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SUMMARY
Somatomedins are the intermediaries through which growth hormone acts on the epiphyseal growth plate to effect linear skeletal growth.
Rat epiphyseal chondrocytes were isolated and cultured in vitro in the presence of somatomedin. Two sources of somatomedin were used, foetal calf serum and rat liver perfusates. The chondrocytes proliferated and synthesized sulphated glycosaminoglycans when grown in the presence of somatomedin from either source, but were not metabolically active in chemically defined medium alone. Some differences in the growth patterns in response to serum or liver somatomedins are reported and discussed.
Chondrocyte metabolic activity in the presence of somatomedin in vitro showed a graded response to alterations in the atmospheric oxygen, being greatest at low oxygen pressure, and almost completely inhibited at 95% oxygen. A gradient of local oxygen tension has been reported to exist across the epiphyseal plate in vivo. The effects of somatomedin combined with changing oxygen levels may help to explain the divergence of cell proliferation and matrix synthesis seen in the various regions of the growth plate.
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Search for other papers by M. J. O. FRANCIS in
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SUMMARY
Plasma somatomedin is the intermediary through which growth hormone (GH) exerts its effects on the growing skeleton. Somatomedin activity may be produced in vitro by perfusion of the liver and kidneys of rats with Waymouth's medium containing GH. The relationship between the activity of plasma somatomedin and somatomedin of hepatic and renal origin has yet to be clarified. Somatomedin from plasma can be separated into active fractions of both high and low molecular weight. Similarly, ultrafiltration of medium containing somatomedin of hepatic origin indicates the existence of two active fractions, one of high molecular weight (greater than 50000) and one of low molecular weight (less than 1000). The latter can be attributed to the release of amino acids, such as serine and glutamine, by the perfused tissue. The high molecular weight fraction is believed to represent GH-dependent somatomedin. Fractions that inhibit production of cartilage matrix are present in liver perfusates as well as in plasma.
These results provide further evidence that the liver is a source of GH-dependent somatomedin in vivo. Furthermore, cartilage growth may be controlled not only by the GH-stimulated release of somatomedin by the liver, but also by its release of acid-labile somatomedin inhibitors.
