Study summary · research use only
IGF-I regulates the age-dependent signaling peptide humanin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using mouse models with altered growth hormone (GH)/insulin-like growth factor-1 (IGF) axis, the authors examined the signaling peptide humanin. The abstract reports a negative correlation between GH-IGF axis activity and humanin levels and a positive correlation between humanin and lifespan: long-lived GH-deficient Ames mice had elevated humanin, while short-lived GH-transgenic mice had reduced humanin. It states that treatment with GH or IGF-I reduced circulating humanin levels in both mice and human subjects. The authors conclude GH and IGF regulate humanin, suggesting humanin is a circulating mitochondrial signal participating in the aging process.
Abstract
Aging is influenced by endocrine pathways including the growth hormone/insulin-like growth factor-1 (GH/IGF) axis. Mitochondrial function has also been linked to the aging process, but the relevant mitochondrial signals mediating the effects of mitochondria are poorly understood. Humanin is a novel signaling peptide that acts as a potent regulator of cellular stress responses and protects from a variety of in vitro and in vivo toxic and metabolic insults. The circulating levels of humanin decline with age in mice and humans. Here, we demonstrate a negative correlation between the activity of the GH-IGF axis and the levels of humanin, as well as a positive correlation between humanin and lifespan in mouse models with altered GH/IGF-I axis. Long-lived, GH-deficient Ames mice displayed elevated humanin levels, while short-lived GH-transgenic mice have reduced humanin levels. Furthermore, treatment with GH or IGF-I reduced circulating humanin levels in both mice and human subjects. Our results indicate that GH and IGF are potent regulators of humanin levels and that humanin levels correlate with lifespan in mice. This suggests that humanin represents a circulating mitochondrial signal that participates in modulating the aging process, adding a coordinated mitochondrial element to the endocrine regulation of aging.
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