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The Latest Molecular Insights into Animal Nutrition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 20 August 2026 | Viewed by 1085

Special Issue Editor


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Guest Editor
Key Laboratory for Animal Disease-Resistant Nutrition of China Ministry of Education, Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu 611130, China
Interests: sow nutrition; reproduction; antioxidation; offspring; molecular nutrition; glucose metabolism; lipids metabolism; insulin signaling

Special Issue Information

Dear Colleagues,

This Special Issue aims to compile and highlight the most significant recent advancements in understanding the molecular and cellular mechanisms governing nutrient utilization, metabolism, and their impacts across diverse animal species. Our primary goal is to foster innovation in sustainable animal production, reproduction, health optimization, and precision nutrition by elucidating the fundamental biological pathways influenced by diet.

This Special Issue will focus explicitly on cutting-edge research employing advanced molecular and omics methodologies (e.g., genomics, transcriptomics, proteomics, metabolomics, epigenomics, microbiomics, CRISPR-based techniques, single-cell sequencing).

Key topics of interest for this Special Issue include the following:

  1. Molecular Mechanisms of Nutrient Action: Deciphering how nutrients (macro and micro) regulate gene expression, signaling pathways (e.g., mTOR, AMPK, inflammasomes), and cellular functions impacting growth, reproduction, immunity, gut health, and metabolic homeostasis.
  2. Nutrient–Gene and Nutrient–Microbiome Interactions: Exploring nutrigenomics, nutrigenetics, and the molecular crosstalk between diet, host physiology, and the gut microbiome, affecting nutrient harvest, efficiency (e.g., feed conversion), and emissions (e.g., methane).
  3. Discovery of Biomarkers: Identifying and validating novel molecular, epigenetic, or microbial biomarkers for assessing nutritional status and predicting performance, disease susceptibility, or metabolic disorders.
  4. Precision Nutrition Applications: Leveraging molecular insights into developing tailored nutritional strategies for specific species, breeds, life stages, health conditions, or production goals.

We welcome the submission of original research, reviews, and perspectives investigating these molecular dynamics in livestock, poultry, aquaculture, and companion animals. This Special Issue emphasizes mechanistic discoveries driving the future of efficient, ethical, and sustainable animal agriculture.

Prof. Dr. Bin Feng
Guest Editor

Manuscript Submission Information

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Keywords

  • reproduction
  • animal production
  • development
  • immunity
  • emissions
  • digestion efficiency
  • microbiome
  • metabolism
  • molecular signaling
  • nutritional strategies

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Published Papers (2 papers)

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Research

13 pages, 1963 KB  
Article
MAPK Phosphatase-3 Mediates Chronic Endoplasmic Reticulum Stress Promoting Hepatic Gluconeogenesis
by Sheng Cao, Yanlin Du, Zhengfeng Fang, Lianqiang Che, Yan Lin, Shengyu Xu, Xuemei Jiang, Guangmang Liu, Yong Zhuo, Lun Hua, Mengmeng Sun, De Wu and Bin Feng
Int. J. Mol. Sci. 2026, 27(6), 2874; https://doi.org/10.3390/ijms27062874 - 22 Mar 2026
Viewed by 373
Abstract
Long-term nutritional excess causes hepatic steatosis, endoplasmic reticulum (ER) stress, hyperglycemia, and hyperlipidemia. Mitogen-activated protein kinase phosphatase-3 (MKP-3) is a well-established stress-regulated protein and a regulator of gluconeogenesis. Our previous study revealed that acute ER stress reduced gluconeogenesis and MKP-3 protein stability. However, [...] Read more.
Long-term nutritional excess causes hepatic steatosis, endoplasmic reticulum (ER) stress, hyperglycemia, and hyperlipidemia. Mitogen-activated protein kinase phosphatase-3 (MKP-3) is a well-established stress-regulated protein and a regulator of gluconeogenesis. Our previous study revealed that acute ER stress reduced gluconeogenesis and MKP-3 protein stability. However, the expression of MKP-3 and its regulatory mechanisms in chronic ER stress remain unclear. The aim of this study was to investigate the effects of chronic ER stress on hepatic MKP-3 expression and its role in the regulation of gluconeogenesis. The results show that long-term administration of thapsigargin (Tg) or palmitic acid promoted gene expression of Mkp-3 and gluconeogenic genes Pepck, G6pc, and Pgc1α in primary mouse hepatocytes. In addition, a long-term high-fat diet (HFD) or Tg administration significantly increased hepatic ER stress and blood glucose level in mice, while inducing the expression of Mkp-3 and hepatic gluconeogenic genes Pepck, G6pc and Pgc1α. Further study revealed that liver-specific Mkp-3 knockout (Mkp-3 LKO) reversed the blood glucose level and expression levels of gluconeogenic genes those were induced by long-term HFD in mice. Moreover, activation of the PKR-like ER kinase (PERK) by its agonist increased hepatic Mkp-3 expression, whereas inhibitor of PERK suppressed the expression of Mkp-3 under Tg administration. These results suggest that chronic high-fat diet might promote hepatic gluconeogenesis via the PERK/MKP-3 pathway. Consequently, this study identified a potential therapeutic target for treating obesity-related hyperglycemia. Full article
(This article belongs to the Special Issue The Latest Molecular Insights into Animal Nutrition)
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15 pages, 2158 KB  
Article
Zearalenone Induces Oxidative Stress and Apoptosis in the Jejunum of Weaned Piglets via the p53/Nrf2 Signaling Pathway
by Yihao Sang, Shaojin Hou, Zhongfang Zhang, Shuzhen Jiang, Weiren Yang and Qun Cheng
Int. J. Mol. Sci. 2026, 27(5), 2401; https://doi.org/10.3390/ijms27052401 - 5 Mar 2026
Cited by 1 | Viewed by 392
Abstract
This study investigated the mechanisms by which ZEA induces oxidative stress and apoptosis in the jejunum of piglets and explored the roles of the tumor suppressor gene p53 and nuclear factor E2-related factor 2 (Nrf2) signaling pathways. Twelve weaned piglets were randomized into [...] Read more.
This study investigated the mechanisms by which ZEA induces oxidative stress and apoptosis in the jejunum of piglets and explored the roles of the tumor suppressor gene p53 and nuclear factor E2-related factor 2 (Nrf2) signaling pathways. Twelve weaned piglets were randomized into Control (basal diet) and ZEA groups (basal diet + 1.0 mg/kg ZEA; 6 piglets/group). No differences were observed between the control and ZEA groups for all production performance indicators. Compared with the jejunum of the control group, the ZEA group exhibited reduced levels of total superoxide dismutase, glutathione peroxidase activity, and total antioxidant capacity, along with elevated malondialdehyde content. Morphological examination revealed increased crypt depth and decreased villus height and villus-to-crypt ratio, as well as swollen, vacuolated spherical mitochondria with disrupted cristae. Immunohistochemistry showed enhanced p53 and Nrf2 immunoreactivity. The relative mRNA levels of Nrf2, Ho1, Gpx1, Cytc1, p53, Caspase1, and Bax increased. The Bax/Bcl-2 ratio increased, and Keap1 and Bcl-2 mRNA levels decreased. The relative protein levels of Nrf2, p53, Bax, Caspase1, and Gpx1 increased, whereas that of Bcl-2 decreased. All differences were significant at p < 0.05. Dietary supplementation with ZEA altered the morphological structure of intestinal tissues and mitochondria. By affecting the expression of genes related to the p53 and Nrf2 signaling pathways, it induces intestinal oxidative stress and apoptosis, thereby impairing intestinal health in weaned piglets. Full article
(This article belongs to the Special Issue The Latest Molecular Insights into Animal Nutrition)
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