ArticleAmerican journal of physiology. Endocrinology and metabolism2023
GCN2 is required to maintain core body temperature in mice during acute cold.
Article in American journal of physiology. Endocrinology and metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- A metabolic basis for motor deficits in mice lacking BCKDK.The Journal of nutritional biochemistry · 2026Article
- Therapeutic effects of cold plasma-activated water on MCF7 breast cancer tumors in a mouse model.BMC pharmacology & toxicology · 2026Article
- YTHDC1 promotes postnatal brown adipose tissue development and thermogenesis by stabilizing PPARγ.The EMBO journal · 2025Article
- DELE1 maintains muscle proteostasis to promote growth and survival in mitochondrial myopathy.The EMBO journal · 2024Article
- DELE1 promotes translation-associated homeostasis, growth, and survival in mitochondrial myopathy.bioRxiv : the preprint server for biology · 2024Article
- ATF4 expression in thermogenic adipocytes is required for cold-induced thermogenesis in mice via FGF21-independent mechanisms.Scientific reports · 2024Article
- Hyperactive browning and hypermetabolism: potentially dangerous element in critical illness.Frontiers in endocrinology · 2024Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Nonshivering thermogenesis in rodents requires macronutrients to fuel the generation of heat during hypothermic conditions. In this study, we examined the role of the nutrient sensing kinase, general control nonderepressible 2 (GCN2) in directing adaptive thermogenesis during acute cold exposure in mice. We hypothesized that GCN2 is required for adaptation to acute cold stress via activation of the integrated stress response (ISR) resulting in liver production of FGF21 and increased amino acid transport to support nonshivering thermogenesis. In alignment with our hypothesis, female and male mice lacking GCN2 failed to adequately increase energy expenditure and veered into torpor. Mice administered a small molecule inhibitor of GCN2 were also profoundly intolerant to acute cold stress.
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