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

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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 3865

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Prof. Dr. Wenqiang Ma

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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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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. Stress–Gut 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 (6 papers)

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Research

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23 pages, 5594 KB

Open AccessArticle

Dietary Chlorogenic Acid Attenuates Hepatic Lipid Accumulation and Reprograms Lipid Metabolism in Heat-Stressed Laying Hens: Integrated Transcriptomic and Metabolomic Analyses

by Dan Wang, Haiqiu Tan, Lin Peng, Xuanfu Wu, Jiang Gao and Wenqiang Ma

Biology 2026, 15(12), 917; https://doi.org/10.3390/biology15120917 (registering DOI) - 12 Jun 2026

Viewed by 36

Abstract

Heat stress leads to excessive hepatic lipid deposition and oxidative imbalance in laying hens, especially during peak laying period. Chlorogenic acid (CGA), a dietary polyphenol with antioxidant and lipid-modulating properties, may improve hepatic lipid homeostasis, yet its effects under heat-stress conditions remain unclear. In this study, 240 Hy-Line Brown laying hens at 36 weeks of age were randomly assigned to one of two treatments (120 hens per treatment, with six replicates of 20 hens each): a basal diet or a basal diet supplemented with 300 mg/kg CGA and subjected to heat-stress conditions for 8 weeks. CGA supplementation significantly reduced liver weight (25.3%), liver index (14.4%), hepatic triglyceride content (29.1%), and serum triglyceride level (61.7%) (p < 0.05). Histological assessment revealed lower steatosis and inflammation scores, alongside increased hepatic SOD activity (13.6%) and decreased MDA content (58.7%) (p < 0.05). RNA-seq analysis identified 420 differentially expressed genes that were significantly enriched in PPAR signaling and fatty acid β-oxidation pathways. CGA upregulated fatty acid oxidation-related genes (ACSL1, CPT1A, ACOX1, ACAA1) and downregulated lipogenic markers (FASN, ACACA). Serum metabolomics revealed coordinated changes in lipid and carbon metabolism. These results indicate that dietary CGA alleviates hepatic lipid accumulation and oxidative stress in heat-stressed peak-laying hens, potentially via PPARα-mediated enhancement of fatty acid oxidation and inhibition of de novo lipogenesis. Full article

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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19 pages, 9380 KB

Open AccessArticle

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 516

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 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

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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18 pages, 3122 KB

Open AccessArticle

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 693

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 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

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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23 pages, 9985 KB

Open AccessArticle

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

Cited by 1 | Viewed by 853

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 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

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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15 pages, 1218 KB

Open AccessArticle

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 580

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. 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

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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Review

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29 pages, 459 KB

Open AccessReview

Consequences of Heat Stress on Physiology, Microbiome Dynamics, and Multi-Omics in Dairy Cows: More than Meets the Eye

by Themistoklis Giannoulis, Eleni Dovolou, Zissis Mamuris and Georgios S. Amiridis

Biology 2026, 15(12), 918; https://doi.org/10.3390/biology15120918 (registering DOI) - 12 Jun 2026

Abstract

Heat stress (HS) is at the top of the challenges facing modern dairy production, with annual losses according to global projections, under high-emission scenarios, reaching US$14.7–40.0 billion by the end of the century. This review emphasizes three interconnected topics that account for most of the proportion of the productive and reproductive losses during HS. First, the physiological consequences of HS are reviewed, with emphasis on the pair-fed thermal neutral (PFTN) paradigm, which established that reduced dry matter intake (DMI) accounts for only 35–50% of the observed milk yield decline, with the remainder arising from tissue-level effects of hyperthermia on mammary function, metabolism, and reproductive performance. Second, HS-induced microbiome disruption is examined as an active pathophysiological amplifier, whereby rumen dysbiosis compromises intestinal barrier integrity and drives systemic endotoxaemia, chronically amplifying the immune suppression already imposed by the thermal insult. Third, we focus on the integration of multi-omics platforms as a management approach, since single-omics analyses capture only a fraction of the biological complexity underlying the HS response. As the available datasets expand in coverage and scale, their integration through AI-driven analytical frameworks has the potential to substantially advance beyond the current fragmented picture, progressively building toward a systems-level model of thermal stress. Evidence-based mitigation strategies spanning environmental cooling, targeted nutritional supplementation, and genomic selection are critically evaluated within this framework, with emphasis on equity of access to evidence-based solutions across global dairy production systems. Full article

(This article belongs to the Special Issue Environmental and Nutritional Stress: Metabolic Consequences and Regulatory Strategies in Animals)

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