Growth Hormone Glucose uptake

The promotion by insulin of glucose uptake by muscle and fat cells (adipocytes), of glycogen deposition in liver and muscle, and its stimulation of growth soon emerged as the purified hormone became available for study. Although insulin was crystallized by Abel in 1926, its primary structure established by Sanger in 1953 (see Chapter 10),... 

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. 

Herrera and Renold (1960) have observed that cortisol in vitro decreases the recovciy of C from glycine-i-C in the trichloroacetic acid-precipitable protein of epididymal adipose tissue (sec Section IV, H). Interest in this observation centers on the possibility that it may reflect the well-known effects of the glucocorticoids on protein metabolism. It has also been noted that cortisol in vitro decreases the glucose uptake of epididymal adipose tissue incubated in the presence of adrenaline, ACTH, or growth hormone (Renold et al., 1960b). 

This insulin effect of growth hormone observed in vivo may also explain some of the discrepancies observed between in vivo and in vitro effects of growth hormones on glucose uptake by muscle. Whereas growth hormone inhibits glucose uptake in vitro, in vivo its inhibitory effect is compensated for by the insulin secreted as a result of liver gluconeogenesis. 

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