DIETS CONTAINING SOLUBLE OAT EXTRACTS REDUCE URINARY MALONDIALDEHYDE IN MODERATELY HYPERCHOLESTEROLEMIC MEN AND WOMEN

Citation
J. Hallfrisch et al., DIETS CONTAINING SOLUBLE OAT EXTRACTS REDUCE URINARY MALONDIALDEHYDE IN MODERATELY HYPERCHOLESTEROLEMIC MEN AND WOMEN, Journal of nutritional biochemistry, 8(9), 1997, pp. 497-501
Citations number
27
Categorie Soggetti
Nutrition & Dietetics",Biology
ISSN journal
09552863
Volume
8
Issue
9
Year of publication
1997
Pages
497 - 501
Database
ISI
SICI code
0955-2863(1997)8:9<497:DCSOER>2.0.ZU;2-M
Abstract
Soluble oat extracts have been used successfully in a number of diet s tudies to lower plasma blood lipids. One of the mechanisms proposed fo r this reduction in lipids is the production of short-chain fatty acid s in the large intestine, which, in turn, may inhibit low-density lipo protein cholesterol synthesis thereby limiting oxidation. Urinary excr etion of malondialdehyde (MDA) is proportional to endogenous lipid per oxidation. The purpose of this report is to examine the effects of con suming oat extracts with low (1%) or high (10%) levels of soluble beta -glucans on lipid peroxidation as measured by urinary malondialdehyde excretion. Twenty-four subjects with moderately elevated cholesterol l evels (6.0 mmol/L) were selected for the study. A I-week equilibration period was followed by two 5-week experimental periods during which d efined diets contained the 1% or 10% oat extracts in a crossover desig n. Seventy-two-hr urine samples (3 x 24-hr) were collected at the end of each period Urinary levels of MDA excreted were 10-18% of dietary M DA consumed. Consumption of either of the oat extracts resulted in hig hly significant reductions in urinary excretion of malondialdehyde (P < 0.0001). These data would support the hypothesis that oar extracts i nhibit endogenous lipid peroxidation by reduction of MDA (a marker for fatty acid oxidation); however, because no significant differences we re found in MDA excretion after subjects consumed the two levels of be ta-glucans, this is apparently not the responsible component. Further examination of this mechanism in the control of lipid metabolism is wa rranted. (C) Elsevier Science Inc. 1997.