We have previously demonstrated in hepatocyte suspensions prepared after in vivo GH deprivation [hypophysectomy (hypox)] that rates of esterification of [1-14C]oleic acid into triglyceride (TG) and phospholipid (PL) were diminished, and that these esterification rates were correspondingly restored by repletion with recombinant GH. The current studies were designed to determine if GH exerts a similar effect on the secretion of very low density lipoprotein (VLDL), the primary plasma carrier of TG. We assessed rates of secretion of VLDL lipid and apoprotein by perfused livers prepared from cortisol/T3-replaced hypox female rats in the presence and absence of recombinant human (h) GH infusion. We also determined rates of synthesis and secretion of VLDL TG from infused [1-14C]oleic acid. After hypox, rates of secretion of VLDL lipid (TG, PL, and cholesterol) and apoprotein (total) were significantly decreased. In addition, VLDL secreted under these conditions was depleted of PL, relative to the other lipid components. Secretion of newly synthesized VLDL TG from [1-14C]oleic acid was also decreased; however, neither intracellular accumulation of labeled TG nor absolute tissue levels of TG were significantly changed. Conversely, GH treatment of hypox rats effectively restored rates of secretion of VLDL TG, PL, cholesterol (C) and apoprotein to control levels. These findings support the putative role of GH in regulating VLDL secretion in vivo by demonstrating that alterations in plasma GH are accompanied by changes in VLDL secretion. The findings further suggest that GH may regulate VLDL secretion by altering the amount of PL and/or apoprotein available for formation of the VLDL particle.