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Animals
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Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases
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Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases

A special issue of Animals (ISSN 2076-2615). This special issue belongs to the section "Animal Physiology".

Deadline for manuscript submissions: 10 November 2026 | Viewed by 2983

Editor

Dr. Fan Yang

E-Mail Website
Guest Editor
College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China
Interests: prevention and control of nutritional metabolic diseases and toxicoses in livestock and poultry; organelle interactions

Special Issue Information

Dear Colleagues,

In modern intensive livestock production, nutritional metabolic diseases pose severe threats to animal health, welfare, and economic efficiency. This Special Issue directly addresses this critical challenge by focusing on translational strategies that bridge the laboratory and the farm.

We are pleased to invite you to submit your work to this Special Issue, aimed at collecting research on innovative clinical management and nutritional regulation strategies for various disorders. The focus of this Special Issue aligns perfectly with the Animals journal scope, intersecting its core areas of animal nutrition, veterinary internal medicine, and production animal health and welfare. We seek to bridge foundational research and practical application.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Pathogenesis of metabolic and toxicological diseases in animals.
  • Functional networks and interaction mechanisms of cellular organelles.
  • Regulation of gut health and systemic metabolic homeostasis in animals.
  • A One Health perspective on animal disease interactions across the human–animal–environment interface.
  • Efficacy and mechanisms of action of natural plant extracts in improving animal health.

We look forward to receiving your contributions.

Dr. Fan Yang
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. Animals is an international peer-reviewed open access semimonthly 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 2400 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

  • nutritional metabolic diseases
  • clinical management
  • nutritional regulation
  • metabolic biomarkers
  • transition cow

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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16 pages, 1936 KB  
Article
Proteomic Analysis of Dairy Cows with Persistent Subclinical Hypocalcemia
by Yunlong Bai, Junbo Hu, Jingyi Liu, Xudong Sun, Chuang Xu, Jiajing Liu, Xiaochen Jia, Yu Yang, Lianying Wang, Guang Shao, Qitao Zhu, Caixia Ru, Mengjiao Wang, Cheng Xia and Yuxi Song
Animals 2026, 16(15), 2378; https://doi.org/10.3390/ani16152378 - 3 Aug 2026
Viewed by 266
Abstract
To delineate the serum proteomic profile of persistent subclinical hypocalcemia (pSCH) in periparturient dairy cows, elucidate its molecular pathogenesis, and provide a theoretical basis for early warning and precision prevention and control, we selected 12 Holstein dairy cows of similar age (2.92 ± [...] Read more.
To delineate the serum proteomic profile of persistent subclinical hypocalcemia (pSCH) in periparturient dairy cows, elucidate its molecular pathogenesis, and provide a theoretical basis for early warning and precision prevention and control, we selected 12 Holstein dairy cows of similar age (2.92 ± 0.12 years), parity (1.56 ± 0.21), body condition score (BCS) (2.84 ± 0.04), milk yield (26.81 ± 0.22 kg/d), and day in milk (DIM) (6.60 ± 0.24 d) and no significant between-group differences as experimental animals. Based on serum calcium concentrations on postpartum days 1 to 4 and clinical presentation, the cows were divided into a healthy control group (serum calcium > 1.77 mmol/L on day 1 and >2.20 mmol/L on day 4 postpartum, n = 6) and a persistent subclinical hypocalcemia group (serum calcium ≤ 1.77 mmol/L on day 1 and ≤2.20 mmol/L on day 4 postpartum, n = 6). Serum samples were collected on postpartum days 1, 2, and 4 and analyzed using 4D-DIA quantitative proteomics. A total of 178 significantly differentially expressed proteins were identified (fold change > 1.2, p < 0.05), including 59 up-regulated and 119 down-regulated proteins. These differentially expressed proteins were mainly enriched in pathways involving endocrine and other factor-regulated calcium reabsorption, regulation of actin cytoskeleton, the tricarboxylic acid cycle (TCA cycle), and lipoic acid metabolism. The results indicate that the pathological state of pSCH is closely associated with abnormalities in calcium reabsorption regulation, actin cytoskeleton maintenance, and mitochondrial energy metabolism-related signaling pathways. The key proteins and pathways identified in this study provide a theoretical foundation for future in-depth research on the pathogenesis, prevention, and treatment of pSCH. Full article
(This article belongs to the Special Issue Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases)
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15 pages, 4466 KB  
Article
Role of Autophagy in Goose Astrovirus-Induced Renal Injury in Goslings
by Jun Kuang, Zhenni Liu, Haoyu Huang, Yan Shi, Meiqin Wu, Zhixian Wang, Xiaona Gao, Xiaoquan Guo, Xinjun Liao and Haiqin Li
Animals 2026, 16(14), 2214; https://doi.org/10.3390/ani16142214 - 16 Jul 2026
Viewed by 368
Abstract
Goose astrovirus (GoAstV) is a newly identified virus affecting geese, leading to goose gout, which is marked by urate deposits in organs and joints. This research investigates the role of autophagy in renal damage caused by GoAstV in goslings. The findings indicated that [...] Read more.
Goose astrovirus (GoAstV) is a newly identified virus affecting geese, leading to goose gout, which is marked by urate deposits in organs and joints. This research investigates the role of autophagy in renal damage caused by GoAstV in goslings. The findings indicated that GoAstV infection in goslings resulted in characteristic clinical manifestations, with renal tissues displaying tubular swelling, inflammatory infiltration, and autophagosome formation. In vivo experiments demonstrated a significant upregulation of mRNA levels for autophagy-related factors, including AMPK, LC3A, ATG5, ATG7, P62, Beclin1, AMBRA1 and GABARAPL1, while mTOR and LC3B levels were notably decreased. At 3 dpi, the protein expression levels of ATG5, Beclin1, and LC3B II/I increased, while P62 levels decreased, suggesting autophagy activation. In vitro analyses revealed that GoAstV infection led to enhanced autophagy; however, the concurrent upregulation of LC3B II/I and P62 proteins suggested an obstruction in the autophagic flux. Upon the inhibition of autophagy with 3-methyladenine (3-MA, autophagy inhibitor), there was a significant reduction in the expression of autophagy-related factors, accompanied by a marked decrease in viral replication rates. In conclusion, GoAstV infection in gosling kidney cells initially triggers enhanced autophagy and subsequently causes a blockage in the autophagic flux. The virus exploits autophagosomes for replication, ultimately resulting in kidney damage. The application of 3-MA effectively inhibits this autophagic process and diminishes viral replication. Full article
(This article belongs to the Special Issue Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases)
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16 pages, 2729 KB  
Article
Free Fatty Acids Induce Endoplasmic Reticulum Stress-Mediated Apoptosis of Macrophages in Dairy Cows with Ketosis
by Hongdou Jia, Xinyuan Sun, Wantong Cheng, Yue Yu, Yutong Wu, Jiayi Yan, Yunhui Fan, Qiushi Xu, Juan J. Loor, Chuang Xu, Shixin Fu and Xudong Sun
Animals 2026, 16(7), 1070; https://doi.org/10.3390/ani16071070 - 1 Apr 2026
Cited by 1 | Viewed by 1016
Abstract
Dairy cows with ketosis display immune dysfunction and a high incidence of infectious diseases, which may partly be attributed to excessive endoplasmic reticulum stress (ERS) and apoptosis in macrophages. The objective of the present study was to assess the role of ERS in [...] Read more.
Dairy cows with ketosis display immune dysfunction and a high incidence of infectious diseases, which may partly be attributed to excessive endoplasmic reticulum stress (ERS) and apoptosis in macrophages. The objective of the present study was to assess the role of ERS in macrophage apoptosis of ketotic dairy cows. Compared with healthy cows, the apoptosis number of macrophages and the protein abundance of glucose regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), and activating transcription factor 6 (ATF6); the ratio of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK)/PERK, phosphorylated inositol-requiring enzyme 1 (p-IRE1)/IRE1 and phosphorylated eukaryotic translation initiation factor 2α (p-eIF2α)/eIF2α; and mean fluorescence intensity of C/EBP homology protein (CHOP) were greater in cows with clinically ketosis (CK). Treatment with FFA increased protein abundance of GRP78, CHOP, ATF6 and p-IRE1/IRE1, and mean fluorescence intensity of CHOP. Furthermore, FFA increased the protein abundance of cysteinyl aspartate-specific proteinase-3 (Caspase-3) and mean fluorescence intensity of Caspase-3 but decreased the Bcl-2/Bax protein abundance ratio, which was accompanied by an increase in the number macrophage apoptosis. Inhibition of ERS via TUDCA attenuated the increased macrophage apoptosis and the activated apoptotic pathways induced by Tn or FFA. Thus, hyperphysiological concentrations of FFA induce apoptosis in macrophages by triggering ERS in ketotic dairy cows. Full article
(This article belongs to the Special Issue Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases)
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Review

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22 pages, 2266 KB  
Review
Promoting Bone Health in Layer Chickens from the Perspective of Mitochondrial Energy Metabolism in Osteoclasts
by Zhiyu Su, Shuo Tian, Ruilong Song, Zongping Liu and Xishuai Tong
Animals 2026, 16(13), 2046; https://doi.org/10.3390/ani16132046 - 3 Jul 2026
Viewed by 842
Abstract
Layer chickens have dual physiological demands for rapid growth and continuous egg production. The maintenance of skeletal homeostasis in layer chickens relies on the precise coordination among OCs, osteoblasts (OBs), and osteocytes. The imbalances in the supply of nutrients such as calcium (Ca) [...] Read more.
Layer chickens have dual physiological demands for rapid growth and continuous egg production. The maintenance of skeletal homeostasis in layer chickens relies on the precise coordination among OCs, osteoblasts (OBs), and osteocytes. The imbalances in the supply of nutrients such as calcium (Ca) and phosphorus (P), as well as dysfunction of the “gut–bone” axis, can disrupt normal bone development in layer chickens, leading to bone diseases such as tibial dyschondroplasia (TD) and osteoporosis (OP), seriously damaging the production performance of layer chickens. This review systematically summarizes the knowledge background of the metabolic reprogramming of OCs in layer chickens, especially mitochondria-mediated biological processes, including oxidative phosphorylation (OXPHOS), glycolysis, reactive oxygen species (ROS) signaling, mitophagy, etc. Notably, the co-culture system of OCs derived from the bone marrow cavity of embryos in vitro has been established in laying chickens. However, there are few reports on the study of mitochondrial metabolism of OCs using this model. Therefore, this review particular focuses on the bone metabolism mediated by OCs in layer chickens and proposes future research priorities, including the application of gene editing and multi-omics methods to ultimately achieve targeted nutritional or pharmacological interventions for optimizing mitochondrial function and promoting bone health. Full article
(This article belongs to the Special Issue Clinical Management and Nutritional Regulation of Livestock Nutritional Metabolic Diseases)
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