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- W8969960 abstract "Ultrastructural analysis of lipid vesicle populations by TEM and light microscopy show lipid trafficking patterns in normal and obese mice (C57BL/6J lep ob) treated for 9 days with combinations of leptin, thyroid hormone (T3), iopanoic acid (reduces thyroxine deiodination), and 6-Hydroxydopamine (blocks peripheral sympathetic neurons). Hepatic lipids selectively traffick into the VLDL export pathways in response to hormones that characterize a well-fed nutritional status (leptin and T3) but are diverted to a distinct microvesicular pool with hypernutrition (elevated T3). Endocrine profiles associated with hyponutrition (low 5′Monodeiodinase activity, decreased T3, leptin deficiency) promote macrovesicular storage due to reduced VLDL export and/or reduced adrenergic receptor-mediated macrovesicle breakdown. In the case of nonalcoholic fatty liver disease (NAFLD), it is likely that the bottlenecking of VLDLs at the site of export leads to excess microvesicular storage or, alternatively, a reduction in macrovesicular breakdown for VLDL export. We propose an integrated model of hepatic lipid trafficking in which leptin promotes mobilization of both stored and newly-synthesized lipids into the VLDL export pathway through direct and sympathetic-mediated mechanisms while T3 directly promotes lipogenesis and microvesicle formation plus indirectly retains both micro- and macrovesicles." @default.
- W8969960 created "2016-06-24" @default.
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- W8969960 date "2007-04-01" @default.
- W8969960 modified "2023-09-26" @default.
- W8969960 title "Leptin and Thyroid Hormone Regulate Hepatic Lipid Trafficking into Macro‐ and Microvesicular Pools" @default.
- W8969960 doi "https://doi.org/10.1096/fasebj.21.5.a699-c" @default.
- W8969960 hasPublicationYear "2007" @default.
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