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Effects of Environmental Stress on the Metabolic Dysfunction and Its...
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Effects of Environmental Stress on the Metabolic Dysfunction and Its Mechanism

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 2687

Special Issue Editor

Prof. Dr. Wenqiang Ma

E-Mail Website
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

Special Issue Information

Dear Colleagues,

Stress is the general non-specific response of the body to various external or internal stimuli. Stress activates the hypothalamic–pituitary–adrenocortical (HPA) axis to produce glucocorticoid, resulting in altered feeding, modifying gut microbiota, metabolic disorders, and so on. A variety of intrinsic and external factors determine the metabolic outcome of stress exposure. In recent years, environmental change has negatively affected metabolic outcomes and is becoming a growing concern for humans and animals. Emerging evidence exhibits the link between environmental factors (temperature, light, pathogens, allergens, noxious gas, and so on) and metabolic dysfunction. This Special Issue is devoted to the publication of research papers involved in relationships between environmental stress and metabolic dysfunction in vivo and in vitro.

The aim of this Special Issue is to highlight the advancements in stress-induced nutritional disorders, metabolic disorders, gut microbiota modification, and stress regulation, i.e.,:

  • (1) Stress and nutritional disorders (disorders of nutrient metabolism, growth);
  • (2) Stress and metabolic disorders (Obesity, insulin resistance, diabetes, nonalcoholic fatty liver disease, cardiovascular diseases);
  • (3) Stress and gut microbiota;
  • (4) Biologically-active substance and stress regulation.

Prof. Dr. Wenqiang Ma
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly 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 2700 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

  • stress
  • glucocorticoid
  • nutritional disorders (disorders of nutrient metabolism, growth)
  • metabolic disorders (obesity, insulin resistance, diabetes, nonalcoholic fatty liver disease, cardiovascular diseases)
  • gut microbiota
  • biologically-active substance

Published Papers (2 papers)

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Research

14 pages, 3496 KiB  
Article
Effects of Chronic Stress from High Stocking Density in Mariculture: Evaluations of Growth Performance and Lipid Metabolism of Rainbow Trout (Oncorhychus mykiss)
by Zhao Li, Qinfeng Gao, Shuanglin Dong, Kang Dong, Yuling Xu, Yaoping Mei and Zhishuai Hou
Biology 2024, 13(4), 263; https://doi.org/10.3390/biology13040263 - 16 Apr 2024
Viewed by 381
Abstract
(1) Background: In aquaculture, chronic stress due to high stocking density impairs animals’ welfare and results in declined fishery production with low protein quality. However, most previous studies evaluated the effects of high stocking density on trout in freshwater rather than seawater. (2) [...] Read more.
(1) Background: In aquaculture, chronic stress due to high stocking density impairs animals’ welfare and results in declined fishery production with low protein quality. However, most previous studies evaluated the effects of high stocking density on trout in freshwater rather than seawater. (2) Methods: Juvenile trout were reared for 84 days in circular tanks under three stocking densities, including low density (“LD”, 9.15 kg/m3), moderate density (“MD”, 13.65 kg/m3), and high density (“HD”, 27.31 kg/m3) in seawater. The final densities of LD, MD, and HD were 22.00, 32.05 and 52.24 kg/m3, respectively. Growth performance and lipid metabolism were evaluated. (3) Results: Growth performance and feeding efficiency were significantly reduced due to chronic stress under high density in mariculture. The digestive activity of lipids was promoted in the gut of HD fish, while the concentration of triglycerides was decreased in the blood. Furthermore, decreased acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), increased hormone-sensitive lipase (HSL) concentrations, and activated hepatic β-oxidation processes were observed in trout under HD. Redundancy analysis showed that glycerol and HSL can be used as potential markers to evaluate the growth performance of trout in mariculture. (4) Conclusions: We showed that chronic high stocking density led to negative effects on growth performance, reduced de novo synthesis of fatty acids, and enhanced lipolysis. Full article
(This article belongs to the Special Issue Effects of Environmental Stress on the Metabolic Dysfunction and Its Mechanism)
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16 pages, 2929 KiB  
Article
Chronic Corticosterone Exposure Suppresses Copper Transport through GR-Mediated Intestinal CTR1 Pathway in Mice
by Shihui Guo, Zijin Chen, Yingying Dong, Yingdong Ni, Ruqian Zhao and Wenqiang Ma
Biology 2023, 12(2), 197; https://doi.org/10.3390/biology12020197 - 28 Jan 2023
Cited by 1 | Viewed by 1825
Abstract
Numerous studies have discovered that chronic stress induces metabolic disorders by affecting iron and zinc metabolism, but the relationship between chronic stress and copper metabolism remains unclear. Here, we explore the influence of chronic corticosterone (CORT) exposure on copper metabolism and its regulatory [...] Read more.
Numerous studies have discovered that chronic stress induces metabolic disorders by affecting iron and zinc metabolism, but the relationship between chronic stress and copper metabolism remains unclear. Here, we explore the influence of chronic corticosterone (CORT) exposure on copper metabolism and its regulatory mechanism in mice. Mice were treated with 100 μg/mL CORT in drinking water for a 4-week trial. We found that CORT treatment resulted in a significant decrease in plasma copper level, plasma ceruloplasmin activity, plasma and liver Cu/Zn-SOD activity, hepatic copper content, and liver metallothionein content in mice. CORT treatment led to the reduction in duodenal expression of copper transporter 1 (CTR1), duodenal cytochrome b (DCYTB), and ATPase copper-transporting alpha (ATP7A) at the mRNA and protein level in mice. CORT treatment activated nuclear glucocorticoid receptor (GR) and down-regulated CRT1 expression in Caco-2 cells, whereas these phenotypes were reversible by an antagonist of GR, RU486. Chromatin immunoprecipitation analysis revealed that GR bound to the Ctr1 promoter in Caco-2 cells. Transient transfection assays in Caco-2 cells demonstrated that the Ctr1 promoter was responsive to the CORT-activated glucocorticoid receptor, whereas mutation/deletion of the glucocorticoid receptor element (GRE) markedly impaired activation of the Ctr1 promoter. In addition, CORT-induced downregulation of Ctr1 promoter activity was markedly attenuated in Caco-2 cells when RU486 was added. These findings present a novel molecular target for CORT that down-regulates intestinal CTR1 expression via GR-mediated trans-repression in mice. Full article
(This article belongs to the Special Issue Effects of Environmental Stress on the Metabolic Dysfunction and Its Mechanism)
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