Journal
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume 64, Issue 2, Pages 67-75Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-19-0207
Keywords
HSP60; ER stress; mitochondrial stress; mTORC1-SREBP1 signaling; hepatic lipogenesis
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Funding
- National Nature Science Foundation of China [91957113, 31871180, 31471131, 81800758]
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Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are associated with hepatic steatosis and insulin resistance. Molecular mechanisms underlying ER stress and/or mitochondrial dysfunction that cause metabolic disorders and hepatic steatosis remain to be fully understood. Here, we found that a high fat diet (HFD) or chemically induced ER stress can stimulate mitochondrial stress protein HSP60 expression, impair mitochondrial respiration, and decrease mitochondrial membrane potential in mouse hepatocytes. HSP60 overexpression promotes ER stress and hepatic lipogenic protein expression and impairs insulin signaling in mouse hepatocytes. Mechanistically, HSP60 regulates ER stress-induced hepatic lipogenesis via the mTORC1-SREBP1 signaling pathway. These results suggest that HSP60 is an important ER and mitochondrial stress cross-talking protein and may control ER stress-induced hepatic lipogenesis and insulin resistance.
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