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Abstract
In this review, we propose that actions of the lipid-lowering, apoptosis-inhibiting
effects of certain "longevity genes" oppose the life-shortening consequences of lipotoxicity
and lipoapoptosis. We note that lipotoxicity occurs whenever leptin action is deficient,
or whenever satiety is overridden, as in forced or voluntary overfeeding ("supersizing").
The role of hyperleptinemia, we suggest, is to extend survival during famine by permitting
the storage of surplus calories in adipocytes without concomitant injury to nonadipose
tissues from ectopic lipid deposits. It achieves this lipid partitioning by (1) restraining
the level of overnutrition so as not to exceed the available adipocyte storage space
and (2) enhancing oxidation of any ectopic lipid overflow: The mechanisms of lipoapoptosis
are discussed, and the possibility that metabolic syndrome is the human equivalent
of rodent lipotoxicity is suggested.