THE INHIBITORY EFFECT OF GLUCOSE ON GROWTH-HORMONE SECRETION IS LOST IN OBESITY BUT NOT IN HYPERTENSION

In obesity there is a clear reduction of both spontaneous and stimulat ed GH secretion. Furthermore, in obese patients the somatotrope respon siveness to provocative stimulation is selectively refractory to the i nhibitory effect of glucose load. It has been hypothesized that hyperi nsulinism of obese patients could play a role in the pathogenesis of t hese alterations. Aim of the present study was to verify the GH respon se to GHRH and the ability of glucose load to inhibit it in patients w ith essential hypertension in whom hyperinsulinism and insulin resista nce are frequently present. To this goal, 7 patients with essential hy pertension (HP, age, mean+/-SE: 29.6+/-2.4 yr, 3 females and 4 males, BMI: 21.7+/-1.2 kg/m(2)), 7 obese (OB, 4 females and 3 males, 31.9+/-4 .1 yr, 35.6+/-2.0 kg/m(2)) and 7 normal subjects (NS, 4 females and 3 males, 28.3+/-3.9 yr, 21.0+/-1.6 kg/m(2)) underwent the following test s: GHRH (1 mu g/kg iv at time 0) alone and preceded by oral glucose lo ad (OGTT, 100 g po at -45 min). Basal insulin levers were similar in H P and OB (11.3+/-0.5 and 12.7+/-2.2 mu U/ml, respectively); these, in turn, were higher (p<0.005) than those in NS (6.8+/-0.8 mu U/ml). Basa l plasma glucose levels in HP were similar to those in OB and NS (80.3 +/-3.6, 86.9+/-6.7 and 84.4+/-1.7 mg/dl, respectively). In HP and OB a nd NS basal GH (1.0+/-0.5, 1.0+/-0.6 and 0.3+/-0.1 mu g/l, respectivel y) and IGF-I levels (132.6+/-14.8, 137.3+/-13.2 and 138.8+/-12.2 mu g/ l, respectively) were similar. In HP the GH response to GHRH (AUC: 105 8.8+/-347.8 mu g/l/min) was similar to that observed in NS (959.0+/-16 7.8 mu g/l/min) and higher than that in OB (344.8+/-67.2 mu g/l/min, p <0.01). OGTT clearly blunted (p<0.01) the GHRH-induced GH response in HP as well as in NS (401.8+/-104.4 and 521.6+/-76.6 (gl/min, respectiv ely) but not in OB (387.4+/-78.8 (g/l/min). The OGTT-induced insulin l evels in HP did not differ from those of OB, both being higher (p<0.05 ) than those recorded in NS. Glucose levels after OGTT were similar in the three groups. In conclusion, this study demonstrates that, like i n normal subjects but differently from in obese patients the GH respon se to GHRH is normal in patients with essential hypertension and it is normally inhibited by oral glucose load even when these patients show high insulin levels. Thus, it is unlikely that the low somatotrope se cretion and its refractoriness to inhibition by glucose load in obesit y is due to hyperinsulinism. (C) 1997, Editrice Kurtis.