{"topic_id":"evidence_exotic_mini_pig_nutrition","category":"evidence","context":"---\ntopic_id: evidence_exotic_mini_pig_nutrition\ncategory: evidence\ntitle: \"Evidence cluster — Miniature pig (Sus scrofa) nutrition (peer-reviewed, Europe PMC)\"\nlang: en\nsource: \"Europe PMC (Europe PubMed Central) REST search, first-hand peer-reviewed abstracts, pulled 2026-08-01\"\nsource_file: pdf-raw/evidence/europepmc_mini_pig_nutrition_2026-08-01.txt\ndate_parsed: 2026-08-01\ntokens_estimated: 5627\nverification:\n  method: substring_match\n  claims: 12\n  passed: 12\n  date: 2026-08-01\nsource_document: \"Peer-reviewed Miniature pig nutrition literature (Europe PMC, first-hand abstracts)\"\ncitation:\n  authority: \"Europe PMC\"\n  title: \"Evidence cluster — Miniature pig (Sus scrofa) nutrition (peer-reviewed, Europe PMC)\"\n  url: \"https://www.ebi.ac.uk/europepmc/\"\n  retrieved: \"2026-08-01\"\n  doc_type: \"first-hand abstracts (Europe PMC REST)\"\n  needs_review: false\n---\n\n# Evidence: Miniature pig (Sus scrofa) nutrition\n\nSource: Europe PMC (Europe PubMed Central) REST search — first-hand peer-reviewed abstract records, pulled 2026-08-01.\nQueries covered nutrient requirements, diet formulation, supplementation and deficiency for Sus scrofa.\nThe cluster returns **12** representative nutrition studies with abstracts below. Abstract text is verbatim from source; each study is traceable by PMID.\n\n## Studies\n- **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.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42237168/\n- **PMID 42233182 (2026, Cell transplantation)** — Autologous chemically induced liver progenitor cell transplantation ameliorates steatosis and fibrosis in a preclinical miniature pig model of metabolic dysfunction-associated fatty liver disease: A pilot study.. Abstract (opening): Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disorder and can progress to steatohepatitis and fibrosis; although approved pharmacotherapies for metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis remain limited. Autologous chemically induced liver progenitor (CLiP) cells, generated from mature hepatocytes without genetic modification, have shown therapeutic promise in rodents, but their efficacy has not been tested in large animals. Six female Clawn miniature pigs (15-42 kg) were fed a high-fat, high-cholesterol diet to induce MASLD with biopsy-proven fibrosis (Brunt stage ≥1). Animals were assigned to CLiP transplantation (<i>n</i> = 3) or saline control (<i>n</i> = 3). Autologous CLiPs (5 × 10<sup>7</sup>) were generated from laparoscopically resected liver wedges, expanded <i>ex vivo</i>, and infused intraportally. Safety was assessed by monitoring, liver function tests, and lipid profiles. Efficacy was evaluated 1 month later by blinded histology and immunohistochemistry. CLiP transplantation was feasible and well tolerated. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) showed minimal changes in both groups, but total cholesterol and triglycerides decreased in treated pigs and increased in controls. Histologically, two of three CLiP-treated livers regressed from Brunt stage 1 to 0, with resolution of steatosis and reduced stellate cell activation, whereas controls showed no regression. These findings support CLiP therapy as a regenerative option for MASLD.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42233182/\n- **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.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41897953/\n- **PMID 42245910 (2026, JBMR plus)** — From farm to lab: gene-edited sheep transforming bone research.. Abstract (opening): For more than half a century, mice have been the workhorse of biomedical research. Their small size, rapid reproduction, and well-characterized genetics make them ideal disease models, and genome editing has enabled transgenic, knock-out, and knock-in lines that mimic numerous human conditions. These advances transformed modern biology, yielding fundamental insights into cancer, metabolism, immunity, and more. Their strengths notwithstanding, mouse models have important limitations, as biology does not scale neatly across species. Differences in physiology, size, and metabolism can obscure-or even distort-experimental outcomes. Nowhere is this clearer than in musculoskeletal research. Human bones are dynamic tissues that undergo Haversian remodeling, whereas mice exhibit limited Haversian remodeling and display distinct temporal growth trajectories. Moreover, mice have monophyodont dentition and craniofacial development diverges in ways that impact maxillofacial studies, and aging timelines differ. These differences limit our ability to understand human bone disorders from murine models alone. Biotechnology offers a new path forward: advances in genome sequencing, assembly and molecular engineering enable precise DNA editing in larger domesticated species-sheep, goats, and pigs-whose skeletal size, biomechanics, growth patterns, and remodeling dynamics more closely mirror humans. By introducing targeted, patient-relevant mutations, large-animal models can replicate mechanisms difficult to capture in mice and support longitudinal, clinically-relevant phenotyping-imaging, histomorphometry, serum biomarkers, and functional testing-in a translatable human-like context. The implications are profound. Large-animal models can validate disease pathways, refine biomarkers, and evaluate drugs, biologics, and implants, potentially improving treatment strategies and reducing clinical failures and costs. This shift does not diminish the value of mice, whose genetic tractability and cost-effectiveness ensure a central and continued important role in discovery. Rather, it adds a complementary strategy: expand to gene-edited large-animal models when human skeletal-like biology matters and where mice fall short, thereby bridging the gap between fundamental research and clinical reality.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42245910/\n- **PMID 41747715 (2026, Cartilage)** — Critical Size Defect in Adult Articular Cartilage: A Preclinical Study.. Abstract (opening): ObjectiveLesions of adult articular cartilage occur due to trauma or disease, such as osteoarthritis. If they do not penetrate the subchondral bone, they are called partial-thickness defects (PTDs), which are believed not to heal. However, some reports indicate that minor PTDs can be repaired. We hypothesize that a critical-size PTD exists below which spontaneous healing occurs.Design/MethodsIn an adult pig model, we created PTDs of minimal width (a scalpel cut) and systematically increased their width up to 0.5 mm. Defect analyses were conducted at 1 and 3 months post-surgery using light microscopy and histomorphometry.ResultsNone of the defects healed by repair cartilage; therefore, all PTDs are of a critical size. Surprisingly, a critical defect-size range was identified where significant mesenchymal tissue (MT) formation occurs, specifically in defects measuring 50-100 μm in width. The presence of this MT was limited to a 1-month time window. Furthermore, physiological joint loading during the postsurgical phase was associated with substantial structural tissue deformation, often leading to an overlapping of the side walls of the smallest defects. This results in a pseudo-covering of the defect void, which may thus be invisible when observed from above.ConclusionsThe main novel finding of this study is that there is no critical width below which PTDs undergo repair.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41747715/\n- **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.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42075046/\n- **PMID 41526338 (2026, International journal of oral science)** — Wnt3a promotes in situ dentin formation through NKD1-MSX1 axis-mediated odontogenic differentiation of dental pulp stem cells.. Abstract (opening): The functional regeneration of the dentin-pulp complex is pivotal for tooth preservation, yet the molecular mechanisms governing odontoblast differentiation remain poorly understood. In the current study, we revealed a distinct NKD1<sup>+</sup> subpopulation exhibiting secretory odontoblast characteristics, which was specifically induced in dental pulp stem cells (DPSCs) by Wnt3a, but not by Wnt5a or Wnt10a through single-cell transcriptomic profiling. We then found that the NKD1<sup>+</sup> subpopulation was functional conservation, which were consistently identified in the odontoblast layers of developing tooth germs in both murine and miniature pig models, as well as within the apical open area in human molars. This conserved spatial distribution and co-localization with DSPP strongly indicates that NKD1<sup>+</sup> cells were active dentin-secreting odontoblasts. Analysis of gene regulatory networks using SCENIC identified MSX1 as a key transcription factor regulating the specification of NKD1<sup>+</sup> lineage. Mechanistically, Wnt3a orchestrates a tripartite cascade: upregulating NKD1/MSX1 expression, triggering NKD1 membrane detachment, and facilitating direct NKD1-MSX1 interaction to promote MSX1 nuclear translocation. CUT&Tag analysis demonstrated MSX1 occupancy at promoters of odontogenic regulators, establishing its necessity for odontogenic gene activation. Murine pulp exposure models validated that Wnt3a-activated NKD1-MSX1 signaling significantly enhances reparative dentin formation. This study delineates an evolutionarily conserved Wnt3a-NKD1-MSX1 axis that resolves stem cell heterogeneity into functional odontoblast commitment, providing both mechanistic insights into dentin-pulp regeneration and a foundation for targeted regenerative therapies.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41526338/\n- **PMID 41997141 (2026, Cell reports. Medicine)** — A pig model of human radiation-induced veno-occlusive liver disease reveals ferroptosis as a therapeutic target.. Abstract (opening): Radiation-induced liver disease (RILD) poses a major clinical challenge in radiotherapy, transplantation preconditioning, or radiation accidents, yet its pathogenesis is poorly understood due to limited animal models. Here, we establish a translational pig model recapitulating human RILD pathology within 4 weeks post-40 Gy irradiation, featuring veno-occlusive disease (VOD) and centrilobular necrosis. Single-cell atlas analyses identify ferroptosis as a key driver of hepatocyte death during RILD initiation. Ferroptosis inhibition with liproxstatin-1 (Lip-1) not only prevents RILD progression but also reverses histological damage and restores liver function. Mechanistically, Lip-1 treatment restores dysregulated gene expression profiles, particularly associated with hepatocyte ferroptosis, while stimulating hepatic regeneration via coordinated proliferation of hepatocytes and endothelial cells. Our findings establish ferroptosis inhibition as a therapeutic strategy for RILD, demonstrating its dual role in cytoprotection and regeneration. This large animal model provides a robust platform to optimize radiotherapy regimens, improve transplant conditioning, and develop targeted radioprotectants.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41997141/\n- **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.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41630470/\n- **PMID 42484922 (2026, Food science of animal resources)** — Wild boar (Sus scrofa) meat quality research at the crossroads of genetics and nutrition: a global bibliometric mapping.. Abstract (opening): This study provides a comprehensive bibliometric analysis of global research on wild boar (Sus scrofa) meat quality and related attributes, including carcass traits, fatty acid composition, and nutritional characteristics. A total of 423 articles indexed in the Web of Science Core Collection were retrieved and analyzed using RStudio with the Bibliometrix package, complemented by VOSviewer for network visualization. The results indicate a marked increase in scientific production, reflecting growing interest in both genetic and quality-related aspects of wild boar meat. Leading journals such as Journal of Animal Science and Meat Science dominate the field in terms of productivity and citation impact, highlighting the strong linkage between animal genetics and meat science. Author and country collaboration networks reveal the presence of core research groups, primarily concentrated in Europe, with increasing international cooperation. Keyword co-occurrence and thematic evolution analyses identify three principal research directions: (i) genetic improvement and production traits, (ii) molecular mechanisms and genome-wide association studies, and (iii) meat quality and lipid composition. Overlay and thematic evolution analyses reveal a transition from traditional studies on carcass and growth traits toward genomic approaches and nutritional evaluation in recent years. Multiple Correspondence Analysis (MCA) further confirms the coexistence of production genetics, molecular biology, and meat quality as the field's main conceptual pillars. This study covers the gap of literature by summarizing research output on this individual topic. Overall, the presented work clarifies the intellectual structure, thematic development, and emerging trends in wild boar meat research, providing a valuable reference framework for future investigations integrating genomics, meat science, and nutritional evaluation.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42484922/\n- **PMID 42084768 (2026, Tropical animal health and production)** — Effects of a multi-nutrient feed additive on the growth performance, gut health, and antioxidant status of weaned piglets.. Abstract (opening): Weaning stress commonly leads to impaired intestinal function, diarrhoea, and growth retardation in piglets. As restrictions on antibiotic use in animal feed continue to increase, practical nutritional alternatives are urgently needed to support post-weaning health and performance. This study evaluated the effects of Grosol®Plus, a multi-nutrient feed additive containing vitamins, amino acids, and isomaltooligosaccharides, on growth performance, intestinal health, oxidative status, and selected microbial indicators in weaned piglets. A total of 100 weaned piglets were randomly assigned to a control group (basal diet) or a treatment group (basal diet + 0.1% Grosol®Plus) for a 45-day trial. Each group consisted of five pens, with ten piglets per pen. Body weight and feed intake were recorded throughout the experiment. On days 7 and 14 post-weaning, 12 piglets per group were selected for blood and fecal sampling to determine biochemical parameters and related molecular indices. Growth performance was analyzed using pen-based data, whereas biochemical indices were analyzed using individual piglet data. The results showed that Grosol®Plus supplementation tended to increase average daily gain during days 15–45 post-weaning (P = 0.10) and final body weight (P = 0.09). It also reduced diarrhoea incidence during days 8–14 (P = 0.06) and significantly reduced diarrhoea incidence during days 15–45 (P < 0.01). At the molecular level, the treatment group exhibited higher fecal mRNA expression of the tight junction proteins ZO-1 and occludin on days 7 and 14, along with increased TGF-β expression, whereas pro-inflammatory markers such as IL-1β and lipocalin-2 showed decreasing trends. On day 14 post-weaning, the fecal abundance of Escherichia coli was significantly lower in the treatment group (P < 0.01). Meanwhile, plasma antioxidant indicators (T-AOC, GSH-Px, and SOD) increased significantly, whereas MDA decreased. Collectively, dietary supplementation with Grosol®Plus may alleviate weaning stress by enhancing intestinal barrier function, attenuating inflammation and oxidative stress, and promoting gut microbial balance, thereby improving piglet health and growth under antibiotic-free conditions. This study provides a promising nutritional intervention strategy to reduce post-weaning losses and decrease (or replace) the use of therapeutic medications.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42084768/\n- **PMID 41984519 (2026, Archives of animal nutrition)** — Early high-energy diet induces a systemic metabolic alteration in light weaning body weight piglets that persists after dietary normalization.. Abstract (opening): Light weaning body weight (LWBW) piglets exhibit inferior growth performance, and their energy requirement vary dynamically with increasing body weight. Although high-energy diets improve growth, they risk impairing liver health. Therefore, we investigated a multi-phase, high-net energy (HNE) regimen with stepwise-decreasing energy concentration with increasing body weight, assessing its impact on growth performance, liver health, and gut microbiota in LWBW piglets. Thirty LWBW piglets (28 days of age, initial body weight: 6.09 ± 0.47 kg) were randomly assigned to two groups; a high-net energy diet based on the energy requirement curve (HNE diet), and a low-net energy diet formulated according to NRC recommendations (NRC diet). Each treatment consisted of five physically separated pens (experimental unit and replicate, <i>n</i> = 5), with three piglets housed per pen throughout the 42-day trial. Results showed that the HNE diet tended to reduce feed to gain ratio (<i>p</i> = 0.075) but failed to improve average daily gain (ADG) in LWBW piglets. Relative to the NRC diet, the HNE diet exhibited significant elevations in serum concentrations of glucose, triglycerides, total cholesterol, bile acids, and alanine aminotransferase (<i>p</i> < 0.05), as well as in hepatic the content of malondialdehyde and the activity of total superoxide dismutase contents (<i>p</i> < 0.05). In addition, HNE diet upregulated the mRNA expression of lipogenic genes acetyl-CoA carboxylase (<i>p</i> < 0.05) and fatty acid synthase (<i>p</i> = 0.076), along with the protein levels of pro-inflammatory cytokines and endoplasmic reticulum stress marker glucose-regulated protein 78 (<i>p</i> < 0.05). Serum metabolomic profiling revealed that HNE diet induced alterations in a series of metabolites associated with oxidative stress, specifically increasing the concentrations of LysoPC, LysoPE, and guanosine while reducing levothyroxine abundance in LWBW piglets. <i>Prevotella copri</i> was the key microbe in the colon of HNE group piglets. Furthermore, HNE diet significantly elevated colonic concentrations of acetate, propionate, and butyrate (<i>p</i> < 0.05). Collectively, these findings suggest that the high-net energy diet reduced the feed-to-gain ratio, it did not significantly increase the ADG of piglets. This phenomenon may be associated with liver function and gut microbiota. Notably, the early high-net energy diet induces a systemic metabolic alteration that persists after dietary normalisation.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41984519/\n\nSource text: `pdf-raw/evidence/europepmc_mini_pig_nutrition_2026-08-01.txt` (Europe PMC first-hand abstracts, pulled 2026-08-01).\n","sources":["Europe PMC — Evidence cluster — Miniature pig (Sus scrofa) nutrition (peer-reviewed, Europe PMC) (retrieved 2026-08-01)"],"source":{"authority":"Europe PMC","title":"Evidence cluster — Miniature pig (Sus scrofa) nutrition (peer-reviewed, Europe PMC)","url":"https://pubmed.ncbi.nlm.nih.gov/42237168/","retrieved":"2026-08-01","ref":"PMID 42237168","doc_type":"official PDF","source_document":"Peer-reviewed Miniature pig nutrition literature (Europe PMC, first-hand abstracts)","verification_file":"pdf-raw/evidence/europepmc_mini_pig_nutrition_2026-08-01.txt"},"source_document":"Peer-reviewed Miniature pig nutrition literature (Europe PMC, first-hand abstracts)","source_file":"pdf-raw/evidence/europepmc_mini_pig_nutrition_2026-08-01.txt","tokens_estimated":600,"generated_at":null,"tip":"Use /api/v1/topics to discover more topics. /api/v1/nutrient for precise single-point queries. /api/v1/cross_compare for 2-3 standard comparisons."}