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Submitted on April 11, 2005
Accepted on May 17, 2005
Depts. of Physiology and Internal Medicine, Southern Illinois University School of Medicine
* To whom correspondence should be addressed. E-mail: abartke{at}siumed.edu.
The important role of insulin-like growth factor (IGF) and insulin related signaling pathways in the control of longevity of worms and insects is very well documented. In the mouse, several spontaneous or experimentally-induced mutations that interfere with growth hormone (GH) biosynthesis, GH actions, or sensitivity to IGF-1 lead to extended longevity. Increases in the average life span in these mutants range from approximately 20% to 70% depending on the nature of the endocrine defect, gender, diet, and/or genetic background. Extended longevity of hypopituitary and GH resistant mice appears to be due to multiple mechanisms including reduced insulin levels, enhanced insulin sensitivity, alterations in carbohydrate and lipid metabolism, reduced generation of reactive oxygen species, enhanced resistance to stress, reduced oxidative damage, and delayed onset of age-related disease. There is considerable evidence to suggest that the genetic and endocrine mechanisms that influence aging and longevity in mice may play a similar role in other mammalian species, including the human.
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