The Merits of Late Life Suppression of Growth Hormone Signaling

The longest lived mice are those in which growth hormone or growth hormone receptor are knocked out, a gain of 70% or so in life span. They exhibit dwarfism, like the human population with the analogous inherited Laron syndrome, caused by a loss-of-function mutation in growth hormone receptor. The Laron syndrome population may be somewhat more resistant to some age-related diseases, that data still to be rigorously confirmed, but do not appear to live any longer than the rest of us. Studies on growth hormone metabolism and longevity conducted in mice should be read with that in mind, particularly when used to advocate therapeutic approaches. One of the most potent interventions used to extend lifespan in laboratory mice is targeted disruption of the growth hormone (GH) receptor (GHR). In fact, the current record holder for the Methuselah Mouse Prize for Longevity - a mouse that lived one week shy of five years - is the GHR "knockout" (GHRKO) mouse. A new study by our laboratory suggests that partial knockdown of the GHR beginning at 6 months of age can also extend median and maximal lifespan in female mice. GH secretion decreases with age (referred to as somatopause), causing some to consider the use of GH replacement as a means to counteract aging-related conditions. Counterintuitively, diminished GH action in model organisms, either by way of natural mutations or inactivation of the GH or GHR genes, increases lifespan and slows the aging process through reducing IG...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs