Oxidized low density lipoproteins (LDLs) are thought to play an important role in atherogenesis. Nutritional and biochemical studies suggest that diet can modulate the susceptibility of plasma LDL to undergo oxidative degradation by affecting the concentration of polyunsaturated fatty acids and antioxidants in the lipoprotein particle. In the present study 11 healthy male volunteers underwent two diet phases. In one phase the diet was enriched in oleic acid (mono), while in the other it was high in linoleic acid (poly). Both diets lowered plasma total and LDL cholesterol contents. The sensitivity of plasma LDL to oxidation was estimated by challenging these lipoproteins with 2,2'-azobis(2-amidinopropane)dihydrochloride, a free-radical initiator. Although neither diet affected the antioxidant content of plasma LDL, the resistance to lipid peroxidation, measured after the consumption of antioxidants present in the lipoprotein, was higher during the mono phase. Indeed, the peroxidation rate of plasma LDL was inversely correlated with the oleic acid to linoleic acid ratio in the LDL particle. These results support the thesis that diets rich in monounsaturated fatty acids increase the resistance of plasma LDL to oxidative modification, independent of their content of antioxidants. This effect could lower the atherogenicity of these lipoproteins.
Nineteen patients affected by non-insulin dependent diabetes mellitus (NIDDM), in good glycemic control (fasting plasma glucose 7.2 +/- 0.3 mmol/L, glycosylated hemoglobin 6.3 +/- 0.2%), underwent three isocaloric dietary phases. In phases 1 and 3 the diet was rich in complex carbohydrates (Carbo) whereas in phase 2 it was rich in monounsaturated fatty acids (Mono). Plasma glucose concentrations were 7.1 +/- 0.3 and 7.2 +/- 0.3 mmol/L for the two Carbo phases and 7.5 +/- 0.4 mmol/L for the Mono phase (NS). Plasma total cholesterol values for the Carbo phases were 6.2 +/- 0.2 and 6.4 +/- 0.2 mmol/L, respectively, and 6.5 +/- 0.2 mmol/L on the Mono phase (NS). Similarly, no significant changes were noticed for plasma triglycerides and high-density-lipoprotein (HDL) cholesterol. Thus, both diets were well-tolerated and did not alter glucose homeostasis or worsen plasma lipid concentrations. Consequently, these results suggest that a wider dietary choice can be made available to NIDDM patients without producing unwanted side effects.
In a case of 'spur cell anaemia' (SCA) a reduced esterified/free cholesterol ratio was found in plasma, in LDL and HDL fractions and an increased cholesterol/phospholipid (C/PL) molar ratio in erythrocyte membrane. Cation transport was normal with the exception of Li-Na counter-transport was decreased. An increased intrinsic membrane proteolytic activity (IMPA) was demonstrated by the generalized reduction or, sometimes, disappearance of protein bands on SDS-PAGE in patient ghosts when the proteolysis was allowed. This characteristic was found to be transferable to normal cells by incubation in SCA-plasma; moreover membrane C/PL molar ratio was augmented after incubation. Normal plasma was not able to normalize IMPA of SCA cells 'in vitro', even if it induced a remarkable decrease of membrane C/PL molar ratio. Nevertheless IMPA normalization did occur 'in vivo', when the SCA cells were exposed to therapeutic 'plasma exchange' (3.3 litre/week). The results suggest the following conclusions: (a) in our SCA patient there is an increased IMPA; (b) this feature, as well as membrane lipid alteration, is transferable to normal erythrocytes; (c) this case seems to demonstrate, for the first time in our knowledge, a modulating effect of plasma on IMPA in erythrocytes.
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