Journal of Nutritional Science and Vitaminology
Online ISSN : 1881-7742
Print ISSN : 0301-4800
ISSN-L : 0301-4800
Comparison of the Isotopical Tracer and the Triton WR 1339 Methods for Triglyceride Kinetics in Carbohydrate-fed Rats
平野 勉John C. L. MAMO高橋 昭三
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1990 年 36 巻 4-SupplementI 号 p. 399-409

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Radiolabeled tracer [3H] very low density lipoprotein (VLDL)-triglyceride (TG) and non-tracer (Triton WR 1339) methods were used to determine VLDL-TG kinetics in normal rats and in rats given either a 10% glucose or a 10% fructose drinking solution for 16 h ad libitum. The carbohydrate-fed rats were hypertriglyceridemic com-pared to control animals. VLDL-TG was endogenously prelabeled with [3H] glycerol in control, glucose- and fructose-fed rats, and injected into identically treated recipients. Triton WR 1339, a potent inhibitor of VLDL-TG catabolism, was injected into the same animal 30 min after the end of the tracer method to measure TG secretion rate (TGSR). The tracer and non-tracer methods showed that fructose-fed rats had a sig-nificantly lower fractional catabolic rate (FCR) than either control or glucose-fed rats. In contrast, glucose-fed rats had a TGSR greater than control without a reduction in FCR. For all treatments, TG concentra-tion correlated with FCR for the tracer method and with TGSR for the non-tracer method. There was good correlation of TGSR determined by the tracer and non-tracer method for control rats despite the substantial difference in the absolute values. No such relationship was observed in carbohydrate-fed rats. Control rats were made hypertriglyceridemic by Intralipid infusion. A lower FCR was observed when determined by the tracer method, but this was not observed by the triton method. These results suggest that TG kinetics determined by the tracer and the triton methods cannot be readily correlated, especially in hypertriglyceridemic state. However, the two kinetic studies both suggested that overproduc-tion of VLDL-TG in glucose-fed rats and impaired VLDL-TG catabo-lism in fructose-fed rats were the primary cause for their hypertriglycer-idemic, respectively.

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