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. 2006 Jun 2;28(2):163–171. doi: 10.1007/s11357-006-9007-7

Do long-lived mutant and calorie-restricted mice share common anti-aging mechanisms?—a pathological point of view

Yuji Ikeno 1,2,3,, Christie M Lew 1,2, Lisa A Cortez 1,2, Celeste R Webb 1,2, Shuko Lee 3, Gene B Hubbard 4
PMCID: PMC2464730  PMID: 19943137

Abstract

Rodent models are an invaluable resource for studying the mechanism of mammalian aging. In recent years, the availability of transgenic and knockout mouse models has facilitated the study of potential mechanisms of aging. Since 1996, aging studies with several long-lived mutant mice have been conducted. Studies with the long-lived mutant mice, Ames and Snell dwarf, and growth hormone receptor/binding protein knockout mice, are currently providing important clues regarding the role of the growth hormone/insulin like growth factor-1 axis in the aging process. Interestingly, these studies demonstrate that these long-lived mutant mice have physiological characteristics that are similar to the effects of calorie restriction, which has been the most effective experimental manipulation capable of extending lifespan in various species. However, a question remains to be answered: do these long-lived mutant and calorie-restricted mice extend their lifespan through a common underlying mechanism?

Key words: aging, growth hormone receptor/binding protein, knockout mouse, neoplastic disease

Abbreviations

CR

caloric restriction

GH

growth hormone

GHR

growth hormone receptor

GHR/BP

growth hormone receptor/binding protein

KO

knockout

PRL

prolactin

IGF-1

insulin-like growth factor-1

TSH

thyroid stimulating hormone

T3

triiodo-thyronnine

T4

thyroxine

AL

ad libitum

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