As described earlier, GH-deficient adults have increased central adiposity. This contributes to the observed hyperinsulinaemia in GH-deficiency, indicating insulin resistance (10). The presence of insulin resistance has been confirmed by studies using hyperinsulinaemic euglycaemic clamp techniques and using Bergman's minimal model (50-52). In addition there is evidence that adults with GH-deficiency have reduced hepatic glycogen stores (51). GH replacement has been demonstrated to further increase insulin resistance over a period of six weeks therapy (52) but although hyperinsulinaemia persists, carbohydrate metabolism returns to baseline following 3 mo GH treatment (50,52).
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