Effects of Growth Hormone
Direct Effects: Growth Hormone
Growth Hormone Receptors: Growth hormone directly activates cells expressing growth hormone receptors on their surface. These receptors bind growth hormone after being released from the Anterior Pituitary into the blood stream. The binding of growth hormone to the receptor activates the cell.
Fat Reserves: Fat cells (adipocytes) express high levels of growth hormone receptor. The binding of growth hormone to these receptors causes the adipocyte to release lipids into the blood stream and simultaneously prevents them from taking up lipids from the exterior. In other words, growth hormone mobilizes fats for energy usage. The ultimate result is that our fat reserves dwindle when growth hormone levels are high.
Growth hormone also slows the use of glucose for energy metabolism.
Indirect Effects: Insulin-like Growth Factor-1
The majority of growth hormone’s actions, however, are indirect.
The majority of growth hormone’s effects are mediated by Insulin-like Growth Factor 1, or IGF-1. IGF-1 is produced by the liver when stimulated by growth hormone; liver cells (hepatocytes) also express high levels of growth hormone receptor.
Therefore, increases in growth hormone are commonly mirrored by increases IGF-1. When the growth hormone receptor isn’t functioning properly, however, IGF-1 levels are low relative to growth hormone.
Muscle Growth: IGF-1 causes muscle cells (myocytes) to increase protein production (synthesis), reduce protein breakdown, take up amino acids (building blocks of proteins) and to divide (proliferate). In other words, our muscles grow when stimulated by IGF-1.
Bone Growth: Bone cells (chondrocytes) also respond to IGF-1 by proliferating; our bones grow. Connective tissue and cartilage also increase in response to IGF-1.
Kidneys: Our kidneys and internal organs increase in size in response to IGF-1.
Regulatory Feedback: Recall that growth hormone eventually shuts off its own release through a process of regulatory feedback. Well, IGF-1 also feedsback upon the hypothalamus and anterior pituitary to inhibit further growth hormone release. More precisely, IGF-1 promotes the release of somatostatin from the hypothalamus, as well as directly inhibits growth hormone release from the anterior pituitary.
Creatine Supplementation: Intriguing data has just appeared indicating that creatine supplementation increases IGF-1 expression independently of an exercise stimulus, an effect most likely downstream of an enhancement of methylation status. Read the issue of the Creatine Newsletter that discusses these provocative studies.