Nondigestible CHOs (NDCs) such as inulin and oligofructose70 are fermentable in the colon and produce short chain fatty acids (acetic acid, propionid, and butyric acids). A large body of evidence indicates that NDCs can decrease in rodent TG and cholesterol concentrations.71-76 The decrease in TG levels has been ascribed to inhibition of hepatic lipogenesis,74,77 decreased reesterification of fatty acids by the liver,73 and a reduction of VLDL-TG secretion.74 Liver lipogenesis may be inhibited by propionic acid.78
Wolever et al. showed that propionate decreased the incorporation of 13C labelled colonic acetate in plasma TG in humans; the effect on the incorporation in plasma cholesterol was not significant.79 Several studies showed that NDCs reduce TG concentrations in control humans, particularly while on high-CHO diets,80-82 and can also reduce cholesterol levels.82 Negative results have also been reported in normal subjects, probably because of low doses of CHOs and relatively high fat diets.83,84
Hepatic lipogenesis was decreased by inulin80 and the decrease probably participated in the reduction of plasma TG concentrations. Unlike liver lipogenesis, neither cholesterol synthesis nor concentrations of mRNA for lipogenic enzymes in adipose tissue were modified by inulin. More conflicting results were reported in type II diabetic patients and in subjects with moderate hyperlipidemias. NDCs decreased plasma cholesterol but had no effect on plasma TG85-87 or plasma lipids.88 89 These discrepancies suggest that the metabolic effects of NDCs on lipid metabolism may be different in normal subjects and in pathological situations. NDC administration in obese Zucker rats did not decrease circulating TG levels, contrary to findings in control rats, and decreased only malic enzyme activity among all the lipogenic enzymes.90
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