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Abstract <p>Hypothermia is a condition in which body temperature falls below 35&#xa0;°C, resulting from exposure to low environmental temperatures or underlying medical conditions. Postmortem examinations have revealed increased levels of fatty acids in blood and lipid droplet formation in renal tubules during hypothermia. However, the causes and implications of these findings are unclear. This study aimed to analyze the biological significance of these phenomena through lipidomics and transcriptomics analyses of specimens from emergency hypothermia patients and mouse hypothermia models. Both human hypothermia patients and murine models exhibited elevated plasma concentrations of fatty acids and their derivatives compared with controls. Hypothermic mouse kidneys displayed lipid droplet formation, with gene expression analysis revealing enhanced fatty acid uptake and β-oxidation in renal tubular cells. In primary cultured mouse renal proximal tubular cells, low temperatures increased the expression levels of Fatty acid transport protein 1 (FATP1), a fatty acid transporter, and boosted oxygen consumption via β-oxidation. Mice treated with FATP1 inhibitors showed a more rapid decrease in body temperature upon exposure to low temperatures compared with untreated mice. In conclusion, increased fatty acid uptake mediated by FATP1 in renal tubular cells plays a protective role during hypothermia.</p> Key messages <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Low temperatures increase FATP1 expression and fatty acid uptake in renal proximal tubular cells, resulting in enhanced β-oxidation.</p> </ItemContent> <ItemContent> <p>Renal proximal tubular cells play an important role in the resistance to hypothermia via lipid uptake.</p> </ItemContent> <ItemContent> <p>Maintaining renal lipid metabolism is essential for cold stress adaptation.</p> </ItemContent> </UnorderedList></p>

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FATP1-mediated fatty acid uptake in renal tubular cells as a countermeasure for hypothermia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月5日

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  • Kie Horioka,
  • Hiroki Tanaka,
  • Shimpei Watanabe,
  • Shinnosuke Yamada,
  • Shuhei Takauji,
  • Akira Hayakawa,
  • Shotaro Isozaki,
  • Keisuke Okaba,
  • Namiko Ishii,
  • Ayumi Motomura,
  • Hiroyuki Inoue,
  • Lynda Addo,
  • Daisuke Yajima,
  • Yoichiro Takahashi,
  • Henrik Druid,
  • Lasse Pakanen,
  • Katja Porvari

摘要

Abstract

Hypothermia is a condition in which body temperature falls below 35 °C, resulting from exposure to low environmental temperatures or underlying medical conditions. Postmortem examinations have revealed increased levels of fatty acids in blood and lipid droplet formation in renal tubules during hypothermia. However, the causes and implications of these findings are unclear. This study aimed to analyze the biological significance of these phenomena through lipidomics and transcriptomics analyses of specimens from emergency hypothermia patients and mouse hypothermia models. Both human hypothermia patients and murine models exhibited elevated plasma concentrations of fatty acids and their derivatives compared with controls. Hypothermic mouse kidneys displayed lipid droplet formation, with gene expression analysis revealing enhanced fatty acid uptake and β-oxidation in renal tubular cells. In primary cultured mouse renal proximal tubular cells, low temperatures increased the expression levels of Fatty acid transport protein 1 (FATP1), a fatty acid transporter, and boosted oxygen consumption via β-oxidation. Mice treated with FATP1 inhibitors showed a more rapid decrease in body temperature upon exposure to low temperatures compared with untreated mice. In conclusion, increased fatty acid uptake mediated by FATP1 in renal tubular cells plays a protective role during hypothermia.

Key messages

Low temperatures increase FATP1 expression and fatty acid uptake in renal proximal tubular cells, resulting in enhanced β-oxidation.

Renal proximal tubular cells play an important role in the resistance to hypothermia via lipid uptake.

Maintaining renal lipid metabolism is essential for cold stress adaptation.