ArticleJournal of animal science2018
Cytosolic phosphoenolpyruvate carboxykinase is a response gene involved in porcine adipocyte adaptation to heat stress.
Article in Journal of animal science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Comparative ubiquitinome analysis reveals the roles of protein ubiquitination in the heat stress response fromApplied and environmental microbiology · 2025Article
- Phosphoenolpyruvate Carboxykinase (PCK) in the Brain Gluconeogenic Pathway Contributes to Oxidative and Lactic Injury After Stroke.Molecular neurobiology · 2021Article
- Temperature training improves transcriptional homeostasis after heat shock in juvenile Atlantic sturgeon (Acipenser oxyrinchus).Fish physiology and biochemistry · 2020Article
- Chronic heat treatment positively impacts metabolic profile of ovariectomized rats: association with heat shock response pathways.Cell stress & chaperones · 2020Article
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Authors and funding
2 authors.
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Abstract
Heat stress (HS) leads to increased lipid storage and expression of cytosolic phosphoenolpyruvate carboxykinase (PCK1) in pig adipocytes. However, the importance of PCK1 activation and lipid storage in the adaptive response to HS is unknown. Therefore, in vitro experiments were conducted to investigate the effect of PCK1 inhibition with 3-mercaptopicolinic acid (3MPA) on lipid storage and adipocyte response during HS. In vitro culture of adipocytes under HS (41.0 °C) increased (P < 0.05) triacylglycerol accumulation compared with control (37.0 °C). HS increased (P < 0.05) reactive oxygen species level and 3MPA further upregulated (P < 0.05) its level. Heat shock protein 70 (HSP70) gene expression was induced (P < 0.05) by HS compared to control, and PCK1 inhibition with 3MPA attenuated (P < 0.05) its induction by HS. The endoplasmic reticulum (ER) stress markers, C/EBP homologous protein (CHOP) was also upregulated by HS and 3MPA further upregulated (P < 0.05) CHOP mRNA level. These results suggest that with inhibition of PCK1 during HS, in vitro cultured adipocytes were less able to induce adaptive responses such as upregulation of HSP70 and triglycerides, and this exacerbated ER stress during HS. Thus, PCK1 may function to alleviate ER stress that occurs during HS.
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