Historical text by DatBTrue, written between 2008 and 2016 and reproduced verbatim. It records what was argued then; it is not dosing guidance and not medical advice. Read the disclaimer.

In plain language, GH in certain circumstances increases glucose uptake identical to that of insulin into both muscle and adipose tissue. This involves translocations of glut 4 and to a lesser extent glut 1 from an intracellular pool to the plasma membrane. BUT in order for this to happen there must be an absence of GH for prolonged periods of time. It appears that this rarely occurs because the base level of GH is still too high to create this effect. *

Of more importance is the “likely” effect of GH on glucose transport into adipose tissue. GH, dose dependently reduces glucose transport (diabetogenic effect). The addition of GH to adipocytes in vitro and dose dependently in vivo reduces the rate of glucose uptake in a way that we could characterize as the opposite of the insulin effect.

“The data reported here not only confirm the earlier findings but also further demonstrate the importance of GH in vivo for the restriction of basal glucose transport in adipocytes. … The data give evidence for the importance of GH in vivo, in balance with insulin, for the control of the activity of the glucose carrier in adipose tissue.” – Glucose transport in adipocytes and its control by growth hormone in vivo, Schoenle et al. 242 (6): E368. (1982)

So there is a good possibility that although GH in the presence of insulin will not lead to substantial fat lossvia lipolysis, it will inhibit the uptake of glucose into adipose tissue. This leads us to the generalization that concurrent administration of GH & insulin will skew nutrient partitioning in favor of muscle tissue and away from adipose tissue.

One further note of interest though is this glucose uptake inhibiting effect of GH leads to a restoration of sensitivity to insulin in that tissue.

  • – Cellular mechanism of the insulin-like effect’ of growth hormone in adipocytes Rapid translocation of the HepG2-type and adipocyte/muscle glucose transporters, Tanner, J. W. et al, Biochem. J. (1992) 282, 99-106