抄録
Hypertriglyceridemia (HTG) is considered to be a risk factor for development of ischemic heart disease. Previously, the authors reported on a simplified intravenous fat emulsion tolerance test (FETT). In the present study, FETT is applied for the analysis of the pathogenesis of HTG and to determine the nutrient composition of a diet in HTG treatment.
The subjects were 9 patients with primary HTG and one with secondary HTG and obesity. The serum triglyceride level was determined before treatment, and subjects were admitted to the hospital for two weeks. The effects of two kinds of diet (A and B) were compared in terms of serum triglyceride (Table 2).
Diet A consisted of 20% calories as fat, 60% as carbohydrate, and 20% as protein. Diet B consisted of 40% calories as fat, 40% as carbohydrate, and 20% as protein. Total diet calory intake was limited to 25-30kcal/kg of ideal b. w. per day. After one week of diet treatment (either one), the serum TG levels of patients were determined for 24hr.
FETT was done as follows: After an overnight fast, an indwelling catheter was inserted into an antebrachial vein, and 0.25ml 10% Intralipid/kg b. w. was injected intravenously in 90 seconds.
Time measurements were started at midpoint of injection, and blood was sampled at 2-3, 5, 7, 9, 11, 14, 17 and 20min, respectively. Light scattering index (LSI) of serum diluted 1:100 in physiological saline, was determined by the nephelometric method. The zero-time value was then subtracted from the value for each post-injection sample. Removal rate was calculated by the method of least squares, using the logarithmic values of LSI. The TG levels in all subjects improved with either diet A or B (Fig. 1). In cases 1, 2, 3, 4, 5 and 6, the TG levels improved more in a day with diet B than diet A (Fig. 2). Cases 7 and 8 showed more TG improvement on diet A (Fig. 2).
Assuming that a multiplication of total serum TG by K2 is a crude estimate of VLDL-TG production, HTG in cases 1 and 2 might be caused by increased VLDL-TG production, and HTG in cases 3, 4 and 5 by both increased VLDL production and decreased VLDL removal from circulation. In the serum of cases 7 and 8 on diet A, chylomicrons of the layer overlying a turbid infranatant layer were observed to correspond to a TG peak concentration in the serum following the meal. HTG in cases 7 and 8 may have been caused by both decreased VLDL removal and decreased chylomicron removal from the circulation.
From these results, diet A with less fat (20% of total calories) should be given to HTG patients with a K2 level under 2%/min. The pathogenesis of HTG could be known by FETT. And FETT is a useful method to determine the nutrient composition of the diet to be used in treating HTG.
