The role of fat depletion in the biological benefits of caloric restriction

Nir Barzilai, I. Gabriely

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

One of the most robust observations in the biology of aging is that caloric restriction (CR) extends life in a variety of species. Although CR results in substantial decrease in fat mass, the role of fat in life extension was considered minimal. Indeed, in the fields of obesity and diabetes, the amount of fat has been directly implicated in the metabolic consequences. Since it became apparent that fat is a massive endocrine tissue, some of its roles have been recently revised. Many of the systemic effects of CR can now be explained by the chronic effects related to decreased plasma levels of peptides, cytokines, complement factors and substrates that are produced in fat. Most of the benefits of CR on the neuroendocrine system and those related to the improvement in glucose homeostasis can be attributed to a decrease in adipose cells and their products. If all or most of the life-extending benefits of CR can be attributed to decreased fat stores, the expression of specific candidate substrates and proteins may be explored and manipulated in searching for the most powerful adipose-dependent signals that modulate life expectancy.

Original languageEnglish (US)
JournalJournal of Nutrition
Volume131
Issue number3
StatePublished - 2001

Fingerprint

Caloric Restriction
Fats
lipids
Life Expectancy
neurosecretory system
Neurosecretory Systems
diabetes
long term effects
homeostasis
complement
obesity
Homeostasis
cytokines
Obesity
peptides
Cytokines
Glucose
Biological Sciences
Peptides
glucose

Keywords

  • Caloric restriction
  • Fat mass
  • Fat-derived peptides
  • Insulin sensitivity
  • Obesity
  • Visceral fat

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

The role of fat depletion in the biological benefits of caloric restriction. / Barzilai, Nir; Gabriely, I.

In: Journal of Nutrition, Vol. 131, No. 3, 2001.

Research output: Contribution to journalArticle

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