The Influence of Growth Hormone on Bone and Adipose Programming.

“In utero growth hormone exposure is associated with distinct immediate growth responses and long term impacts on adult physiological parameters that include obesity, insulin resistance, and bone function. Growth hormone accelerates cellular proliferation in many tissues but is exemplified by increases in the number of cells within the cartilaginous growth plate of bone{can it increase the number of growth plate progenitor cells?}. In some cases growth hormone also potentiates differentiation as seen in the differentiation of adipocytes that rapidly fill upon withdrawal of growth hormone. Growth hormone provokes these changes either by direct action or through intermediaries such as insulin-like growth factor-I and other downstream effector molecules. The specific mechanism used by growth hormone in programming tissues is not yet fully characterized and likely represents a multipronged approach involving DNA modification, altered adult hormonal milieu, and the development of an augmented stem cell pool capable of future engagement as is seen in adipose accrual.”

“Early therapeutic provision of GH to SGA[small for gestational age] neonates having sufficient GH enhances the velocity of bone growth transiently but only for the duration of GH treatment”

“between birth and 28 days is most influential on bone elongation and adult size. Initiating the elevated GH beyond 28 days of age increases growth but not to the
extent realized with earlier exposure despite the presence of a functional growth plate. At the cellular level, GH accelerates bone growth by hyperplasia[an increase in the number of cells] as opposed to growth plate chondrocyte hypertrophy”<-hyperplasia is more powerful than chondrocyte hyertrophy if it increases the amount of growth plate progenitor cells.  If it only increases chondrocyte proliferation then the effect is transient as chondrocytes have a finite proliferative capacity.