理学最新文献

Zinc, an essential trace element, plays a pivotal role in maintaining animal health and physiological functions. This review comprehensively examines zinc metabolism-including absorption dynamics across species (poultry, ruminants, and non-ruminants), transport mechanisms, storage in tissues, e.g., the liver, and excretion pathways-and its multifaceted effects on animal health. Zinc critically regulates aspects of growth and development, particularly bone formation, as its deficiency induces skeletal deformities in young animals. It modulates immune function through zinc finger proteins, influencing immune organ integrity, lymphocyte proliferation, and cytokine expression. Reproductive performance is significantly affected by zinc, with its deficiency causing impaired spermatogenesis; delayed sexual maturity in males; and reduced litter size, embryonic survival, and placental function in females. At the molecular level, zinc regulates the activity of enzymes (e.g., SOD), signaling pathways (MAPK, NF-κB), and transcription factors (MTF-1, Sp1) to maintain homeostasis. Both zinc deficiency (due to dietary insufficiency, malabsorption, or physiological stress) and zinc excess (from environmental pollution or feed oversupplementation) adversely affect health, disrupting mineral balance, enzyme function, and gut microbiota. In animal production, inorganic (zinc oxide, zinc sulfate) and organic (zinc methionine) sources of zinc increase growth, immunity, and productivity, although sustainable strategies are needed to mitigate environmental risks. Future research should focus on novel zinc formulations, precision nutrition, and interactions with gut microbiota to optimize livestock health and sustainable husbandry.

Background: Weaning-induced diarrhoea and growth retardation in piglets are associated with impaired intestinal barrier function and decreased levels of colonic short-chain fatty acids (SCFAs). Although SCFA supplementation has been proposed to mitigate these issues, the efficacy and optimal dosage of sodium isobutyrate remain unclear.

Results: We investigated the effects of sodium isobutyrate supplementation (500, 1,000, 2,000, and 4,000 mg/kg diet) on weaned piglets (Duroc × Landrace × Yorkshire, 28 d of age; n = 8). After a 28-d feeding trial, supplementation at 500-2,000 mg/kg significantly improved average daily gain and feed efficiency and reduced diarrhoea frequency, with maximal benefits observed at 1,000 mg/kg (P < 0.0001). Additionally, 500-1,000 mg/kg sodium isobutyrate supplementation increased the apparent digestibility of crude protein, organic matter, and crude fibre (P < 0.05). Serum biochemical parameters were unaffected, although secretory immunoglobulin A (SIgA) levels significantly increased upon supplementation with 500-1,000 mg/kg (P < 0.05). 16S rRNA gene sequencing indicated that sodium isobutyrate increased the abundance of beneficial colonic microbiota. The 1,000 mg/kg group presented the most pronounced effect, with a significant increase of the relative abundance of Prevotella and the greatest improvement in SCFA concentrations (P < 0.05). Metabolomics revealed elevated levels of colonic indole-3-lactic acid and 3-hydroxybutyrate upon supplementation with 1,000 mg/kg (P < 0.05). Transcriptomic analyses indicated activation of protein digestion and absorption pathways, and PI3K-Akt signalling, marked by TSG-6 upregulation and the suppression of ISG15 and DDIT4 expression (P < 0.05). Supplementation with 1,000 mg/kg was associated with improved intestinal barrier-related markers, including reduced serum D-lactate, diamine oxidase, and lipopolysaccharide levels, increased tight junction protein expression; activation of G protein-coupled receptors; and inhibition of TLR4/MyD88/NF-κB signalling (P < 0.05), suggesting enhanced barrier function.

Conclusions: In conclusion, dietary supplementation with 1,000 mg/kg sodium isobutyrate was associated with improved intestinal morphology, reduced serum permeability, increased expression of tight junction proteins, and enhanced immune function in weaned piglets, suggesting enhanced colonic barrier function and providing dosage guidance and mechanistic insights for future applications.

Background: Our previous study demonstrated that dietary supplementation of Bacillus subtilis enhanced growth performance and intestinal integrity in weaned pigs challenged with enterotoxigenic Escherichia coli (ETEC). Therefore, this study aimed to explore the impact of Bacillus subtilis on gut health and its role in modulating host-microbe interactions in post-weaning pigs.

Results: ETEC infection disrupted key metabolic pathways in distal colon, including glutathione, beta-alanine, and pyrimidine metabolism, indicating increased oxidative stress, impaired nucleotide balance, and amino acid catabolic stress. Bacillus subtilis supplementation induced distinct metabolomic and microbiome profiles in colon digesta of weaned pigs challenged with ETEC. Bacillus subtilis-treated pigs under ETEC challenge exhibited significant enrichment in amino acid- and energy-related pathways such as arginine biosynthesis, phenylalanine metabolism, pantothenate and CoA biosynthesis. ETEC infection induced microbial dysbiosis in the distal colon, resulting in decrease (P < 0.05) in abundance of Streptococcaceae and Enterobacteriaceae compared to healthy controls. Bacillus subtilis supplementation mitigated the ETEC-induced disruptions by increasing the relative abundance of beneficial bacterial families, including Lachnospiraceae and Bacteroidaceae.

Conclusion: Supplementation of Bacillus subtilis improves intestinal health and resilience against ETEC challenge by mitigating infection-induced metabolic disruptions and gut dysbiosis in weaned pigs.

Background: Fatty liver syndrome is a prevalent metabolic disorder in transition dairy cows, characterized by excessive hepatic lipid accumulation that impairs liver function and leads to systemic metabolic disturbances. Docosahexaenoic acid (DHA), a prominent n-3 polyunsaturated fatty acid (PUFA), not only exhibits anti-inflammatory and anti-oxidative properties, but also holds potential in ameliorating lipid metabolism. This study integrated in vitro bovine primary hepatocyte models and in vivo dairy cow trials to investigate the regulatory effects of DHA on hepatic lipid deposition.

Results: In vitro, 40 μmol/L DHA significantly reduced triglyceride (TAG) accumulation in steatotic hepatocytes by downregulating genes involved in fatty acid transport (FABP-1, CD36) and lipogenesis (DGAT2, FAS, SREBP-1C), while upregulating markers of lipolysis (CGI-58, ATGL) and fatty acid oxidation (ACADL, CPT1A, CPT2). Transmission electron microscopy (TEM) confirmed DHA-mediated restoration of mitochondrial ultrastructure and enhanced lipid droplet (LD)-mitochondria interactions. In vivo, dietary rumen-protected DHA (180 g/d) supplementation reduced hepatic lipid deposition, improved liver function (evidenced by decreased total bilirubin and alanine aminotransferase), reduced oxidative stress and inflammation (suppressed malondialdehyde, glutathione peroxidase, and lipopolysaccharide), coincided with relieving insulin resistance (reduced insulin and glucose, as well increased adiponectin) in dairy cows with fatty liver. These improvements may be attributed to increased expression of TOMM20 and MtCo-1, promoting mitochondrial biogenesis and β-oxidation, along with an elevated plasma n-3/n-6 ratio.

Conclusions: Collectively, these findings suggest that DHA supplementation represents a promising nutritional strategy for preventing spontaneous fatty liver in transition dairy cows by enhancing hepatic lipid clearance and restoring metabolic homeostasis.

The primary role of the gastrointestinal tract in broiler chickens is nutrient assimilation, with transporter proteins facilitating the uptake of amino acids, peptides, monosaccharides, fatty acids, and minerals across the intestinal epithelium. Among these nutrient transporters, members of the solute carrier family are particularly important, and gene expression analyses targeting these transporters have provided informative insights into how birds adapt to diverse dietary, environmental, and physiological challenges to maintain nutrient homeostasis. These transporters are expressed either at the brush border membrane, where they facilitate the absorption of nutrients from the gut lumen into enterocytes, or at the basolateral membrane, where they mediate the transfer of nutrients from the enterocytes into the bloodstream. The expression of these transporters is influenced by a range of factors, including bird age, sex, intestinal segment, dietary substrate availability and source, as well as external stressors such as heat stress and pathogen exposure. While upregulation of transporter genes often suggests an enhanced capacity for nutrient uptake, it does not always correlate with improved growth performance, due to compensatory physiological responses and fluctuations in nutrient bioavailability. Understanding the regulation and functional dynamics of nutrient transporters presents valuable opportunities to develop targeted dietary and management strategies aimed at optimizing nutrient utilization and improving bird performance. This review summarizes current knowledge on the classification, function, and regulation of key nutrient transporters in broilers, highlights factors influencing their expression, and explores their implications for nutrition and production efficiency.

Skeletal muscle accounts for approximately 40% of body mass and 50%-75% of whole-body protein, playing a central role in meat production and quality. Efficient protein synthesis in skeletal muscle relies on an adequate supply of nutrient substrates and a balanced amino acid profile. Branched-chain amino acids (BCAA), including leucine (Leu), isoleucine (Ile), and valine (Val), are the most abundant essential amino acids in skeletal muscle and contribute to both protein synthesis and oxidative energy production. Additionally, BCAA function as signaling molecules that regulate gene expression and protein phosphorylation cascades, which significantly influence physiological processes, such as protein synthesis and degradation, glucose and lipid metabolism, and cell apoptosis and autophagy. These processes are primarily mediated through the PI3K/AKT/AMPK/mTOR signaling pathways. This review summarizes BCAA transporters and catabolic metabolism, their role as signaling molecules in regulating protein metabolism and glucose and lipid equilibrium, and applications in animal production. These findings offer both theoretical insights and practical guidelines for the precise regulation of feed efficiency and production performance through tailored dietary BCAA supplementations.

Background: Low dietary energy levels can disrupt energy balance, causing metabolic disorders, particularly those involving in hepatic lipid metabolism. Betaine (BET), an important methyl donor, has demonstrated protective effects against liver diseases. However, its effects on hepatic lipid metabolism in pigs fed a low-net energy (NE) diet and the underlying mechanisms remain unclear. Thirty-two pigs (85.52 ± 2.27 kg) were randomly assigned to four treatments: N-NE group (normal NE diet, 2,475 kcal/kg NE), N-NEB group (normal NE diet + 1,500 mg/kg BET, 2,475 kcal/kg NE), R100-NE group (low-NE diet, 2,375 kcal/kg NE), and R100-NEB group (low-NE diet + 1,500 mg/kg BET, 2,375 kcal/kg NE). The experiment lasted 35 d.

Results: There was no significant difference in growth performance among the groups (P > 0.05). Reducing dietary NE levels caused liver dysfunction and increased total glyceride concentration, accompanied by lipid metabolism disorders. BET supplementation in a low-NE diet exhibited hepatoprotective roles, as evidenced by increased TP concentration and reduced ALT level in serum (P < 0.05), as well as decreased fat content, adipocyte size, and total glyceride concentration in the liver (P < 0.05). Meanwhile, dietary BET alleviated low-NE diet-induced hepatic lipid metabolism disorder by downregulating mRNA expressions of genes related to fatty acid transport (FABP3 and CD36) and lipogenesis (SREBP1c and FASN), while upregulating mRNA expressions involved in lipolysis (CPT1 and HSL) (P < 0.05). Furthermore, dietary BET increased serum SAM concentration and the SAM/SAH ratio in pigs fed low-NE diets (P < 0.05), thereby providing sufficient methyl groups through regulating the activities of enzymes participated in BET metabolism. Mechanistically, BET increased m⁶A modification level and regulated mRNA and protein expressions of m⁶A modified proteins including METTL3, METTL14, WTAP, YTHDF1, and ALKBH5. Correlation analysis showed a significant association between m⁶A RNA methylation and hepatic lipid metabolism, suggesting that m⁶A RNA methylation may play a critical role in mediating hepatic lipid metabolism.

Conclusions: Dietary BET supplementation in low-NE diets alleviated hepatic lipid metabolism disorders by regulating m⁶A RNA methylation, ultimately reducing hepatic lipid accumulation in finishing pigs.