Physiology publications

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Browsing Physiology publications by Author "Abbey, M."

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    Body fat distribution as a determinant of the lipoprotein response to dietary fat and cholesterol
    (Louisiana State University Press, 1996) Clifton, P.; Abbey, M.; Noakes, M.; Nestel, P.; Bray, G.A.; Ryan, D.H.
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    Dietary supplementation with orange juice and carrot juice in cigarette smokers lowers oxidation products in copper oxidised low density lipoproteins
    (The Association, 1995) Abbey, M.; Noakes, M.; Nestel, P.

    Objective

    Our objective was to evaluate the effect of daily supplementation with foods high in vitamin C and beta carotene on plasma vitamin levels and oxidation of low-density lipoprotein (LDL) in cigarette smokers.

    Subjects

    Fifteen normolipidemic male cigarette smokers who did not usually take vitamin supplements were recruited into the study.

    Interventions

    Throughout the study, subjects consumed a diet rich in polyunsaturated fatty acids, which provided 36% of energy as fat: 18% from meat, dairy products, vegetable oils, and fat spreads and 18% from walnuts (68 g/day). Subjects consumed a vitamin-free drink daily for 3 weeks; then for 3 weeks they consumed daily supplements of orange juice (145 mg vitamin C) and carrot juice (16 mg beta carotene).

    Results

    Vitamin-rich food supplements raised plasma levels of ascorbic acid (1.6-fold; P < .01) and beta carotene (2.6-fold; P < .01). Malondialdehyde, one end product of oxidation, was lower in copper-oxidized LDL after vitamin supplementation (mean +/- standard error = 65.7 +/- 2.0 and 57.5 +/- 2.9 mumol/g LDL protein before and after supplementation, respectively; P < .01). Rate of LDL oxidation and lag time before the onset of LDL oxidation were not affected by antioxidant supplementation.

    Conclusions

    In habitual cigarette smokers, antioxidant vitamins, which can be feasibly provided from food, partly protected LDL from oxidation despite a diet rich in polyunsaturated fatty acids.
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    Enhanced capacity of n-3 fatty acid-enriched macrophages to oxidise low density lipoproteins: Mechanisms and effects of antioxidant vitamins
    (ELSEVIER SCI IRELAND LTD, 1996) Suzakawa, M.; Abbey, M.; Clifton, P.; Nestel, P.
    We have investigated possible mechanisms by which n-3 fatty acid-enriched macrophages enhance the oxidation of low density lipoprotein (LDL), and the ability of antioxidant vitamins to prevent this. Macrophages were enriched with n-3 fatty acids (eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid) following incubation with fish oil. These macrophages produced large amount of TBARS in medium containing metals, and showed enhanced capacity to oxidize LDL (3-4 fold increase compared to control cells) and to accumulate the modified LDL. 5,8,11,14-eicosatetraynoic acid (ETYA, 15-lipoxygenase inhibitor) and superoxide dismutase (SOD) did not inhibit the enhanced capacity of n-3 fatty acid-enriched cells to oxidize LDL. However antioxidants, (vitamin E-enriched macrophages or vitamin C in the medium), inhibited this enhanced capacity. Medium conditioned by n-3 fatty acid-enriched cells had pro-oxidant effects on metal-initiated LDL oxidation. We conclude that n-3 fatty acid-enriched macrophages display increased oxidant capacity which is not inhibited by ETYA or SOD, and that antioxidant vitamins inhibit the enhanced capacity to oxidize LDL.
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    Hormone replacement therapy is associated with improved arterial physiology in healthy post-menopausal women
    (Wiley, 1996) McCrohon, J.; Adam, M.; McCredie, R.; Robinson, J.; Pike, A.; Abbey, M.; Keetch, A.; Cabermajer, D.
    OBJECTIVE Oestrogen replacement therapy is associated with a marked reduction in coronary event rates in post‐menopausal women. As older age is associated with progressive arterial endothelial damage, a key event in atherosclerosis, we assessed whether hormone replacement therapy (HRT) with oestrogen alone, or oestrogen and progesterone combined, is associated with improved endothelial function in healthy women after the menopause. DESIGN Using high resolution external vascular ultrasound, brachial artery diameter was measured at rest and in response to reactive hyperaemia, with increased flow causing endothelium‐dependent dilatation (flow‐mediated dilatation). PATIENTS  We investigated 135 healthy women; 40 were pre‐menopausal (mean±SD age/26±6 years, group 1), 40 were post‐menopausal and had never taken HRT (aged 58±3 years; group 2) and 55 were age‐matched post‐menopausal women who had taken HRT for >2 years, from within 2 years of the menopause (aged 57±4 years; group 3). In group 3, 40 women were on combined oestrogen and progesterone and 15 on oestrogen‐only HRT. RESULTS In group 2, flow‐mediated dilatation was significantly reduced compared with group 1 (4.4±3.4 vs 9.6±3.6%, P<0.001), consistent with a decline in arterial endothelial function after the menopause. In group 3, however, flow‐mediated dilatation was significantly better than group 2 (6.2±3.3 vs 4.4±3.4%, P=0.01), suggesting a protective effect of HRT. Flow‐mediated dilatation was similar in women taking oestrogen alone and in those on combined HRT (5.5±2.8 vs 6.5±3.4%, P=0.40). CONCLUSIONS Long‐term HRT is associated with improved arterial endothelial function in healthy post‐menopausal women. This benefit was observed in both the combined hormone replacement and unopposed oestrogen therapy groups. This may explain some of the apparent cardioprotective effect of HRT after the menopause.