Growth Hormone Fatty acid synthesis

It has been reported also that epidermal growth factor stimulates fatty acid synthesis and the phosphorylation of ACC in rat liver and adipose tissues (Holland and Hardie, 1985) through phosphorylation of the I-peptide, suggesting that several peptide hormones sharing homology with insulin, such as IGF-1, could enhance lipogenesis similarly. 

Mechanism of Action A polypeptide hormone that stimulates cartilaginous growth areas of long bones, increases the number and size of skeletal muscle cells, influences the size of organs, and increases RBC mass by stimulating erythropoietin. Influences the metabolism of carbohydrates (decreases insulin sensitivity), fats (mobilizes fatty acids), minerals (retains phosphorus, sodium, potassium by promotion of cell growth), and proteins (increases protein synthesis). Therapeutic Effect Stimulates growth. 

Somatropin is a growth hormone, which mimics actions of naturally occurring growth hormone to stimulate hnear and skeletal growth increases the number and size of skeletal muscle cells increases RBC mass and internal organ size increases cellular protein synthesis reduces body fat stores and lipid mobilization, and increases plasma fatty acids. It is indicated in long-term treatment of children with growth... 

Growth hormone increases the sensitivity of the adipocyte to the lipolytic action of the catecholamines and decreases its sensitivity to the lipogenic action of insulin. These actions lead to the release of free fatty acids and glycerol into the blood to be metabolized by the liver. GH also decreases esterification of fatty acids, thereby reducing triacylglycerol synthesis within the fat cell. Recent evidence suggests that GH may impair glucose uptake by both fat and muscle cells by a postreceptor inhibition of insulin action. 

Plane of Nutrition. The plane of nutrition alters the blood level of polyunsaturated fatty acids (mainly arachidonic acid), which are potent stimulators of PG release. These fatty acids can regulate PG production as precursors, as feedback inhibitors (1), or as competitors of arachidonic acid for PG synthase (15) however, other mechanisms of the effect of nutrition on PG release (for example, through nutrition-dependent production of metabolic hormones and growth factors) are not to be excluded (see below). Dietary fatty acids reduced ovarian and endometrial PGF synthesis, decreased ovulation rate in rats, delayed parturition in sheep and humans, and reduced embryonic mortalily in cows (15). 

---