Growth Hormone
Promotion of Linear Growth - Stimulates the eppheseal Cartilage of the long bones
Promotion of protein deposition in tissues
Promotion of Fat utilisation for Energy - mobilisation of FFA from adipose tissue and the peripheral utilisation of FFA for Energy
Impairment of carbohydrate utilisation for energy - Decreases uptake and utilisation of Glucose by many insulin sensitive cells, such as muscle and adipose tissue. Increase Glucose and there is a compensatory increase in Insulin. GH is diabetogenic
Promotes the secretion of Somatomedins or IGF's - secreted by the liver - and the growth promoting effects are due to locally produced and circulating somatomedins in cartilage and muscle. Locally produced somatomedins act in a autocrine or paracrine fashion
Hypothalamus - GHRH stimulates and Somatostatin inhibits - GH
Three general catagories that increase GH secretion:
Promotion of protein deposition in tissues
Promotion of Fat utilisation for Energy - mobilisation of FFA from adipose tissue and the peripheral utilisation of FFA for Energy
Impairment of carbohydrate utilisation for energy - Decreases uptake and utilisation of Glucose by many insulin sensitive cells, such as muscle and adipose tissue. Increase Glucose and there is a compensatory increase in Insulin. GH is diabetogenic
Promotes the secretion of Somatomedins or IGF's - secreted by the liver - and the growth promoting effects are due to locally produced and circulating somatomedins in cartilage and muscle. Locally produced somatomedins act in a autocrine or paracrine fashion
Hypothalamus - GHRH stimulates and Somatostatin inhibits - GH
Three general catagories that increase GH secretion:
- Fasting, Chronic protein deprevation, or a fall in plasma glucose and FFA
- Increased plasma levels of amino acids, after a protein meal
- Exercise and stressful stimuli such as pain and fever.
Abnormalities
- Dwarfism
- Gigantism
- Acromegaly - with DM in states of chronic GH excess
Regulation of circulating and tissue levels of insulin-like growth factors. Most circulating insulin-like growth factors are produced in the liver. Hepatic IGF1 production is subject to complex regulation by hormonal and nutritional factors. Growth hormone (GH), which is produced in the pituitary gland under control of the hypothalamic factors growth-hormone-releasing hormone (GHRH) and somatostatin (SMS), is a key stimulator of IGF1 production. Various IGF-binding proteins (IGFBPs) are also produced in the liver. In IGF-responsive tissues, the ligands IGF1 and IGF2 as well as IGFBPs can be delivered through the circulation from the liver (an 'endocrine' source), but IGFs and IGFBPs can also be locally produced through autocrine or paracrine mechanisms. These mechanisms often involve interactions between stromal- and epithelial-cell subpopulations. |
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