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. 2004 Feb 9;101(7):2058–2063. doi: 10.1073/pnas.0308258100

Fig. 5.

Fig. 5.

Comparison of the effects of endogenous (adipocyte-derived; Left) and ectopic (liver-derived; Right) hyperleptinemia on white adipocyte morphology. (Left) As obesity develops, the accumulation of triglycerides is accompanied by progressively increasing hyperleptinemia. The fat-burning action of the hyperleptinemia on the adipocytes is completely blocked, possibly by factor(s) that are coexpressed with leptin. This blockade preserves the physiologic mission of the adipocytes, which is to store fat so as to provide fat fuel during famine. (Right) When the hyperleptinemia is ectopically derived, as in normal rats treated with recombinant adenovirus containing the leptin cDNA, there is no blockade of leptin action on adipocytes. Liver-derived hyperleptinemia rapidly transforms adipocytes into mitochondria-rich, fat-burning postadipocytes that are essentially fatless.

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