Relation of hyperinsulinemia, hyperparathyroidism and hypocalcitriolemia to hypertriglyceridemia in nonobese nondiabetic predialyzed CRF men

ABSTRACT

The aim of the present study was to determine the relation of uremic hyperinsulinemia, hyperparathyroidism and hypocalcitriolemia to hyper triglyceridemia in nonobese nondiabetic, predialyzed CRF men. The present study was conducted on thirty nonobese nondiabetic male subjects suffering from CRF due to different intrinsic renal causes. They were not yet performing dialysis. The patients were categorized according to their fasting serum triglyceride [TG] levels into two groups a hypertriglyceridemic and a normotriglyceridemic, each comprised 15 patients. In addition ten clinically healthy male subjects matched in age and body mass index were enrolled as a reference group. Overnight fasting serum triglycerides [enzymatic], insulin [ELISA], 1,25 [OH]2Da [radioimmunoassay], and plasma parathyroid hormone [chemiluminecence immunoenzymo- metric assay] were carried out for all subjects. There was significant increase in serum insulin [P<0.001] and plasma PTH [P<0.001] values in CRF hypertriglyceridemic group than the corresponding values of CRF nor-motriglyceridemic group which in turn was significantly higher compared to the controls. Alternatively there was significant increase in serum total triglycerides levels in both hyperinsulinemic and severe hyperparathyroid CRF subgroups in comparison with normoinsulinemic and mild hyperparathyroid CRF subgroups [all patients showed secondary hyperparathyroidism] respectively. At the same time there was significant positive correlation between serum triglycerides levels and serum insulin and PTH levels [P<0.05, P<0.02 respectively]. On the other hand, there was significant reduction in serum calcitriol levels in CRF compared to controls with insignificant correlation between serum triglycerides and calcitriol levels in uremic. In conclusion, unlike calcitriol, reactive hyperinsulinemia and secondary hyperparathyroidism in CRF patients might contribute to hypertriglyceridemia in CRF. The mode of such action would be complex, but most probably through changes in the activity of lipases in the uremic milieu