Insulin-Like Signaling, Nutrient Homeostasis, and Life Span (original) (raw)

Abstract

Insulin-like signaling is critical for nutrient homeostasis, growth and survival. However, work with lower metazoans—Caenorhabditis elegans and Drosophila—shows that reduced insulin-like signaling extends life span. In addition, reduced insulin signaling in higher animals—rodents and humans—causes glucose intolerance and hyperinsulinemia that progresses to diabetes and shortens the life span of affected individuals. Hyperinsulinemia usually develops to maintain glucose homeostasis and prevent the progression toward life-threatening type 2 diabetes; however, increased circulating insulin may have negative effects on the brain that promote age-related disease. We discuss the possibility that the brain is the site where reduced insulin-like signaling can consistently extend mammalian life span—just as reduced insulin-like signaling extends the life span of lower metazoans.

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/content/journals/10.1146/annurev.physiol.70.113006.100533

2008-03-17

2024-10-21

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