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Fig. 5 | Lipids in Health and Disease

Fig. 5

From: Pathophysiological importance of bile cholesterol reabsorption: hepatic NPC1L1-exacerbated steatosis and decreasing VLDL-TG secretion in mice fed a high-fat diet

Fig. 5

Schematic illustration of the proposed model for hepatic NPC1L1-mediated steatosis induction. Hepatic NPC1L1-mediated steatosis can be characterized by at least three features that occur sequentially: (1) involvement of multiple cytotoxic factors that could be trigged by lipid overloading mediated by hepatic NPC1L1 localized on the bile canalicular membrane of hepatocytes; (2) activation of innate immune system and the TLR4-mediated pathway during the early progression of the steatosis; and (3) decreased hepatic ability of very low-density lipoprotein (VLDL)-triglyceride (TG) secretion would contribute to the rapid accumulation of hepatic TG

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Lipids in Health and Disease

ISSN: 1476-511X