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Resistant starch is more effective than cholestyramine as a lipid‐lowering agent in the rat
Author(s) -
Younes Hassan,
Levrat MarieAnne,
Demigné Christian,
Rémésy Christian
Publication year - 1995
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02533961
Subject(s) - cholestyramine , chemistry , cholesterol , resistant starch , bile acid , medicine , endocrinology , triglyceride , excretion , lipoprotein , fatty acid , starch , biochemistry , biology
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 on 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.