Lipoapoptosis: Its mechanism and its diseases

Roger H Unger, Lelio Orci

Research output: Contribution to journalReview articlepeer-review

309 Scopus citations


The balance between cell division and cell death determines the cell population of an organ. When cell death exceeds cell replacement in an organ, a functional deficit is created. A metabolic cause of programmed cell death, lipoapoptosis, has recently been identified to occur in obesity and aging. If nonadipose tissues are exposed to an excess of long-chain fatty acids, unless leptin action increases their oxidation sufficiently, unoxidized fatty acids enter nonoxidative pathways. While initially they are sequestered as harmless neutral fat, ultimately some will enter more toxic pathways. One of these, the de novo ceramide pathway, has been implicated in the lipoapoptosis of β-cells and myocardiocytes of congenitally obese rats in which leptin action is defective. Here we review the mechanisms of lipoapoptosis and the diseases that result from this cause of a diminishing cell population of these organs. We suggest that some of the components of the metabolic syndrome of obese humans and the sarcopenia of aging may be result of failure of leptin liporegulation to prevent lipid overload of lean body mass and lipoapoptosis in certain organ systems.

Original languageEnglish (US)
Pages (from-to)202-212
Number of pages11
JournalBiochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
Issue number2-3
StatePublished - Dec 30 2002


  • Lipoapoptosis
  • Obesity
  • β Cell

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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