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The intermediates from de novo lipogenesis in the liver will disrupt mitochondrial function and produce ROS, and then cause endoplasmic reticulum (ER) stress, ultimately leading to inflammation, and the broken cells releasing cytokines will cause more cell death ( The excess free fatty acids (FFAs) and de novo lipogenesis would break the homeostasis of lipid metabolism

11 , e201700377 (2018)

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Preclinical research summary The main evidence includes: (1) studies in tendons that link BPC-157 with cell growth, survival and migration [1]

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