Leptin and Longevity: Blocking the consequences of lipid overload
R.H. Unger
Department of Internal Medicine, UT Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Y8.212, Dallas, TX 75390-8854, USA
Leptin mediates intracellular liporegulation in nonadipocytes and
adipocytes, and, by maintaining intracellular homeostasis, influences
the ability of cells to withstand disease-causing environmental
perturbations. Leptin effectively partitions FA surplus into
adipocytes through its central action, which limits the magnitude of
overnutrition to fit into the slowly expanding adipocyte storage space,
and through a peripheral action to increase oxidation of surplus fatty
acids (FA). Failure of lipid partitioning leads to lipid overload,
dysfunction and apoptosis in organs that are involved in the metabolic
syndrome, and apoptosis due to non-lipid factors may be lipid-requiring
and therefore preventable by lowering intracellular lipids, an action
which others have attribute to at least 2 longevity genes. Exploration
of these pathways may provide novel strategies and treat and prevent
disease and prolong life.
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