Short-term exposure to heat stress attenuates appetite and intestinal integrity in growing pigs1

Pearce, Sarah; Fernández, M. V. Sanz; Hollis, James; Baumgard, Lance H.; Gabler, Nicholas K.

doi:10.2527/jas.2014-8407

Cited by 146 publications

(147 citation statements)

References 43 publications

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“…2014). Briefly, animals increased core temperature from 39.2 ± 0.1°C (thermoneutral group) to approximately 41.2 ± 0.1°C at 2 h and remain elevated at 4 h, and 6 h of heat stress ( P < 0.05).…”

Section: Resultsmentioning

confidence: 99%

“…2003; Pearce et al. 2013c, 2014) and agricultural economics (St‐Pierre et al. 2003; Key et al 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Despite apparent changes in circulating TNF α in the same pigs (Pearce et al. 2014), skeletal muscle TNF α abundance following 6 h of heat stress is ostensibly independent of NF‐ κ B signaling.…”

Section: Discussionmentioning

confidence: 99%

“…Germane to this investigation, heat stress resulted in a progressive increase in endotoxemia concomitant with intestinal damage and leakage (Pearce et al. 2014). While it is likely that endotoxemia contributed to inflammatory signaling in these muscles the possibility of other mediators cannot be eliminated.…”

Section: Discussionmentioning

confidence: 99%

“…A detailed experimental design and phenotypic data have been previously published (Pearce et al. 2014). Briefly, 32 gilts with average body weight of 63.8 ± 2.9 kg were randomly assigned to four groups.…”

Section: Methodsmentioning

confidence: 99%

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Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

et al. 2017

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Despite well‐studied clinical manifestations, intracellular mechanisms of prolonged hyperthermic injury remain unclear, especially in skeletal muscle. Given muscle's large potential to impact systemic inflammation and metabolism, the response of muscle cells to heat‐mediated injury warrants further investigation. We have previously reported increased activation of NF‐κB signaling and increased NF‐κB and AP‐1‐driven transcripts in oxidative skeletal muscle following 12 h of heat stress. The purpose of this investigation was to examine early heat stress‐induced inflammatory signaling in skeletal muscle. We hypothesized that heat stress would increase NF‐κB and AP‐1 signaling in oxidative skeletal muscle. To address this hypothesis, 32 gilts were randomly assigned to one of four treatment groups (n = 8/group): control (0 h: 21°C) or exposed to heat stress conditions (37°C) for 2 h (n = 8), 4 h (n = 8), or 6 h (n = 8). Immediately following environmental exposure pigs were euthanized and the red portion of the semitendinosus muscle (STR) was harvested. We found evidence of NF‐κB pathway activation as indicated by increased protein abundance of NF‐κB activator IKK‐α following 4 h and increased total NF‐κB protein abundance following 6 h of heat stress. Heat stress also stimulated AP‐1 signaling as AP‐1 protein abundance was increased in nuclear fractions following 4 h of heat stress. Interleukin‐6 protein abundance and activation of the JAK/STAT pathway were decreased in heat stressed muscle. These data indicate that heat stress activated inflammatory signaling in the porcine STR muscle via the AP‐1 pathway and early activation of the NF‐κB pathway.

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Section: Resultsmentioning

confidence: 99%

“…2003; Pearce et al. 2013c, 2014) and agricultural economics (St‐Pierre et al. 2003; Key et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

et al. 2017

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Heat stress induced IPEC‐J2 cells barrier dysfunction through endoplasmic reticulum stress mediated apoptosis by p‐eif2α/CHOP pathway

Cui

Chen

Zhou

et al. 2021

Journal Cellular Physiology

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Heat stress (HS) induced by high ambient temperatures compromises intestinal epithelial cell. However, the underlying mechanisms by which HS causes intestinal barrier dysfunction remain unclear. In this study, we established an in vitro acute-HS-induced intestinal damage using porcine small intestinal epithelial cell (IPEC-J2) that exposed to the high temperatures (43°C) for 2 h. The cell proliferation, apoptosis, tight junction (TJ) barrier integrity and transcriptomic profiles were measured. The results showed that HS decreased cell viability while increased proapoptotic signaling evidenced by Bax/bcl2 ratio, cytochrome C release to cytosol and active-caspase 3 increases (p < 0.01). HS led to decreased transepithelial electrical resistance, increased cell permeability, and downregulated TJ proteins including ZO1, occludin, and claudin 3 (p < 0.05). Transcriptome sequencing and KEGG pathway analysis revealed HS-induced cell cycle arrest and activation of endoplasmic reticulum stress (ERS) response mediated by a critical transcript eif2α and proapoptotic molecule DDIT3 (known as CHOP). Furthermore, inhibition of ERS by 4-phenylbutyrate (4-PBA) administration and knockdown of eif2α and CHOP significantly attenuated IPEC-J2 cells apoptosis (p < 0.05). Transmission electron microscopy analysis suggested that 4-PBA inhibited HS-induced increase in ER lumen diameter, indicating ultrastructural sign of ERS. In addition, HS-induced impairment of TJs was significantly attenuated by 4-PBA (p < 0.05). Collectively, HS induces ERS and activates the p-eif2α/CHOP signaling pathway to impair epithelial barrier integrity through triggering the intestinal epithelial cell apoptosis.

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Proteomic changes of the porcine skeletal muscle in response to chronic heat stress

et al. 2018

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The results indicate that HS-induced changes in the expression of myofibrillar proteins, glucose and energy metabolism-related proteins, heat shock protein and antioxidant enzymes might, at least partly, contribute to increase in meat tenderness. These findings will provide the foundation for developing future mitigating solutions and preventative therapies to reduce the detrimental effects of chronic HS on muscle function, metabolism and meat quality. © 2017 Society of Chemical Industry.

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Short-term exposure to heat stress attenuates appetite and intestinal integrity in growing pigs1

Cited by 146 publications

References 43 publications

Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

Heat stress induced IPEC‐J2 cells barrier dysfunction through endoplasmic reticulum stress mediated apoptosis by p‐eif2α/CHOP pathway

Proteomic changes of the porcine skeletal muscle in response to chronic heat stress

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