R.H. Unger

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.

Keywords (Optional):