Dietary effects of partial or total substitution of sucrose for starch on glucose and lipid metabolism in dyslipidemic rats

被引:16
作者
Chicco, A [1 ]
Bernal, C [1 ]
Soria, A [1 ]
Giangrossi, G [1 ]
Lombardo, Y [1 ]
机构
[1] Univ Litoral, Dept Biochem, RA-3000 Santa Fe, Argentina
关键词
sucrose-rich diet; hypertriglyceridemia; insulin resistance; glucose intolerance; dyslipidemia;
D O I
10.1016/S0271-5317(98)00191-2
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Rats fed on a sucrose-rich diet (SRD) (63 % w/w) up to 30 weeks develop stable hypertriglyceridemia, impaired glucose tolerance and insulin insensitivity. At present only scarce and non-systematic information is available concerning the possible reversion of these metabolic derangements by nutritional or metabolic interventions. The present study was designed to investigate the effect of the isocaloric substitution of sucrose for starch (during 15 weeks) on lipid and glucose metabolisms in rats in which a well-established hypertriglyceridemia and glucose intolerance were present before the amount of sucrose (63% w/w) was partially (33% w/w) or totally (0% w/w) replaced by an isocaloric amount of starch. Our findings show that: i) when the amount of fructose (sucrose moieties) is partially replaced by starch (from 33 to 18% of the total calories) most of its undesirable effects on lipid metabolism are still present and no significant improvement in glucose regulation is noticed; ii) hypertriglyceridemia and glucose intolerance can be completely reversed, without detectable changes in circulating insulin levels, by shifting completely to starch as the source of carbohydrate in the diet. Moreover, when sucrose was removed from the diet, it took 7 weeks for plasma triglyceride levels to become completely normal while plasma free fatty acids and glucose levels needed twice that time. These findings suggest that manipulation of dietary fructose may play a role in the management of lipid disorders associated with glucose intolerance and insulin resistance. (C) 1999 Elsevier Science Inc.
引用
收藏
页码:281 / 293
页数:13
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