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LPIAT1/MBOAT7 depletion increases triglyceride synthesis fueled by high phosphatidylinositol turnover

As the other mechanism, the hypothalamic inflammation, the role of endoplasmic reticulum stress and defective autophagy are suggested to be involved

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These basic and translational neuroscience findings point to this mitochondrial signaling pathway as a potential target to identify novel mechanisms of brain plasticity and potential unique targets for therapeutic intervention targeted to specific clinical phenotypes

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