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: 31 March 2026 | Viewed by 74

Special Issue Editor


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Guest Editor
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China
Interests: high-fat food; mammals; fish; metabolic blocks; toxosis; treatment of disease
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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

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Keywords

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

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Published Papers (1 paper)

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Research

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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
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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