Skrha J, Sindelka G, Haas T, Hilgertová J, Justová V
III. interní klinika 1. LF UK a VFN, Praha.
Cas Lek Cesk. 1994 Aug 22;133(16):496-9.
Insulin resistance and hypertriacylglycerolaemia are part of the X syndrome and are supposed to be interrelated. The objective of the present trial was to evaluate the impact of hypolipidaemic treatment on the action of insulin evaluated by means of a so-called hyperinsulimaemic clamp and by examination of insulin receptors.
To eight type 2 diabetics with mild hypertriacylglycerolaemia for three months ethophylline clofibrate (Duolip) was administered and for three months phenofibrate (Lipanthyl). Before and during treatment parameters of diabetes compensation were examined (blood sugar level, fructosamine and glycolysate haemoglobin), insulin sensitivity, using an isoglycaemic hyperinsulinaemic clamp and insulin receptors on red blood cells. Lipanthyl caused a more marked drop of triacylglycerol (by 46%) than Duolip forte (by 20%). Hypolipidaemic treatment did not affect diabetes compensation. As compared with healthy subjects, in diabetics before treatment a reduced insulin sensitivity was found, evaluated either by the index of insulin sensitivity (24.0 +/- 0.8, as compared with 35.5 +/- 4.9 mumol/kg/min per mU/l x 100, p < 0.05) or metabolic glucose clearance (3.7 +/- 0.9, as compared with 6.3 +/- 1.0 ml/kg/min, p < 0.01) and a slightly reduced insulin bond with receptors (p < 0.05). Duolip treatment led to a drop of insulin sensitivity and concurrent rise of affinity of insulin receptors (p < 0.01), while Lipanthyl was not manifested by marked changes. The authors did not find a significant correlation between the drop of triacylglycerol levels and insulin sensitivity in different types of treatment, which obviously is due to the small number of examinations.
Therapy with ethophylline clofibrate of fenofibrate was not manifested in type 2 diabetics by a changes in the compensation of the disease. Hypertriacylglycerolaemia exists as an independent factor which is rather the consequence than cause of insulin resistance.
