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Metabolites
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Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition
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Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Animal Metabolism".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 2908

Editor

Prof. Dr. Mengyao Guo

E-Mail Website
Guest Editor
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China
Interests: high-fat food; mammals; fish; metabolic blocks; toxosis; treatment of disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will cover animals and fish. The main research content focuses on nutritional metabolic disorders, including the dysregulation of autoregulation and foodborne over-intake or under-intake. Nutrients can be proteins, lipids, sugars, or trace elements, with new processes existing for regulating or supplementing nutrients. At the same time, the focus of this Special Issue is animal toxicosis-related research content, especially new environmental toxicants, aiming of explore the relevant pathogenic mechanism and harm caused to animals. Moreover, related animal nutritional metabolic diseases and toxicosis treatment measures or drugs are also covered by the scope of this Special Issue. We welcome research dedicated to dealing with the digestion, absorption, transport, and metabolism of carbohydrates, amino acids, lipids, vitamins, minerals, organic acids, alkaloids, and drugs, as well as metabolomics, lipidomics, and crosstalk between gastrointestinal microbiota and the host involved in nutritional and metabolic diseases in animals. This Special Issue will not only detail results of studies on nutritional and metabolic diseases in domestic animals and in vitro models but also provide the results of studies on cell and animal models for human nutritional and metabolic diseases.

Prof. Dr. Meng-yao Guo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • high-fat food
  • mammals, fish
  • metabolic blocks
  • toxosis
  • treatment of disease

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Published Papers (4 papers)

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Research

22 pages, 14729 KB  
Article
Metabolic Mechanisms of Hexavalent Chromium-Induced Splenic Immune Injury via Oxidative Stress and Ferroptosis Pathways in New Zealand Rabbits
by Junzhao Yuan, Jiaqi Zhang, Jinxing Song, Lingling Liu, Hang Liu, Shuangxing Jin and Xiaoli Ren
Metabolites 2026, 16(6), 430; https://doi.org/10.3390/metabo16060430 - 18 Jun 2026
Viewed by 321
Abstract
Background: Hexavalent chromium (Cr(VI)) is a widespread environmental toxic heavy metal with strong oxidative properties; however, its immunotoxicity and metabolic mechanisms in rabbit spleen remain largely unclear. Methods: In this study, New Zealand rabbits were exposed to 0, 12.5, 25, and [...] Read more.
Background: Hexavalent chromium (Cr(VI)) is a widespread environmental toxic heavy metal with strong oxidative properties; however, its immunotoxicity and metabolic mechanisms in rabbit spleen remain largely unclear. Methods: In this study, New Zealand rabbits were exposed to 0, 12.5, 25, and 50 mg/L Cr(VI) (as potassium dichromate, K2Cr2O7) via drinking water for four weeks to investigate splenic damage and the underlying molecular pathways. Spleen pathological injury was evaluated by hematoxylin and eosin (H&E) staining, and the distribution of T cells, B cells, and macrophages was assessed by immunohistochemistry. Antioxidant enzyme activities and antioxidant substance levels were determined using ELISA, and the relative mRNA expression of immune factor genes, antioxidant-related genes, and ferroptosis-related genes was quantified by quantitative real-time PCR (qRT-PCR). In addition, the distribution of iron in splenic tissue was detected by enhanced Prussian blue staining. Results: Our results demonstrate that high-dose Cr(VI) significantly inhibited body weight gain, induced lymphocyte atrophy, vacuolization, and widening of intercellular spaces in the splenic white pulp. Furthermore, Cr(VI) reduced T and B lymphocyte populations, promoted macrophage infiltration and inflammatory cytokine gene expression in a concentration-dependent manner, impaired total antioxidant capacity, and led to a decrease in glutathione (GSH) levels in the spleen. Additionally, Cr(VI) exposure increased iron accumulation, activated the ACSL4–NOX lipid peroxidation cascade, and downregulated GPX4 expression, ultimately triggering ferroptosis. Conclusions: These findings reveal that Cr(VI) causes splenic immune injury by disrupting oxidative homeostasis and inducing ferroptosis, providing novel insights for evaluating immunotoxicity and identifying metabolic targets under Cr(VI) pollution. Full article
(This article belongs to the Special Issue Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition)
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17 pages, 4855 KB  
Article
GDF15 Improves Renal Injury Induced by Ectopic Lipid Deposition via AMPK/SIRT1 Pathway-Mediated Autophagy
by Qiang Zhang, Xidong Yang, Yuxuan Yang, Min Wang, Yulin Wu, Xin Xie, Yongjun Jin, Ming Yang and Meizi Yang
Metabolites 2026, 16(5), 336; https://doi.org/10.3390/metabo16050336 - 18 May 2026
Viewed by 387
Abstract
Objectives: Obesity precipitates excessive lipid accumulation within the kidney, culminating in ectopic lipid deposition that compromises target organ function through lipotoxicity. Given the pivotal role of GDF15 in lipid metabolism, this study aims to determine whether GDF15 can ameliorate ectopic lipid deposition and [...] Read more.
Objectives: Obesity precipitates excessive lipid accumulation within the kidney, culminating in ectopic lipid deposition that compromises target organ function through lipotoxicity. Given the pivotal role of GDF15 in lipid metabolism, this study aims to determine whether GDF15 can ameliorate ectopic lipid deposition and mitigate the resulting renal injury. Methods: C57BL/6J mice were used to establish a high-fat diet-induced obesity model. Based on Lee’s index, the mice were categorized into a diet-induced obesity group and an obesity-resistant group. Subsequently, the diet-induced obesity group received an injection of AAV-shGFRAL to knock down the GFRAL receptor. Results: In obesity resistant mice, ectopic lipid deposition in the kidneys was markedly reduced, accompanied by decreased expression of the renal injury marker KIM-1 and significantly elevated levels of GDF15. Modulation of the GDF15-GFRAL axis demonstrated that reduced autophagy levels led to increased lipid accumulation and exacerbated renal injury. Conversely, GDF15 activates the AMPK/SIRT1 signaling pathway to promote cellular autophagy, thereby mitigating renal damage induced by ectopic lipid deposition. Consistent with this mechanism, the suppression of autophagy results in the aggravation of renal injury caused by ectopic lipid accumulation. Conclusions: GDF15 ameliorates renal injury induced by ectopic lipid deposition in the kidney primarily through activation of autophagy via the AMPK/SIRT1 signaling pathway. Full article
(This article belongs to the Special Issue Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition)
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21 pages, 2788 KB  
Article
Enhancement of Disease Resistance in Pengze Crucian Carp (Carassius auratus var. Pengze) by Carvacrol Through Modulation of Intestinal Microbiota and Serum Metabolism
by Yuzhu Wang, Xiaoze Guo, Jingjing Lu, Lingya Li, Yanqiang Tang, Haihong Xiao, Siming Li and Wenshu Liu
Metabolites 2026, 16(3), 151; https://doi.org/10.3390/metabo16030151 - 25 Feb 2026
Viewed by 676
Abstract
Objectives: This study aimed to investigate the regulatory effects of dietary carvacrol on intestinal micro biota composition, serum metabolic profiles, and their association with increased resistance to Aeromonas hydrophila in Pengze crucian carp. Methods: Juvenile fish (5.63 ± 0.35 g) were randomly allocated [...] Read more.
Objectives: This study aimed to investigate the regulatory effects of dietary carvacrol on intestinal micro biota composition, serum metabolic profiles, and their association with increased resistance to Aeromonas hydrophila in Pengze crucian carp. Methods: Juvenile fish (5.63 ± 0.35 g) were randomly allocated into two experimental groups: a control group (CK) fed a basal diet and a treatment group (CA) supplemented with 600 mg/kg microencapsulated carvacrol. Following an 8-week feeding trial, nine specimens per group were sampled for venous blood and intestinal tract collection. Remaining individuals were subjected to a 12-h A. hydrophila challenge prior to identical sample collection. Results: Key findings revealed that carvacrol supplementation induced significant microbial modulations, notably reducing Firmicutes abundance while enhancing Cetobacterium populations by 33.25% compared to controls. Post-challenge analysis demonstrated marked declines in intestinal microbial diversity indices (Observed ASV, Chao1, ACE, and PD whole tree) in the CK group, whereas the CA group maintained stable microbial diversity. Pathogenic genera including Aeromonas, Shewanella, and Vibrio showed significant proliferation in challenged controls, contrasting with maintained microbial homeostasis in carvacrol-fed specimens. Serum metabolomic profiling identified the most significantly altered metabolic pathways associated with carvacrol administration: glycerophospholipid metabolism, linoleic acid metabolism, arachidonic acid metabolism, α-linolenic acid metabolism, GPI-anchor biosynthesis, and autophagy-animal pathways. Conclusions: Our results demonstrate that dietary carvacrol may reinforce intestinal microbial barrier function by optimizing beneficial microbial composition and reducing the proportion of pathogens, and modulate immune-related metabolic pathways critical for host defense, which might be involved in enhanced disease resistance. Full article
(This article belongs to the Special Issue Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition)
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25 pages, 6097 KB  
Article
Hexavalent Chromium Induces Defense Responses, Hepatocellular Apoptosis, and Lipid Metabolism Alterations in New Zealand Rabbit Livers
by Junzhao Yuan, Lei Zhang, Xiuqing Li, Xinfeng Li, Pandeng Zhao, Xiaoli Ren and Yuzhen Song
Metabolites 2025, 15(10), 637; https://doi.org/10.3390/metabo15100637 - 23 Sep 2025
Cited by 2 | Viewed by 1159
Abstract
Background: Hexavalent chromium (Cr(VI)) can migrate into soil and water, posing risks to animal health. However, it remains unclear whether Cr(VI) perturbs essential trace elements and antioxidant gene expression, triggers apoptosis, or disrupts hepatic lipid metabolism in New Zealand rabbits. Methods: [...] Read more.
Background: Hexavalent chromium (Cr(VI)) can migrate into soil and water, posing risks to animal health. However, it remains unclear whether Cr(VI) perturbs essential trace elements and antioxidant gene expression, triggers apoptosis, or disrupts hepatic lipid metabolism in New Zealand rabbits. Methods: To address this knowledge gap, twenty-four 30-day-old New Zealand rabbits were randomly allocated to one control and three Cr(VI)-treated groups (differing in Cr(VI) concentration) and maintained for 28 days. Livers were then harvested for analysis. Total Cr and essential trace elements were quantified by ICP-OES. Hematoxylin–eosin staining and transmission electron microscopy were employed to assess histopathological and ultrastructural alterations, respectively. Hepatic lipid accumulation was visualized with Oil Red O staining. QRT-PCR was used to determine the expression of antioxidant and lipid-metabolism-related genes. Results: Cr(VI) was detectable in liver tissue at all exposure levels and was accompanied by significant decreases in four essential trace elements (Fe, Mn, Zn, and Se); Cu displayed a biphasic response, rising at lower Cr(VI) doses before declining at higher doses. Histopathological and ultrastructural analyses revealed overt hepatic injury. Notably, all Cr(VI) treatments elevated antioxidant gene expression, indicating activation of hepatic defense pathways. Lipid metabolism was also disrupted, evidenced by increased lipid deposition and up-regulation of genes governing hepatic fat metabolism. Conclusions: Collectively, these findings demonstrate that Cr(VI) elicits dose-dependent activation of hepatic antioxidant defenses, promotes apoptosis, and induces lipid-metabolic disorders in New Zealand rabbit hepatocytes. This study provides novel mechanistic insights into Cr(VI)-induced hepatotoxicity and offers a valuable reference for evaluating the hepatic risks of environmental Cr(VI) exposure in this species. Full article
(This article belongs to the Special Issue Animal Nutritional Metabolism and Toxicosis Disease, 2nd Edition)
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