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Growth Hormone Requirement for a Normal Human Adipocyte Glucose Carrier Function^*

Children's University Hospital CH-8032 Zürich, Switzerland

Address requests for reprints to: Dr. Eugen J. Schoenle, Children's University Hospital, Steinwiesstrasse 75, CH-8032, Zürich, Switzerland.

One of the most prominent actions of insulin is stimulation of the glucose carrier in different cell types, especially adipose cells. However, the exact mechanism of the mode of action of insulin, between receptor binding and stimulation of glucose transport, is not understood in detail. We have shown earlier, that GH plays an important role in the control of the insulin-sensitive glucose carrier system in rat fat cells. In this study, we measured glucose transport in fat cells of normal probands, GH-deficient (GHD) and GH-treated GHD patients. From sc fat tissue biopsies of three GHD patients, fat cells were isolated after digestion with collagenase. In normal fat cells, basal glucose transport was slow (t/2 = 2.5 min) and stimulated by insulin (t/2 = 0.8 min), as expected. In fat cells of GHD patients glucose transport was maximal already in the basal state (t/2 = 0.8 min) without an additional effect of insulin. After GH administration during several months to GHD patients, glucose transport was again slow in the basal state (t/2 = 3.2 min) and could be stimulated by insulin (t/2 = 0.7 min). These results confirm our earlier findings in rat adipocytes for human adipocytes: GH in vivo is responsible for a glucose transport-limiting factor in the plasma membrane that restricts basal glucose transport and is acutely inhibited by insulin resulting in enhanced glucose transport. These results demonstrate the physiological importance of GH for a normal function of the insulin transmembrane signaling system in fat tissue and indicate a possible benefit of GH administration in adult GHD patients.

^* Dedicated to Professor Andrea Prader on the occasion of his 70th birthday. This work was supported by Nordisk Gentofte A/S Denmark and by the Swiss National Science Foundation.

Received October 17, 1989.