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Triacylglycerol Secretion in Rats: Validation of a Tracer Method Employing Radioactive Glycerol¹

Michael Bird^2,*, Mary Ann Williams^3,* and Nome Baker

^* Department of Nutritional Sciences, University of California, Berkeley, CA 94720 Department of Medicine, UCLA School of Medicine and Crump Institute for Medical Engineering, University of California, Los Angeles, CA 90024

A two-compartment model was developed to analyze the temporal changes in plasma triacylglycerol (TG)-specific radioactivity after injection of [2-³H]glycerol into rats. The analysis, which yielded fractional rate constants of TG secretion, was tested in rats fed diets either adequate or deficient in essential fatty acids (EFA) and containing either glucose, fructose or sucrose as the dietary carbohydrate. The method of analysis appeared valid, first, because of a close agreement between experimental and computer-fitted TG-specific radioactivity curves, and second, because the fractional rate constants obtained were quite similar to fractional rate constants determined previously by the Triton WR-1339 technique in rats maintained on identical diets. The results show that EFA deficiency increased the fractional rate constant of TG secretion 1.7-, 1.8- and 3.3-fold and the rate of TG secretion 1.8-, 1.6- and 1.4-fold when the dietary carbohydrate was glucose, sucrose and fructose, respectively, in comparison with control rats fed diets supplying these same carbohydrates but adequate in EFA. In the latter groups, the rates of plasma TG secretion were in the range of 0.14–0.17 mg/min per 100 g body weight, and the rate of secretion in the fructose-fed rats was only 20% higher than in the glucose-fed rats.

KEY WORDS: • triacylglycerol secretion • plasma triacylglycerol turn-over • sucrose • glucose • fructose • [2-³H]glycerol • tracer kinetics

¹ Supported in part by California Agricultural Experiment Station Project 1166A and U.S. Public Health Service Grants AM12024 from the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases (to M. A. W.) and CA15813 from the National Cancer Institute (to N. B.).

² Present address: Department of Biochemistry, University College, London, Gower Street, London WC1E 6BT, U.K.

³ To whom reprint requests should be addressed.

Manuscript received 16 May 1984.

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