RESISTANT STARCH IS MORE EFFECTIVE THAN CHOLESTYRAMINE AS A LIPID-LOWERING AGENT IN THE RAT

Amylase-resistant starch (RS) represents a substrate for the bacterial flora of the colon, and the question arises as whether RS shares with soluble fibers common mechanisms for their lipid-lowering effects. It is uncertain whether a cholesterol-lowering effect depends basically on an enhanced rate of steroid excretion or whether colonic fermentations also play a role in this effect. In the present study, the effect of RS (25% raw potato starch), of a steroid sequestrant (0.8% cholestyramine), or both were compared an bile acid excretion and lipid metabolism in rats fed semipurified diets. RS diets led to a marked rise in cecal size and the cecal pool of short-chain fatty acids (SCFA), as well as SCFA; absorption; cholestyramine did not noticeably affect cecal fermentation. Whereas cholestyramine was particularly effective at enhancing bile acid excretion, RS was more effective in lowering plasma cholesterol (-32%) and triglycerides (-29%). The activity of 3-hydroxy-3-methylglutaryl-CoA reductase was increased fivefold by cholestyramine and twofold by RS. This induction in rats fed RS diets was concomittant to a depressed fatty acid synthase activity. In rats fed the RS diet, there was a lower:concentration of cholesterol in all lipoprotein fractions, especially the (d = 1.040 - 1.080) fraction high-density lipoprotein (HDL(1)), while those fed cholestyramine had only a significant reduction of HDL(1) cholesterol. In contrast to cholestyramine, RS also depressed the concentration of triglycerides in the triglyceride-rich lipoprotein fraction. There was no noticeable synergy between the effects of RS and cholestyramine when both were present in the diet. This suggests that the cholesterol-lowering effect of RS is not limited to its capacity to enhance bile acids excretion. The difference between RS and cholestyramine could relate to the capacity of fermentation end-products to counteract the upregulation of cholesterol and bile acid biosynthesis. Thus, in the absence of fermentation in the large intestine, a high rate of bile acids excretion is not always sufficient to elicit a cholesterol-lowering effect.