Abstract
NYGGF4 is a recently discovered gene that is involved in obesity-associated insulin resistance. The exact mechanism by which NYGGF4 induces insulin resistance has not yet been fully elucidated. In this study, we demonstrated that the overexpression of NYGGF4 in 3T3-L1 adipocytes decreased mitochondrial mass, mitochondrial DNA, and intracellular ATP synthesis. In addition, NYGGF4 overexpression also led to an imbalance of the mitochondrial dynamics and excess intracellular ROS production. Collectively, our results indicated that the overexpression of NYGGF4 caused mitochondrial dysfunction in adipocytes, which might be responsible for the development of NYGGF4-induced insulin resistance.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3-L1 Cells
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Adenosine Triphosphate / metabolism
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Adipocytes / metabolism*
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Adipocytes / pathology
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Animals
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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DNA, Mitochondrial / metabolism
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Insulin Resistance* / genetics
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Membrane Potential, Mitochondrial
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Mice
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Mitochondria / metabolism*
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Mitochondria / pathology
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Reactive Oxygen Species / metabolism
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Trans-Activators / metabolism
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Transcription Factors
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Transfection
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Up-Regulation
Substances
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Carrier Proteins
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DNA, Mitochondrial
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PID1 protein, human
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Ppargc1a protein, mouse
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Reactive Oxygen Species
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Trans-Activators
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Transcription Factors
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Adenosine Triphosphate