Longevity, lipotoxicity and leptin

The adipocyte defense against feasting and famine

Research output: Contribution to journalArticle

110 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)57-64
Number of pages8
JournalBiochimie
Volume87
Issue number1 SPEC. ISS.
DOIs
StatePublished - Jan 2005

Fingerprint

Starvation
Leptin
Adipocytes
Lipids
Overnutrition
Choristoma
Rodentia
Deposits
Genes
Tissue
Apoptosis
Oxidation
Survival
Wounds and Injuries

Keywords

  • Apoptosis
  • Ceramide
  • Leptin
  • Lipodystrophy
  • Lipotoxicity
  • Longevity
  • Metabolic syndrome
  • Obesity

ASJC Scopus subject areas

  • Biochemistry

Cite this

Longevity, lipotoxicity and leptin : The adipocyte defense against feasting and famine. / Unger, Roger H.

In: Biochimie, Vol. 87, No. 1 SPEC. ISS., 01.2005, p. 57-64.

Research output: Contribution to journalArticle

@article{a4859e25554c4b8493bba7789ea12b2d,
title = "Longevity, lipotoxicity and leptin: The adipocyte defense against feasting and famine",
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.",
keywords = "Apoptosis, Ceramide, Leptin, Lipodystrophy, Lipotoxicity, Longevity, Metabolic syndrome, Obesity",
author = "Unger, {Roger H}",
year = "2005",
month = "1",
doi = "10.1016/j.biochi.2004.11.014",
language = "English (US)",
volume = "87",
pages = "57--64",
journal = "Biochimie",
issn = "0300-9084",
publisher = "Elsevier",
number = "1 SPEC. ISS.",

}

TY - JOUR

T1 - Longevity, lipotoxicity and leptin

T2 - The adipocyte defense against feasting and famine

AU - Unger, Roger H

PY - 2005/1

Y1 - 2005/1

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Ceramide

KW - Leptin

KW - Lipodystrophy

KW - Lipotoxicity

KW - Longevity

KW - Metabolic syndrome

KW - Obesity

UR - http://www.scopus.com/inward/record.url?scp=14544279805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14544279805&partnerID=8YFLogxK

U2 - 10.1016/j.biochi.2004.11.014

DO - 10.1016/j.biochi.2004.11.014

M3 - Article

VL - 87

SP - 57

EP - 64

JO - Biochimie

JF - Biochimie

SN - 0300-9084

IS - 1 SPEC. ISS.

ER -