[Blood glucose regulation in Bartter's syndrome. Observations in 2 cases]. / La regolazione glicemica nella sindrome di Bartter. Osservazioni su due casi.

Two cases (two sisters) of Bartter's syndrome are reported in which evident disturbance of the glycaemia regulation system was observed alongside other elements typical of the syndrome. The data are discussed in the light of recent aetiopathogenetic hypotheses about Bartter's syndrome. It is concluded that the physiopathological condition is also directly responsible for the disturbance in glycoregulation.

Possible glucagon-mediated hypocholesterolemic activity of a nicotinic acid derivative (sorbinicate).

The antilipolytic activity of nicotinic acid was investigated in 7 patients with type II b hyperlipoproteinemia and in 7 with type IV hyperlipoproteinemia treated for two months with a nicotinic acid derivative, sorbinicate (1600 mg daily, ie 1454 mg NA). Before and after treatment the blood levels of total cholesterol and triglycerides were determined and three dynamic tests -- oral glucose tolerance test, insulin test and tolbutamide test -- were done to check in each test the variations in blood glucose, NEFA, insulin (excluding obviously the insulin test), glucagon and growth hormone levels. At the end of the treatment, there was a significant reduction of cholesterol (type IIb and type IV) and of triglycerides (type IV), a marked reduction of the glucagon response, a slight increase in the insulin response and in the basal secretion of the growth hormone. It is suggested that the antilipolytic activity of nicotinic acid (and hence of sorbinicate) is at least partly mediated by an inhibition of glucagon secretion (and/or synthesis).