Endocrine Abstracts

GH has well documented insulin antagonistic effects. By inference, GHD may be expected to result in increased insulin sensitivity. Young GHD children have a tendency to both fasting and readly provoked hypoglycaemia probably resulting from impaired hormonale counter-regolation. Increased insulin sensitivity could also contribute to their hypoglycaemia; however, this has not been directly demonstrated. Interestingly, susceptibility to hypoglycaemia in GHD children diminishes with increasing age and, paradoxically, GH deficient adults demonstrate insulin resistance even prior to GH replacement therapy. The mechanism underlying this apparent age-related deterioration in insulin sensitivity in GHD subjects is unknown (changes in body composition or metabolic responses to GH, or interaction with pubertal increases in sex steroids e.g.). The transition period is defined as the period between end of linear growth and attainment of full adult somatic development. It can be defined as late teenage years, ‘Post-adolescence’, ‘Young adulthood’ with a duration of ∼ 3–10 years and the ESPE consensus of december 2003 underline the transition period defined as ending around 25 years. In order to examinate the life span insulin sensitivity index a group of GHD patients have been selected (n=81); in particular group A (n=10) (<25 yrs), group B (n=4) (26–30 yrs), group C (n=11) (31–40 yrs), group D (n=14) (41–50 yrs), group E (n=30) (51–60 yrs) and group F (n=12) (>60 yrs). The insulin sensitivity was evaluated using HOMA index (basal insulin levels x blood glucose/22) reflecting, in particular, the ‘value’ of insulin resistance. Our preliminary results indicated that insulin sensitivity decresed significantly in the group of patients after the transition phase (group B) respect to the other period of life (P<0.05, vs A, C, E). We are not aware of any other works evaluating insulin sensitivity in a large group of GHD patients. In our patients reduced insulin sensitivity in the period after transition age could support the hypothesis to treat this patients also in this period of life due to possible high incidence of insulin resistance after the transition period. There is some debate as to whether a reduced insulin sensitivity is only a transiet phenomenon or a persistent one. This data is reflecting somatic immaturity of patients who suffer for two components: developmental existing since childhood (in childhood onset GHD) and metabolic acquired in the transition period so this data support the hypothesis that patients must be treated also in transition phase due to the possible incidence of metabolic alteration in the following period of life.