Anti-aging effects of caloric restriction: Involvement of neuroendocrine adaptation by peripheral signaling

Takuya Chiba, Haruyoshi Yamaza, Yoshikazu Higami, Isao Shimokawa

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Many hormonal signals from peripheral tissues contribute to the regulation of energy homeostasis and food intake. These regulators including leptin, insulin, and ghrelin, modulate the orexigenic and anorexigenic neuropeptide expression in hypothalamic nuclei. The anti-aging effects of caloric restriction have been explained from an evolutional viewpoint of the adaptive response of the neuroendocrine and metabolic response systems to maximize survival during periods of food shortage. In organisms, excess energy is stored in adipose tissues as a triglyceride preparation for such survival situations. Adipose tissue has recently been recognized as an endocrine organ, and leptin, as secreted by adipocyte, seems to be an especially important factor for the adaptive response to fasting and neuroendocrine alterations under caloric restriction. In this review, we discuss the potential involvement of neuroendocrine modulators in longevity and the anti-aging effects of caloric restriction.

Original languageEnglish
Pages (from-to)317-324
Number of pages8
JournalMicroscopy Research and Technique
Volume59
Issue number4
DOIs
Publication statusPublished - Nov 15 2002

Fingerprint

anti-aging properties
Caloric Restriction
leptin
adipose tissues
adipose tissue
constrictions
Aging of materials
Tissue
Leptin
ghrelin
food shortages
Adipose Tissue
energy
neuropeptides
food intake
fasting
adipocytes
homeostasis
insulin
Ghrelin

All Science Journal Classification (ASJC) codes

  • Anatomy
  • Histology
  • Instrumentation
  • Medical Laboratory Technology

Cite this

Anti-aging effects of caloric restriction : Involvement of neuroendocrine adaptation by peripheral signaling. / Chiba, Takuya; Yamaza, Haruyoshi; Higami, Yoshikazu; Shimokawa, Isao.

In: Microscopy Research and Technique, Vol. 59, No. 4, 15.11.2002, p. 317-324.

Research output: Contribution to journalArticle

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