Introduction

Growth hormone (GH) deficiency (GHD) in adults exhibits many clinical abnormalities, including central obesity, hypertension, dyslipidaemia, coagulopathy, insulin resistance and glucose intolerance (Carroll et al., 1998; Hew et al., 1998), features that closely resemble those seen in patients with the metabolic insulin resistance syndrome (MIRS). This combination of metabolic abnormalities may be responsible for the higher cardiovascular mortality and morbidity demonstrated in earlier epidemiological studies in GH-deficient adults (Rosén & Bengtsson, 1990; Erfurth et al., 1996; Markussis et al., 1997). The obesity of GH-deficient adults is predominantly central in distribution (Carroll et al., 1998; Hew et al., 1998), which is known to be metabolically more active (Bjørntorp, 1991). The pattern of dyslipidaemia present in GH-deficient adults is characterized by elevated triglyceride (TG) and reduced high density lipoprotein (HDL) cholesterol levels (Hew et al., 1998), together with an increased prevalence of more atherogenic, small diameter low density lipoprotein (LDL) particles (O'Neal et al., 1996). In addition to the central obesity and dyslipidaemia, plasminogen activator inhibitor-1 and fibrinogen are increased, and are likely to be important contributory factors to the enhanced cardiovascular disease of GHD (Hew et al., 1998). Thus, given the importance of MIRS to long-term health of GH-deficient individuals, this review will explore, in detail, the defects of glucose metabolism and insulin action in GH-deficient adults, particularly in respect to which site(s) (liver and/or periphery muscle) and in vivo and in vitro glucose metabolic pathways are involved. We will also examine the impact of GII replacement on these metabolic defects.