Effects of intravenously administered fructose and glucose on splanchnic secretion of plasma triglycerides in hypertriglyceridemic men

Abstract

Studies were undertaken in man to test the hypothesis that fructose produces higher rates of triglyceride secretion from the liver than equimolar amounts of glucose. Splanchnic metabolism of triglycerides and other substrates was studied during prolonged intravenous administration of 9,10- 3H-palmitate and either fructose or glucose (30 g/hr) to hypertriglyceridemic men maintained on a highcarbohydrate diet for 2 wk. The secretion of plasma triglycerides from the splanchnic region was quantified from splanchnic flow and chemical (and radio-chemical) measurements of the transsplanchnic gradients of 3H-labeled free fatty acids and triglycerides. Very high rates of release of triglycerides from the splanchnic region (average 84 g triglyceride/day) were observed during the infusion of hypercaloric amounts of either hexose. Mean values for splanchnic secretion of plasma triglyceride fatty acids were not significantly different during administration of fructose versus glucose [values for chemical production: 108 ± 28 (SE) and 96 ± 20 μmole/min/sq m, respectively] and were more than one-half the rate of transport of plasma free fatty acids. In contrast to the postabsorptive state, labeled plasma free fatty acids did not comprise a major source of the secreted plasma triglyceride fatty acids. During intravenous infusion of fructose versus glucose, the mean fraction of triglyceride fatty acids of plasma very low-density lipoproteins derived from plasma free fatty acids was 14.8% versus 8.9%, respectively; after a 12-hr infusion of either labeled hexose, that derived from fructose or glucose, though it increased with time, it reached only 5.1% and 3.6%, respectively. Elevated rates of secretion of plasma triglycerides, evidently derived from stored liver fat or glycogen, contribute to the accentuation of lipemia by either fructose or glucose. Considering the high capacity for triglyceride release of the human liver during hypercaloric carbohydrate administration, the results imply that impaired peripheral removal mechanisms may underlie the elevation of serum triglyceride levels in many patients with endogenous hyperlipemia.