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Resistance to cirrhotic lesions is a general characteristic of Western diet-based mouse models of NASH, possibly explained by mice not living long enough to develop manifest cirrhosis or, alternatively, have high capacity to handle dietary lipids and carbohydrates in the context of sustained nutrient overload that could otherwise exhaust liver regenerative responses and thereby perpetuate cirrhotic injury 52

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Microglial density was similarly significantly increased in both OHT-groups (OHT HBSS: 10.6 cells/0.01 mm 2 , OHT SEM: 9.1 cells/0.01 mm 2 ) compared to NT HBSS ((OHT HBSS) = 66.5%, p 0.05), but not as a variable

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