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This version published online on January 5, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-1239
A more recent version of this article appeared on April 1, 2005
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Submitted on June 30, 2004
Accepted on December 22, 2004

Adiponectin, Leptin, and Erythrocyte Sodium/Lithium Countertransport Activity, but not Resistin, are Related to Glucose Metabolism in Growth Hormone Deficient Adults

Johan Svensson MD, Ph.D.*, Hans Herlitz MD, Ph.D., Per-Arne Lundberg B.Sc., and Gudmundur Johannsson MD, Ph.D.

Research Centre for Endocrinology and Metabolism (J.S., G.J), Department of Nephrology (H.H), and Department of Clinical Chemistry (P-A.L), Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden

* To whom correspondence should be addressed. E-mail: Johan.Svensson{at}medic.gu.se.

In a randomized, placebo-controlled, crossover study under metabolic ward conditions, ten growth hormone (GH) deficient (GHD) adults received one-week GH replacement therapy (9.5 µg/kg/day). The effect of this treatment on the erythrocyte sodium/lithium countertransport (SLC) activity, and on serum levels of adiponectin, resistin, leptin, insulin-like growth factor binding globulin-1 (IGFBP-1) and interleukin-6 (IL-6), was determined.

The one-week GH replacement impaired glucose homeostasis determined from an oral glucose tolerance test (OGTT). The other measured variables in serum were unchanged by GH replacement. At baseline, serum adiponectin level was inversely correlated and serum leptin level was positively correlated with measures of glucose tolerance and insulin sensitivity. The changes in serum leptin level and erythrocyte SLC activity were positively, and the change in serum IGFBP-1 level was negatively, correlated with changes in measures of glucose metabolism.

In conclusion, short-term GH treatment induced glucose intolerance, but did not significantly change the erythrocyte SLC activity and the serum levels of adipokines, arguing against direct effects of GH on these measures. However, baseline values or changes in erythrocyte SLC activity, adiponectin, leptin, and IGFBP-1 correlated with glucose metabolism. This suggests that these factors are of importance for glucose homeostasis in GHD adults, most likely through GH-independent mechanisms.


Key words: growth hormone deficiency • glucose • insulin • adipokine • sodium/lithium countertransport




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