March 24/Lund, Sweden/Cardiovascular Device Liability Week -- According to recent research published in the British Journal of Nutrition, "Cholesterol-lowering effects of oats have been demonstrated in both animals and human subjects. However, the crucial properties of oat-containing diets that determine their health effects need to be further investigated to optimize their use."
"A mouse model would be a valuable tool, but few such studies have been published to date. We investigated the effects of oat bran on plasma cholesterol and lipoproteins in two substrains of C57BL/6 mice. Western diet was made atherogenic by the addition of 0.8 % cholesterol and 0.1 % cholic acid. After four weeks on atherogenic diet, total plasma cholesterol had increased from 1.86-2-53 to 3.77-4-40mmol/l. In C57BL/6NCrl mice, inclusion of 27% and 40% oat bran reduced total plasma cholesterol by 19% and 24 %, respectively, reduced the shift from HDL to LDL + VLDL and caused increased fecal cholesterol excretion. There was no effect of oat bran on plasma levels of the inflammatory markers fibrinogen, serum amyloid A or TNF-alpha. Contrary to findings in C57BL/6NCrl mice, there was no sustained effect of oat bran (27% or 40 %) on plasma cholesterol in C57BL/6JBomTac mice after four weeks of feeding. Thus, C57BL/6NCrl mice fed an atherogenic diet are a good model for studies of physiological effects of oats, whereas a substrain derived from C57BL/6J, raised in a different breeding environment and likely possessing functional genetic differences from C57BL/6N, is considerably less responsive to oats," wrote K.E. Andersson and colleagues, Lund University.
The researchers concluded, "The present finding that two substrains of mice respond differently to oats is of practical value, but can also help to elucidate mechanisms of the cholesterol-lowering effect of oats."
Andersson and colleagues published their study in British Journal of Nutrition ("Effects of Oats on Plasma Cholesterol and Lipoproteins in C57BL/6 Mice are Substrain-specific." British Journal of Nutrition, 2010;103(4):513-521).
For additional information, contact K.E. Andersson, Lund University, Dept. of Expt Med Sci, BMC D12, SE-22184 Lund, Sweden.
From the March 29, 2010, Prepared Foods E-dition
