Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 2943

Special Issue Editor


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Guest Editor
Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China
Interests: animal metabolic diseases (obesity and fatty liver); biologically active substance and stress regulation; regulation of iron and copper metabolism; oxidative stress; ferroptosis; non-coding RNA; egg quality
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Special Issue Information

Dear Colleagues,

Stress represents the body’s nonspecific response to diverse external or internal challenges, triggering adaptive physiological changes through the activation of the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system. While acute stress promotes survival, chronic exposure disrupts metabolic homeostasis, altering nutrient utilization, gut microbiota composition, and energy balance. A growing body of evidence underscores the interplay between environmental stressors (e.g., climate extremes, pollution) and nutritional stressors (e.g., feed scarcity, imbalanced diets) in driving metabolic dysfunction across species.

Topics of Interest​

We invite original research, reviews, and translational studies that address topics including (but not limited to) the following:

​1. Environmental Stressors and Metabolic Dysfunction​

  • Climate-related stress: Heat/cold stress-induced alterations in energy expenditure, thermoregulation, and feed efficiency.
  • Toxicant exposure: Air/water pollutants (e.g., heavy metals, pesticides) disrupting endocrine and hepatic function.
  • Photoperiod and circadian disruption: Implications for seasonal metabolic disorders (e.g., adiposity, reproductive cyclicity).

​2. Nutritional Stress and Metabolic Adaptation​

  • Nutrient scarcity or excess: Protein/energy restriction vs. high-fat diets in terms of stress susceptibility.
  • Micronutrient imbalances: Vitamin D deficiency or iron overload in stress-responsive pathways.
  • Feed-associated toxins: Mycotoxins triggering oxidative stress and intestinal barrier dysfunction.

​3. StressGut Microbiota Interactions​

  • Microbial shifts under stress (e.g., reduced Lactobacillus, increased Enterobacteriaceae) and their metabolic consequences (e.g., SCFA depletion, endotoxemia).
  • Probiotics/prebiotics as modulators of stress resilience.

​4. Therapeutic and Regulatory Approaches​

  • Bioactive compounds: Phytochemicals (e.g., polyphenols), omega-3 fatty acids, or adaptogens (e.g., ginsenosides) targeting HPA axis or inflammatory pathways.
  • Nutritional interventions: Precision feeding strategies to counteract stress-induced metabolic impairments.

Prof. Dr. Wenqiang Ma
Guest Editor

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Keywords

  • stress physiology
  • metabolic dysfunction
  • environmental stress
  • nutritional stress
  • gut microbiota
  • bioactive compounds

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Published Papers (4 papers)

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Research

19 pages, 9380 KB  
Article
High Temperature Stress Impairs Muscle Quality in Largemouth Bass (Micropterus salmoides) Through Textural Deterioration and Flavor Compounds Depletion
by Wanjie Cai, Hui You, Meiyu Wang, Yanjian Jin, Zhiyong Dong, Bo Shi, Yuexing Zhang and Liying Huang
Biology 2026, 15(8), 634; https://doi.org/10.3390/biology15080634 - 17 Apr 2026
Viewed by 461
Abstract
While the detrimental effects of high temperature stress on fish growth and disease resistance have been widely reported, its impact on muscle quality has received limited attention. In this study, largemouth bass Micropterus salmoides with an initial body weight of 45.73 g were [...] Read more.
While the detrimental effects of high temperature stress on fish growth and disease resistance have been widely reported, its impact on muscle quality has received limited attention. In this study, largemouth bass Micropterus salmoides with an initial body weight of 45.73 g were subjected to a 60-day growth trial (~25 °C), followed by a 5-day acute warming phase and a subsequent 30-day chronic high temperature exposure (32 °C). Through integrated analyses of morphological parameters, texture characteristics, TUNEL assay, gene expression analysis, and metabolomics in muscle, the effects of high temperature stress on the meat quality of largemouth bass were systematically examined. The results showed that high temperature stress significantly upregulated key genes in the ubiquitin-proteasome pathway (trim13, foxo1α) and key genes in the autophagy-lysosome pathways (lc3α, lc3β, bcl2l1, ctsl2), induced apoptosis in muscle cells, and led to significant reductions in myofiber diameter and density. In terms of textural properties, high temperature stress significantly decreased parameters such as springiness, adhesiveness, and cohesiveness, as well as water holding capacity. Metabolomic analysis further revealed that high temperature induced remodeling of energy metabolism and significant reprogramming of purine and amino acid metabolic pathways, resulting in decreased levels of key flavor compounds, including IMP, GMP, flavor amino acids (glutamic acid, alanine, methionine, arginine, proline), and peptides (glu-glu-lys and glu-cys-gly), thereby adversely affecting muscle flavor quality. The findings of this study provide a theoretical basis for understanding the impact of thermal stress on the eating quality of farmed fish. Full article
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18 pages, 3122 KB  
Article
Study on the Role of the AMPK/PGC-1α Pathway in Cold-Induced Vascular Endothelial Cell Apoptosis and Uterine Damage
by Sufen Bai, Xiaojin La, Yiting Yang, Yu Li, Di Wang, Yanqing Ren, Huimin Fang, Xinhua Li, Xiaodan Song, Xiumei Cheng and Dingjie Xu
Biology 2026, 15(5), 436; https://doi.org/10.3390/biology15050436 - 6 Mar 2026
Viewed by 642
Abstract
Cold exposure may influence reproductive health through vascular changes, yet its mechanisms remain underexplored. This study aimed to investigate the impact of cold exposure on uterine blood vessels and the expression of the AMPK/PGC-1α gene and protein in adult female SD rats. A [...] Read more.
Cold exposure may influence reproductive health through vascular changes, yet its mechanisms remain underexplored. This study aimed to investigate the impact of cold exposure on uterine blood vessels and the expression of the AMPK/PGC-1α gene and protein in adult female SD rats. A primary dysmenorrhea model was established in female Sprague Dawley rats and subjected to continuous cold exposure. Changes in body weight, ear temperature, and estrous cycle were observed. Superoxide dismutase (SOD) activity and adenosine triphosphate (ATP) levels were measured to assess oxidative stress. Uterine tissue morphology was assessed via small animal ultrasound, microcirculation observed using RFLSI imaging, and vascular morphology along with caspase-3 and AMPK expression evaluated histologically and immunohistochemically. CD31 and TUNEL double immunofluorescence were used to assess vascular endothelial apoptosis levels. Western blot was used to analyze Bax, BCL-2, and pAMPK/AMPK expression levels. In vitro injury models were used to treat human umbilical vein endothelial cells (HUVECs) with cold stimulus using the AMPK inhibitor Compound C. RT-PCR quantified Bax, AMPK, p53, and PGC-1α expression. Hypothermia-exposed rats exhibited significantly reduced body weight and ear temperature (p < 0.05), prolonged estrous cycle (p < 0.01), and decreased uterine index (p < 0.01), accompanied by reduced SOD and ATP levels (p < 0.01, p < 0.05). Ultrasound and flow imaging revealed decreased uterine blood flow velocity in the hypothermia group (p < 0.01). Histomorphology revealed disorganized uterine cell arrangement, reduced uterine vessel count (p < 0.01), and increased mean vessel area (p < 0.01) in cold-exposed uteri. Immunofluorescence detection revealed increased vascular endothelial cell apoptosis (p < 0.05). Western blot results showed that proapoptotic protein Bax was upregulated (p < 0.01), Bcl-2 was downregulated (p < 0.05), p-AMPK and p-AMPK/AMPK ratio were elevated (p < 0.01) after cold exposure; Rt-qPCR results indicated that Bax and P53 mRNA were increased (p < 0.01), while PGC-1α expression was elevated (p < 0.01). Rt-qPCR results showed elevated Bax and p53 mRNA (p < 0.01), along with increased AMPK and PGC-1α expression (p < 0.01) in the cold-exposed group. In human umbilical vein endothelial cells (HUVECs), compound C attenuated cold-induced effects (p < 0.01) and downregulated Bax and AMPK expression (p < 0.01). Cold exposure exacerbates uterine oxidative stress and energy imbalance, disrupts microcirculatory homeostasis, and induces endothelial cell apoptosis. Excessive phosphorylation of AMPK may co-activate PGC-1α, jointly contributing to cold-induced uterine dysfunction and exacerbated dysmenorrhea. This study reveals potential signaling pathways underlying cold-induced uterine vascular abnormalities, providing novel theoretical foundations and targeted intervention strategies for the prevention and treatment of primary dysmenorrhea. Full article
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23 pages, 9985 KB  
Article
Lycopene Attenuates T2 Mycotoxin-Induced Hepatotoxicity and Dysbiosis by Activating PPAR Signaling
by Wael Ennab, Saber Y. Adam, Hao-Yu Liu, Ghaid J. Al-Rabadi, Ping Hu, Baiome Abdelmaguid Baiome, Kaiqi Li, Abdelkareem A. Ahmed, In Ho Kim, Madesh Muniyappan and Demin Cai
Biology 2026, 15(4), 347; https://doi.org/10.3390/biology15040347 - 16 Feb 2026
Viewed by 738
Abstract
Exposure to T2 toxin is known to induce hepatotoxicity and gut dysbiosis, yet effective dietary interventions remain underexplored. This study investigates the hepatoprotective and microbiota-modulating effects of lycopene against T2 toxin-induced toxicity in mice. Mice were exposed to T2 toxin with or without [...] Read more.
Exposure to T2 toxin is known to induce hepatotoxicity and gut dysbiosis, yet effective dietary interventions remain underexplored. This study investigates the hepatoprotective and microbiota-modulating effects of lycopene against T2 toxin-induced toxicity in mice. Mice were exposed to T2 toxin with or without lycopene supplementation at low and high doses. The hepatic function, oxidative stress markers, inflammatory gene expression, detoxification pathway activity, and gut microbiota composition were assessed using histological, biochemical, and molecular analyses. T2 toxin exposure resulted in significant weight loss, oxidative liver damage, and gut dysbiosis—marked by a decline in beneficial phyla and an increase in pathogenic bacteria. Hepatic injury was accompanied by upregulated pro-inflammatory genes and downregulated PPAR pathway genes, leading to impaired lipid metabolism and disrupted liver histology. Lycopene supplementation effectively attenuated these effects: it reduced oxidative stress, enhanced antioxidant defense, lowered inflammatory markers, and restored gut microbial balance. Furthermore, lycopene upregulated PPAR pathway and phase I detoxification genes. Notably, the low-dose lycopene regimen demonstrated superior efficacy compared to the high-dose regimen. In conclusion, lycopene, particularly at a low dose, confers significant protection against T2 toxin-induced hepatotoxicity and gut dysbiosis, highlighting its potential as a dietary strategy for mitigating mycotoxin-induced health risks. Full article
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15 pages, 1218 KB  
Article
Effects of High-Flow-Velocity Stress on Energy Metabolism and Transcription Level of Triplophysa orientalis
by Xin Gao, Hui Wan, Yuxuan Jiang, Liping Qiu, Zhongquan Jiang, Shunlong Meng and Chao Song
Biology 2026, 15(4), 331; https://doi.org/10.3390/biology15040331 - 14 Feb 2026
Viewed by 537
Abstract
River channel development and hydraulic engineering alter natural flow-velocity patterns, subjecting Triplophysa orientalis to heightened hydrodynamic stress and energy expenditure in high-flow-velocity habitats. Regulating the molecular regulatory mechanisms underlying their adaptation to high-flow velocities provides a basis for species conservation and habitat optimization. [...] Read more.
River channel development and hydraulic engineering alter natural flow-velocity patterns, subjecting Triplophysa orientalis to heightened hydrodynamic stress and energy expenditure in high-flow-velocity habitats. Regulating the molecular regulatory mechanisms underlying their adaptation to high-flow velocities provides a basis for species conservation and habitat optimization. Fish were exposed for 3 days to a normal flow velocity (3 BL/s) or a high flow velocity (33 BL/s) in a controlled circular swimming system that maintained a stable current without a deliberate low-flow velocity refuge; fish at 33 BL/s sustained upstream swimming throughout the exposure. RNA-seq differential expression analysis and GO/KEGG enrichment were performed on harvested skeletal muscle, with key genes validated via qPCR. A total of 78 differentially expressed genes (DEGs) were identified between the high-flow-velocity group and the normal-flow-velocity group, including 55 up-regulated genes and 23 down-regulated genes. GO and KEGG analyses revealed that the DEGs were predominantly enriched in mitochondrial energy metabolism and neural regulation, notably oxidative phosphorylation, and were further linked to FoxO and IL-17 signaling. Compared to the normal-flow-velocity group, the high-flow-velocity group exhibited significant down-regulation of multiple oxidative phosphorylation-related subunits, including Mt-co1, Mt-co2, Mt-co3, Mt-nd1, Mt-nd2, Mt-nd4, Mt-nd5, and Mt-atp6. Concurrently, stress response-related genes, such as Selenop, GADD45B, and SIK2, showed a down-regulation trend. These transcriptional changes are consistent with reduced expression of genes involved in antioxidant defense and cellular protection under high-flow conditions, integrating differential-expression and pathway-enrichment results. This decline correlates with the down-regulation of genes associated with antioxidant and stress regulation. Pathways related to energy metabolism show significant enrichment, suggesting enhanced regulation of energy supply and allocation. This pattern indicates metabolic reprogramming characteristics adapted to high-flow-velocity stress. Full article
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