Plasma lipids and fatty acid synthase activity are regulated by short-chain fructo-oligosaccharides in sucrose-fed insulin-resistant rats.

The aim of this study was to evaluate the chronic effects of a short-chain fructo-oligosaccharide (FOS)-containing diet on plasma lipids and the activity of fatty acid synthase (FAS) in insulin-resistant rats. Normal male Sprague-Dawley rats, 5 wk old, were randomly assigned to two groups and fed either a sucrose-rich diet (S, 575 g sucrose /kg diet and 140 g lipids/kg diet) or a sucrose-rich diet supplemented with 10 g/100 g short-chain fructo-oligosaccharides (S/FOS). A third reference group (R) was fed a standard nonpurified diet (g/kg, 575 g starch, 50 g fat). After 3 wk the sucrose-fed rats (compared with the R group) were characterized by the following: 1) higher insulin responses after a glucose challenge (P < 0.05); 2) heavier liver (P < 0.001) and retroperitoneal adipose tissue (P < 0.01); 3) hypertriglyceridemia (P < 0.0001) and higher plasma free fatty acids (P < 0.0001); and 4) higher fatty acid synthase activity in the liver but a low activity in the adipose tissue (P < 0.001). The addition of FOS to the diet resulted in 11% lower liver weight than in the S group (P < 0.05) and tended to result in lower adipose tissue weight (P < 0.11). Plasma triglycerides and plasma free fatty acids were lower in S/FOS- than in S-fed rats (P < 0.05). Chylomicrons + VLDL, and intermediate density lipoprotein (IDL) concentrations did not differ between groups, nor was plasma cholesterol influenced by diet. Hepatic FAS activity was lower in S/FOS-fed rats than in the S-fed rats (P < 0.05). In adipose tissue, however, this activity tended to be greater in rats fed S/FOS than in rats fed the S diet (P < 0.07). In conclusion, in a rat model of diet-induced (57.5% sucrose and 14% lipids) insulin resistance, the addition of short-chain FOS prevented some lipid disorders, lowered fatty acid synthase activity in the liver and tended to raise this activity in the adipose tissue. Short-chain FOS, in addition to being a nondigestible sweetener with good bulking capacity, might be useful in the treatment of insulin resistance and hyperlipidemia.

Effect of simvastatin and fenofibrate on the fatty acid composition of hypercholesterolaemic patients.

1. The effects of simvastatin (one of a new class of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors) and fenofibrate on the fatty acid composition of cholesterol esters, phospholipids and triglycerides of different lipoproteins of 15 patients with primary hypercholesterolaemia were compared in a double-blind study. 2. Fenofibrate (300 mg day-1) increased the relative content of saturated fatty acids of cholesterol esters, phospholipids and triglycerides in VLDL, IDL and HDL. It also increased the relative content of monounsaturated fatty acids of cholesterol esters and phospholipids in all fractions and those of triglycerides in VLDL and IDL. In contrast, it decreased the proportion of polyunsaturated fatty acids of cholesterol esters and phospholipids in all fractions and those of triglycerides in VLDL and IDL. The polyunsaturated/saturated (P/S) ratio was reduced in cholesterol esters and phospholipids in VLDL and in phospholipids in IDL by fenofibrate. The drug significantly increased the 18:1w9/18:2w6 ratio in cholesterol esters and phospholipids in VLDL, LDL and HDL, but produced a non-significant increase in the ratio in IDL. 3. Simvastatin (20 mg day-1) produced a significant decrease in saturated fatty acid and an increase in polyunsaturated fatty acid in triglycerides in VLDL. Simvastatin, in contrast to fenofibrate caused a slight decrease in saturated and monounsaturated fatty acids in the three other lipoprotein fractions, and an increase in polyunsaturated fatty acids. The P/S and 18:1w9/18:2w6 ratios were not modified by simvastatin.

Effect of dietary treatment on the lipid, lipoprotein and fatty acid compositions in type IV familial hypertriglyceridemia.

The effects of a 2-month dietary treatment (1,625 +/- 177 kcal, 40 +/- 2.3% carbohydrate, 35 +/- 3.7% fat, 25 +/- 2% protein, polyunsaturated/saturated fat ratio = 1.02 +/- 0.06) on the overall composition of serum lipids, lipoproteins and the fatty acid composition of cholesterol esters and phospholipids in very low (VLDL), intermediate (IDL), low (LDL) and high (HDL) density lipoprotein in 5 patients with primary familial hypertriglyceridemia type IV were assessed. The data were compared with those for 9 normolipidemic subjects. Treatment decreased serum triglycerides (-52%) and total cholesterol (-12%) due to decrease in free cholesterol (-30%). It produced a significant decrease in all the constituents of VLDL (-58%), but the VLDL remained significantly higher after treatment than those of control subjects. The diet caused a decrease in triglycerides (-16%, -29% and -33%, respectively), and an increase in cholesterol in IDL, LDL and HDL. The IDL level in the treated patients remained significantly higher than in the controls. The LDL cholesterol/HDL cholesterol ratio was unchanged after treatment. The fatty acid compositions of the patients before treatment and the controls were not significantly different. The diet caused a decrease in palmitoleic and oleic acids in the cholesterol ester fraction and an increase in linoleic acid, but this was significant only in VLDL and HDL. The diet decreased the eicosapentaenoic acid but the drop was only significant in IDL and LDL. There was also a decrease in linolenic acid, only significant in IDL. The diet induced only minor changes in the phospholipid fractions. We concluded that a single nutritional regimen can effectively decrease the serum lipids and normalize the lipoprotein composition of type IV hypertriglyceridemic patients.