Insulin paradox, aging, bone health and growth in the context of mitochondrial function
Insulin paradox and bone health
Abstract
Insulin paradox has recently been reported to show up in more than expected scientific investigations. This puzzle has also involved studies in bone health and longevity. Increase in lifespan of mice and c. elegans knockouts of growth hormone receptor gene has opened an interesting area of research. To this effect, an interesting paper [1] seems to integrate certain cardinal aspects of aging, bone health, and growth with mitochondrial function and insulin; indicating role for insulin signaling at several levels in differentiation, growth and maintenance of osteocytes and life span determination. It has been found that growth hormone receptor knockout (GHRKO) mice display increased insulin, insulin like growth factor-1 (IGF-1), cytoplasmic/mitochondrial reactive oxygen species (ROS), life span and decreased mitochondrial membrane potential, glucose transporter-1 (GLUT-1) expression, steady state ATP, NADH redox index, glutathione, oxygen consumption rate, mitochondrial reserve capacity and skeletal health span [1, 2]. Association of increased insulin and IGF-1 with extended life span is a novel finding seemingly not in agreement with previous reports [3]. An imperative facet of these findings is reduced mitochondrial volumetric density and mitochondrial intensity density in vivo with a parallel finding of no reduction in mitochondrial volumetric density and reduced mitochondrial intensity density in the primary osteocyte cultures.
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References
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