HYPERLIPIDEMIA IN RENAL-FAILURE - STUDIES OF PLASMA LIPOPROTEINS, HEPATIC TRIGLYCERIDE PRODUCTION, AND TISSUE LIPOPROTEIN-LIPASE IN A CHRONICALLY UREMIC RAT MODEL

  • 1 January 1978
    • journal article
    • research article
    • Vol. 91  (1) , 176-186
Abstract
To determine whether hypertriglyceridemia in chronic renal failure resulted from altered production and/or removal, Sprague-Dawley rats in which chronic uremia had been induced by 5/6 nephrectomy were studied. In this model, basal plasma TG [triglyceride] levels were higher than in controls (uremic 141 .+-. 52 mg/100 ml; control 83 .+-. 25; mean .+-. SD; P < 0.001) at 1 mo. after nephrectomy and remained significantly elevated throughout the 10 wk duration of study. In the uremic animals hepatic TGSR [triglyceride secretion rate] (Triton) were not increased (uremic 0.56 .+-. 0.11 mg/min; control 0.63 .+-. 0.13), and AcCoAc [acetyl-CoA carboxylase] the rate-limiting enzyme in hepatic lipogenesis, was significantly reduced (control 24.5 .+-. 3.8 nM/min per mg protein; uremic 18.2 .+-. 1.1; P < 0.005). The TG removal system, heparin-elutable LPL [lipoprotein lipase] activities, was similar in control and uremic animals in heart, diaphragm and adipose tissue. Serum from both acute and chronically uremic rats lowered adipose tissue LPL activity (P < 0.01). In uremia TG production was not increased and the clearance of TG-rich lipoprotein from the circulation was reduced because of a functional impairment in LPL.