Deletion, but not antagonism, of the mouse growth hormone receptor results in severely decreased body weights, insulin, and insulin-like growth factor I levels and increased life span.
Level 5 - mechanism / opinion, no new human data
Animal comparative study (non-human laboratory model)
PubMed 12933651 · doi:10.1210/en.2003-0374
What was done
Researchers compared two dwarf mouse models on the same C57BL/6J genetic background: mice expressing a growth hormone antagonist (GHA) and mice with targeted disruption of the growth hormone receptor/binding protein gene (GHR -/-). They assessed post-weaning weight gain profiles, fasting insulin and glucose levels, circulating insulin-like growth factor I (IGF-I), IGF binding proteins (IGFBP-1 through -4), and overall lifespan.
What was found
The abstract reports directional comparisons without numerical values: - Body weight: GHA dwarf weights gradually approached control weights over time, whereas GHR -/- mice remained underweight throughout the analysis period. - Metabolism: Fasting insulin and glucose levels were reduced in GHR -/- mice but normal in GHA mice. - IGF axis: IGF-I and IGFBP-3 were significantly reduced in both lines (by different degrees). IGFBP-1 and -4 levels decreased and IGFBP-2 levels increased in GHR -/- mice, while remaining unaltered in GHA mice. - Lifespan: Life span was significantly extended in GHR -/- mice but remained unchanged in GHA dwarf mice.
Why it matters
This study demonstrates that the degree of growth hormone signaling blockade produces fundamentally different metabolic profiles and longevity outcomes in a mammalian model.
Limits
The study was conducted entirely in mice, limiting direct translation to human aging. The abstract provides no exact sample sizes, numerical values for biochemical assays, or survival metrics.
Cited by
- supports Mice with growth hormone receptor deficiency or growth hormone deficiency live approximately 40% longer than control mice.