Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal

Abstract At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. We have measured their different molecular forms in plasma of six female controls, six normal pregnant (NP) women and six gestational diabetic (GD) women under basal conditions and 30 min after an oral glucose load (100 g) and a liquid mixed meal in order to study if their alteration could contribute to the impaired glucose tolerance in GD. Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. Neurotensin-1–13 was the main molecular form of all neurotensins at basal time in the three groups studied, being higher in GD in comparison with controls and NP. Somatostatin-1–14 was the predominant molecular form in controls and GD under basal conditions and did not show any change after stimuli. In NP, somatostatin-1–14 showed a significant increase following both kinds of stimuli. Total gastrin concentrations in NP and GD showed a significant increase after the glucose load, which was not observed in controls. Gastrin-17 was the main molecular form at basal time and 30 min post-stimuli in GD but not in NP and controls. We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD. The different patterns of circulating small and large molecular forms of neurotensin, gastrin and somatostatin may be due to variations in the rate of their release or degradation in pregnancy and gestational diabetes.