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In Type 1 diabetes an increased total body sodium and an impaired ability to excrete a sodium load have been described. A possible involvement of the renal dopaminergic system in this abnormal sodium handling was evaluated through measurements of the urinary output of dopamine, sodium, the dopamine/sodium correlation, and through examining the effect of a dopamine infusion on urinary sodium excretion. Twenty-four hour urinary dopamine excretion was significantly lower in Type 1 diabetic patients as compared to normal controls. A significant correlation between urinary dopamine and sodium excretion was present in normoalbuminuric Type 1 diabetic patients and in normal controls. However, no such correlation could be found in microalbuminuric patients. The increase in fractional excretion of sodium during a 1 h low-dose dopamine (3 micrograms kg-1 min-1) infusion in Type 1 diabetic patients was negatively correlated with diabetes duration. Patients with short duration of diabetes (less than 15 years) had a comparable dopamine-induced increase in fractional excretion of sodium as normal controls. However, patients with longer duration of diabetes (more than 15 years) and microalbuminuric patients displayed no significant changes in sodium output during dopamine infusion. These findings suggest that in Type 1 diabetes mellitus a deficiency of renal dopamine production could be responsible for the impaired sodium handling. Longer duration of the disease and microalbuminuria seem to be associated with an uncoupling of the urinary dopamine/sodium relationship.

Peripheral levels of basal and tolbutamide-induced somatostatin have been measured in patients with diabetes or impaired glucose tolerance (IGT) and compared with those in normal individuals. Basal somatostatin was significantly higher in patients with Type 1 diabetes than in age-matched control subjects. This increase was most pronounced at diagnosis, and appeared to be related to metabolic control in insulin-treated patients. No increase was noted in patients with Type 2 diabetes or with IGT. Intravenous bolus injection of tolbutamide enhanced peripheral somatostatin levels in healthy volunteers in a biphasic manner. Patients with IGT also exhibited a biphasic response but the amplitude of the first phase was higher. No secretory response was detected in 27/29 Type 1 diabetic patients at diagnosis; a somatostatin response to tolbutamide became detectable again in Type 1 patients with normalization of their basal somatostatin levels but was then paradoxically related to poor blood glucose control. In Type 2 diabetes, basal somatostatin levels were similar to age-matched control subjects, but decreased upon intravenous tolbutamide administration.