Abstract
Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Caveolae / metabolism
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Caveolin 1 / genetics
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Caveolin 1 / physiology*
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Cell Cycle
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Cell Division
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Fatty Acids / blood
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Fatty Acids / metabolism
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Glucose / administration & dosage
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Hepatectomy
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Hepatocyte Growth Factor / metabolism
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Hepatocytes / cytology
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Hepatocytes / metabolism*
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Lipid Metabolism*
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Lipids / blood
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Liver / metabolism
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Liver / ultrastructure
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Liver Regeneration*
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Male
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Mice
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Phosphorylation
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RNA, Small Interfering
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STAT3 Transcription Factor / metabolism
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Signal Transduction
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Triglycerides / blood
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Triglycerides / metabolism
Substances
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Caveolin 1
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Fatty Acids
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Lipids
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RNA, Small Interfering
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STAT3 Transcription Factor
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Stat3 protein, mouse
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Triglycerides
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Hepatocyte Growth Factor
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Glucose