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The authors have studied insulin receptors on peripheral blood monocytes and insulin sensitivity, evaluated by simultaneous infusion of glucose, insulin and somatostatin in 10 control subjects and in 20 obese patients with normal glucose tolerance. The obese patients have been divided into two groups, normo (NO) and hyperinsulinemic (HO), according to the total insulin response during OGTT. We considered HO patients with insulin response higher than M + 2DS of controls. Obese patients showed, in comparison to the controls, a lower specific binding and higher degree of insulin resistance. The subdivision of obese patients allowed us to distinguish two groups. The first was characterized by basal hyperinsulinemia, normal insulin response to the stimulus, reduced number of insulin receptors and normal or slightly reduced sensitivity. The second group showed high basal and after stimulus insulinemic values, reduced number of insulin receptors and high level of insulin resistance. When we compared the two groups of obeses we found that the first has a shorter duration of obesity and lower blood glucose values after OGTT. However both groups show the same reduction of insulin bound and the same degree of basal hyperinsulinemia. These data suggest that a reduction of insulin receptors is not the main factor responsible for insulin resistance in obesity. Furthermore, the presence of basal hyperinsulinemia and normal insulin sensitivity in our first group suggests that the modification of basal insulin concentrations is not dependent on the presence of insulin resistance.

The authors have studied the effects of an oral or intravenous glucose load, of insulinic hypoglycemia, of arginine and the effects of the 2-deoxi-glucose on the plasmatic concentration of HPL and GH on pregnant women at different times during their pregnancy. None of the used tests seemed able to modify in any way the plasmatic concentration of the placental lactogen hormone; the somatotropinic response to the different stimuli happens to be lower than that found in non pregnant women of the same age. We and by asserting that unlike what happens with the GH, there does not exist a direct "feedback" between the modifications of plasmatic concentration of the main underlayers and HPL.