Recent research has shown that disrupting growth hormone signaling in mice can lead to extended lifespan, but the effects may not be as dramatic as in other well-known models. While mice with selective knockout of growth hormone still live longer, the increase is not as significant as in other genetic alterations. This highlights the complexity of cellular biochemistry and the multifunctional nature of proteins. Interestingly, human counterparts with Laron syndrome, a similar condition of growth hormone deficiency, do not exhibit the same lifespan extension. These findings suggest that while growth hormone plays a role in aging, there may be other factors at play influencing lifespan. Further studies are needed to fully understand the impact of growth hormone metabolism on longevity.
The somatotrophic axis, comprised of growth hormone (GH) and GH-releasing hormone (GHRH), plays a crucial role in regulating lifespan in mice. Genetic disruptions at various levels of this axis have shown significant extensions in longevity. However, it is important to note that mice labeled as “GH-deficient” often have additional genetic defects, complicating the direct assessment of growth hormone’s impact. Ames dwarf and Snell dwarf mice, for example, lack GH along with other hormones, making the specific contribution of GH unclear. Further studies with targeted disruptions of the GH gene have shown moderate extensions in lifespan, suggesting a more nuanced role for growth hormone in aging. These findings underscore the need for more research to unravel the complexities of growth hormone metabolism in relation to longevity.
