina MiSeq sequencing of the V3 region of the 16S rRNA genes showed that alfalfa-containing diet significantly decreased the relative abundance of genera Turicibacter, Acidiphilium, Paracoccus, Propionibacterium, Corynebacterium, Pseudomonas, Acinetobacter, and Staphylococcus, and increased the relative abundance of genera Lachnospira, Marvinbryantia, and Desulfovibrio in the caecal digesta. Butyrate concentration was significantly increased in the hindgut by the supplementation of alfalfa meal in diets. The mRNA gene expressions of FFAR3, SMCT1, MCT1, PYY, and GCG were significantly increased in the caecal mucosa of pigs fed alfalfa meal. Our results suggested that alfalfa-containing diet has exerted significant impacts on caecal microbiota composition, butyrate concentration and significantly upregulated mRNA expression of host caecal mucosal genes involved in SCFA sensing and absorption as well as regulation of satiety.

Background: The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Methods: Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Results: Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P < 0.05). The spleen index did not change, but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased, the red pulp increased, and splenocyte apoptosis occurred in the Se deficient group. Se deficiency decreased the Se concentration and selenoprotein expression in the spleen (P < 0.05), blocked the glutathione and thioredoxin antioxidant systems, and led to redox imbalance. Se deficiency activated the NF-κB and HIF-1α transcription factors, thus increasing pro-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-17, and TNF-α), decreasing anti-inflammatory cytokines (IL-10, IL-13, and TGF-β) and increasing expression of the downstream genes COX-2 and iNOS (P < 0.05), which in turn induced inflammation. In addition, Se-deficiency induced apoptosis through the mitochondrial pathway, upregulated apoptotic genes (Caspase3, Caspase8, and Bak), and downregulated antiapoptotic genes (Bcl-2) (P < 0.05) at the mRNA level, thus verifying the results of TUNEL staining. Conclusions: These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins, oxidative stress, inflammation and apoptosis.