UNLABELLED: It is well documented that growth hormone (GH) functions to regulate both cell growth and cell number and is considered the master hormone because it affects almost every cell of the body. Growth hormone stimulates the liver to secrete insulin-like growth factor (IGF-1), which is also capable of binding insulin as well as insulin-like binding receptors on the cell surface. It is possible that GH cellular effects are mediated by IGF-1 rather than GH itself. In this study, RAW 264.7 cells were challenged with a high dose of GH (48 ng/microliter), a low of dose GH (4.8 ng/microliter), a high dose of IGF-1 (26 ng/microliter) or low doses of IGF-1 (6.3 ng/microliter) for 24, 48, 72, and 96 hours. Cell number, cell protein concentration, cell damage, and cellular morphology were measured at each time point and compared to untreated RAW 264.7 cells. The results show significant increases in cell number for cells treated with low doses of GH and IGF-1 at 24 hour phase. Cell proliferative effects were also observed at 48 hours in IGF-1 treated cells. Cellular damage (MDA levels) was not statistically significant for any treated group for the entire duration of the experiment. Most notable differences were observed in cellular morphology for both IGF-1 and GH treated cells. IGF-1 resulted in condensation of the nuclear material as early as 24 hours after treatment. IN CONCLUSION: (1) RAW 264.7 responded to both IGF-1 and GH equally (viability and proliferation), and (2) morphological changes were observed in all cells treated with both hormones compared to control group. This study indicates that GH hormone could induce its effect directly or indirectly through IGF-1.
UNLABELLED: It is well documented that growth hormone (GH) functions to regulate both cell growth and cell number and is considered the master hormone because it affects almost every cell of the body. Growth hormone stimulates the liver to secrete insulin-like growth factor (IGF-1), which is also capable of binding insulin as well as insulin-like binding receptors on the cell surface. It is possible that GH cellular effects are mediated by IGF-1 rather than GH itself. In this study, RAW 264.7 cells were challenged with a high dose of GH (48 ng/microliter), a low of dose GH (4.8 ng/microliter), a high dose of IGF-1 (26 ng/microliter) or low doses of IGF-1 (6.3 ng/microliter) for 24, 48, 72, and 96 hours. Cell number, cell protein concentration, cell damage, and cellular morphology were measured at each time point and compared to untreated RAW 264.7 cells. The results show significant increases in cell number for cells treated with low doses of GH and IGF-1 at 24 hour phase. Cell proliferative effects were also observed at 48 hours in IGF-1 treated cells. Cellular damage (MDA levels) was not statistically significant for any treated group for the entire duration of the experiment. Most notable differences were observed in cellular morphology for both IGF-1 and GH treated cells. IGF-1 resulted in condensation of the nuclear material as early as 24 hours after treatment. IN CONCLUSION: (1) RAW 264.7 responded to both IGF-1 and GH equally (viability and proliferation), and (2) morphological changes were observed in all cells treated with both hormones compared to control group. This study indicates that GH hormone could induce its effect directly or indirectly through IGF-1.