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However, they have subtle, profound differences in how they interact with your bodys fat cellsspecifically regarding how they stimulate fat breakdown (lipolysis) versus how they stop new fat from forming (adipogenic inhibition)

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The persistent limitation is translational: rodent lipid handling differs from human physiology, and even the best diet models only partially recapitulate the slow, heterogeneous fibrotic progression seen in human MASH which is why an animal liver-fat signal is treated as hypothesis-generating rather than confirmatory