Evidence: Miniature pig (Sus scrofa) nutrition
Source: Europe PMC (Europe PubMed Central) REST search — first-hand peer-reviewed abstract records, pulled 2026-08-01. Queries covered nutrient requirements, diet formulation, supplementation and deficiency for Sus scrofa. The cluster returns 4 representative nutrition studies with abstracts below. Abstract text is verbatim from source; each study is traceable by PMID.
Studies
- PMID 42237168 (2026, Animal microbiome) — Multi-omics elucidates the regulatory mechanisms of tryptophan in gut health of weaned piglets.. Abstract (opening): Tryptophan (Trp), an essential amino acid (AA) implicated in diverse physiological and pathological processes, remains incompletely characterized in its mechanisms regulating intestinal health in weaned piglets. In this study, 27 weaned Bama miniature pigs with highly homogeneous genetic characteristics (6.200 ± 0.242 kg) were randomly divided into three groups and fed a basal diet, a diet supplemented with 0.5-fold Trp, or a diet supplemented with 1.5-fold Trp for 21 days. We used multi-omics approaches to investigate the mechanisms by which Trp regulates intestinal health through dietary interventions with different concentrations. Both Trp-supplemented groups exhibited significantly reduced diarrhea incidence (P = 0.012) and improved intestinal morphology compared to the control group (P < 0.05). While Trp-targeted metabolomics showed no statistically significant alterations, metagenomic analysis revealed Trp-driven microbial remodeling, characterized by increased α-diversity, elevated abundances of Deferribacteres, Turicibacter, Clostridials_Bacteria, and Turicibacter_Sanguinis, alongside decreased Tenericutes and Chryseobacterium. Transcriptome analysis further identified immune-related pathways as central targets of Trp action. Subsequent cytokine quantification confirmed Trp's immunomodulatory effects: pro-inflammatory cytokines (IL-1β, IL-6, IL-17) decreased, while anti-inflammatory IL-10 increased. Collectively, our findings demonstrate that Trp alleviates weaning-associated intestinal dysfunction by reshaping microbial ecosystems and regulating immune homeostasis. *[CC BY — Open Access, verbatim with attribution.]*
Source: https://pubmed.ncbi.nlm.nih.gov/42237168/
- PMID 41897953 (2026, Animals : an open access journal from MDPI) — Intestinal Development in Wuzhishan Pigs at Different Growth Phases: Insights from Microbiome and Metabolomics.. Abstract (opening): Wuzhishan pigs are a typical Chinese indigenous miniature pig breed, with thin skin and high amino acid content in muscle; slow weight gain and long feeding phases limit their value. As the primary digestive and absorptive organ, the intestine is crucial for growth, yet current studies on its development are limited. This study aimed to investigate intestinal physiological differences in Wuzhishan pigs across four phases (pre-weaning: 7, 14 days; weaning: 35, 38, 45 days; fattening: 70, 100 days; maturity: 180, 240 days) by evaluating intestinal morphology, digestive enzyme activity, gut microbiota diversity via 16S rRNA gene sequencing, and metabolite characteristics via metabolomic analysis. Results showed poor intestinal morphology and enzyme activity during weaning, significant ileal and colonic microbial diversity differences across phases, increased beneficial bacteria with age, and enriched opportunistic pathogens (<i>Streptococcus</i>, <i>Romboutsia</i>, <i>Terrisporobacter</i>) during weaning; weaning also had lower lipid metabolites, correlated with decreased <i>Fusobacterium</i>, <i>Lactobacillus</i>, and <i>Muribaculaceae</i>. Fattening enhanced amino acid metabolism, with increased <i>Lactobacillus</i> correlated with higher amino acids and muscle-related metabolites, while maturity increased immune-related metabolites (e.g., pyridoxine) in the vitamin B6 pathway. These results explain delayed rapid weight gain in Wuzhishan pigs and provide a theoretical basis for maintaining intestinal stability and production performance. *[CC BY — Open Access, verbatim with attribution.]*
Source: https://pubmed.ncbi.nlm.nih.gov/41897953/
- PMID 42075046 (2026, Nutrients) — Marine-Derived Chitooligosaccharide Attenuates Obesity and Metabolic Syndrome in Bama Pigs Through LXR-Mediated Cholesterol Metabolism and Gut Microbiota Modulation.. Abstract (opening): <b>Background/Objectives:</b> Chitooligosaccharide (COS) is a marine-derived natural product obtained from shrimp and crab shells. Although its anti-inflammatory and antioxidant activities are documented, its potential effects on obesity and metabolic syndrome remain largely unclear. This study aimed to investigate the efficacy of COST (MW ≈ 1000 Da) against high-fat diet (HFD)-induced obesity and metabolic syndrome in Bama pigs. <b>Methods:</b> Bama pigs were fed a HFD for 12 weeks to establish an obesity model, followed by 12 weeks of oral COST administration. Serum biochemical parameters, tissue indicators, histopathology, and gene/protein expression related to cholesterol metabolism were analyzed. Fecal bile acid (BA) profiles, gut microbiota composition, and short-chain fatty acid (SCFA) levels were also examined. <b>Results:</b> COST treatment significantly attenuated weight gain and improved multiple components of metabolic syndrome, including insulin resistance, dyslipidemia, and inflammation. Mechanistically, COST upregulated intestinal ABCG5/ABCG8 to promote cholesterol excretion, increased ABCA1 expression in intestine and liver to enhance reverse cholesterol transport (RCT), and upregulated hepatic LDL-R to facilitate LDL-C clearance from circulation while modulating hepatic cholesterol synthesis via SREBP2 downregulation and RNF145 upregulation. These transcriptional changes were confirmed at the protein level for LXR, LDL-R, and ABCA1. Additionally, COST decreased fecal secondary BA levels, reshaped gut microbiota composition, and increased SCFA production, with significant correlations among these factors. <b>Conclusions:</b> COST ameliorates protective effects against HFD-induced obesity and metabolic syndrome, potentially through the regulation of cholesterol metabolism and the modulation of the gut microbiota-BA-SCFA network. *[CC BY — Open Access, verbatim with attribution.]*
Source: https://pubmed.ncbi.nlm.nih.gov/42075046/
- PMID 41630470 (2026, Animal models and experimental medicine) — Quantitative proteomics identifies clusterin as a novel biomarker for atherosclerosis.. Abstract (opening): <h4>Background</h4>Atherosclerosis (AS), the leading cause of cardiovascular disease, involves complex molecular mechanisms that remain incompletely understood, particularly in the context of diet-induced vascular lesions.<h4>Methods</h4>We established an AS model in Bama miniature pigs using a high-cholesterol, high-fat diet (HCFD) and performed quantitative proteomic analysis on coronary artery tissues. Key proteins were identified using protein-protein interaction (PPI) network analysis and subsequently validated by histopathological evaluation in porcine and murine coronary arteries. The underlying molecular mechanisms were elucidated using Western blot analysis.<h4>Results</h4>The HCFD successfully induced an atherosclerotic phenotype characterized by significantly elevated serum lipid levels. Proteomic analysis identified 108 differentially expressed proteins (DEPs) between the AS and control groups. From four identified hub proteins, we focused on clusterin (CLU), which was markedly upregulated in atherosclerotic coronary tissues, particularly within endothelial cells (ECs) and smooth muscle cells (SMCs). Mechanistically, CLU upregulation activated the LRP1/AKT signaling pathway, thereby promoting atherogenesis.<h4>Conclusion</h4>Our study reveals that elevated CLU expression accelerates the process of AS by activating the LRP1/AKT pathway. These data elucidate a novel pro-atherogenic role for CLU and establish the CLU/LRP1/AKT axis as a promising therapeutic target for managing AS, particularly in pathologies driven by high-fat diets. *[CC BY — Open Access, verbatim with attribution.]*
Source: https://pubmed.ncbi.nlm.nih.gov/41630470/
Source text: pdf-raw/evidence/europepmc_mini_pig_nutrition_2026-08-01.txt (Europe PMC first-hand abstracts, pulled 2026-08-01).
License & attribution
Mixed licensing per COPYRIGHT_POLICY §3: Open Access (CC BY / CC BY-NC / CC BY-NC-ND) studies are reproduced verbatim with attribution under their specific CC license; non-Open-Access studies are paraphrased as derived fact summaries (numbers and proper nouns preserved, sentences rewritten). Original records:
- https://pubmed.ncbi.nlm.nih.gov/42237168/
- https://pubmed.ncbi.nlm.nih.gov/41897953/
- https://pubmed.ncbi.nlm.nih.gov/42075046/
- https://pubmed.ncbi.nlm.nih.gov/41630470/
Cleaning removal log (2026-08-05, codebuddy)
PMID 42233182 — Clawn miniature pig MASLD MODEL testing human liver progenitor cell therapy — model organism, not pet subject PMID 42245910 — subject is sheep (gene-edited bone research), a different species, not miniature pig PMID 41747715 — entry labeled off-topic: adult pig MODEL articular-cartilage defects, orthopaedic repair not mini-pig nutrition — mis-clustered PMID 41526338 — miniature pig MODEL for human dentin-pulp regeneration — model organism, not pet subject PMID 41997141 — pig MODEL of human radiation-induced liver disease — model organism, not pet subject PMID 42484922 — entry labeled off-topic: wild boar meat-quality bibliometric analysis, not mini-pig nutrition — mis-clustered PMID 42084768 — weaned production piglet feed-additive trial — livestock-production nutrition, not pet mini-pig PMID 41984519 — entry labeled off-topic: swine (piglet) high-net-energy diet growth/liver study, not mini-pig (pet) nutrition — mis-clustered