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Biomedical subjects

M F Oliver

Publications and source records attributed to M F Oliver.

At least 37 records · Page 2Linked to original sources
PubMed1997

Influence of n-6 versus n-3 polyunsaturated fatty acids in diets low in saturated fatty acids on plasma lipoproteins and hemostatic factors.

Modification of dietary fat composition may influence hemostatic variables, which are associated with increased risk of coronary heart disease (CHD). To address this question, we performed a controlled feeding study on 26 healthy male nonsmoking subjects with diets of differing fat composition. For the first 3 weeks, the subjects were given a diet calculated to supply 30% energy as total fat: 8% as monounsaturated, 4% as polyunsaturated, and 16% energy as saturated fatty acids, respectively (saturated diet). This was followed immediately by two diets taken in random order, each of 3-week duration and separated by an 8-week washout period on the subject's usual diet. Both diets were calculated to supply 30% of energy as fat: 14% monounsaturated, 6% as polyunsaturated, and 8% energy as saturated fatty acids. They both provided 5 g (approximately 1.7% energy) more of polyunsaturated fatty acids than the saturated fat diet; in one diet as long-chain n-3 fatty acids (n-3 diet) and in the other as linoleic acid (n-6 diet). Fasting plasma lipids, lipoproteins, and hemostatic factors were measured on the final 3 days of each dietary period. In a subset of 9 subjects the postprandial responses to a test meal were studied on the penultimate day of each period, each meal having the fat composition of its parent diet. On the n-3 diet compared with the n-6 diet, plasma triglyceride, HDL3 cholesterol, apoprotein AII, and fibrinogen concentrations were lower and HDL2 cholesterol concentration was higher (P = .0001, P = .003, P = .0001, P = .004, and P = .001, respectively). On both the n-3 and n-6 diets compared with the saturated diet, fasting plasma total and LDL cholesterol, apoprotein B, beta-thromboglobulin concentrations, and platelet counts were lower (P < .0001, P < .0001, P < .001, P < .01, and P < .05 respectively) and plasma Lp(a) and von Willebrand factor concentrations were higher (P = .02 and P < .01, respectively). Fasting factor VII coagulant activity (VIIc) was increased and apoprotein AI concentration reduced following the n-3 diet (P = .004 and P = .01, respectively) compared with the saturated diet. Plasma fibrinogen concentration was significantly greater following the n-6 diet than on the saturated diet (P = .02). Postprandially, plasma triglyceridemia was greater on the n-6 diet and lowest on the n-3 diet (P < .001) with the saturated diet being intermediate. Plasma VIIc was increased at 4 hours following the standardized test meals on the n-3 and n-6 diets (both P < .05) but not on the saturated diet. An increased intake of long chain n-3 fatty acids decreases fasting plasma triglyceride and apoprotein AII concentrations and increases HDL2 cholesterol concentrations and results in less postprandial lipemia but leads to an increase in VIIc. An increased intake of linoleic acid may raise plasma fibrinogen concentration. Decreasing the intake of saturated fatty acids reduces plasma LDL cholesterol and apoprotein B without affecting HDL cholesterol concentration independent of the type of polyunsaturated fatty acids in the diet. When advice is given to reduce saturated fat intake, it is important to ensure an appropriate ratio of n-3/n-6 fatty acids in the diet.

Adult↗
PubMed1997

Relation of plaque lipid composition and morphology to the stability of human aortic plaques.

The propensity of atherosclerotic plaques to disrupt may be influenced by their lipid content and the distribution of these lipids within the plaque. To investigate this, we analyzed the morphological and lipid profiles of 668 human aortic plaques from 30 males who had died of ischemic heart disease. Plaques were classified as disrupted or as intact types A or B, the latter distinction being based on the absence or presence, respectively, of disrupted plaques within the same aorta. Disrupted plaques have a greater content of lipid (P < .001) and macrophages (P < .001) as well as a thinner cap (P < .001) than intact plaques. Lipid concentrations are positively associated with macrophage accumulation in all plaque types and are negatively associated with minimum cap thickness at the edge of disrupted plaques (P < .05). Free cholesterol concentration is inversely associated with minimum cap thickness at the center of type B plaques only (P < .05). At the center of intact type A and B and disrupted plaques, the free-to-esterified cholesterol ratios were 0.9 (range, 0.0 to 2.7), 0.8 (0.0 to 3.9), and 1.6 (0.2 to 4.0), respectively. Esterified cholesterol concentrations were higher at the center of type B plaques, and those of free cholesterol were higher at the center of disrupted plaques. At the edge of disrupted plaques, the free-to-esterified cholesterol ratio was 0.5 (0.0 to 2.7) because of the accumulation of esterified cholesterol. Concentrations of all fatty acids were increased at the edge of disrupted plaques compared with the center, but as a proportion of total fatty acids, omega 6-polyunsaturated fatty acids (PUFAs) were lower (44% versus 46%, P < .01), possibly reflecting oxidation of PUFAs. These data demonstrate differences in lipid composition and intraplaque lipid distribution between intact and disrupted plaques. At the edge of advanced plaques, increased esterified lipid concentrations, inversely associated with cap thickness, may reflect macrophage activity and a predisposition to rupture.

Aged↗
PubMed1994

Dietary polyunsaturated fatty acids and composition of human aortic plaques.

How long-term dietary intake of essential fatty acids affects the fatty-acid content of aortic plaques is not clear. We compared the fatty-acid composition of aortic plaques with that of post-mortem serum and adipose tissue, in which essential fatty-acid content reflects dietary intake. Positive associations were found between serum and plaque omega 6 (r = 0.75) and omega 3 (r = 0.93) polyunsaturated fatty acids, and monounsaturates (r = 0.70), and also between adipose tissue and plaque omega 6 polyunsaturated fatty acids (r = 0.89). No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered.

Adipose Tissue↗
PubMed1994

Effects of glucose and fatty acids on myocardial ischaemia and arrhythmias.

Evidence for the utilisation of substrates by the ischaemic myocardium and its dependence for viability on a critical supply of glucose was established many years ago. It was recognised that an excess of free fatty acids (FFA) could increase the severity of ischaemic damage and possibly be arrhythmogenic. But metabolic intervention to improve survival during acute myocardial infarction was not regarded as a priority, perhaps because of uncertainty about its value and the advent of trials of beta-blocker and antiarrhythmic drugs. There has never been an adequate trial of the benefit to the ischaemic or infarcting myocardium of increasing local glucose concentrations or reducing the availability of FFA. We have taken into account new knowledge of the effects of fatty acids on cation channels and brought up to date the arguments for metabolic intervention with glucose-insulin solutions or antilipolytic drugs sustained ischaemia.

Animals↗
PubMed1994

Insulin resistance in chronic heart failure.

The objective of this study was to investigate the existence of abnormalities of insulin sensitivity in patients with chronic heart failure. Glucose metabolism and insulin resistance were assessed in 10 male patients with severe, chronic heart failure and in 10 matched control subjects. Glucose, insulin and C-peptide concentration profiles were measured following a 0.5 g.kg-1 intravenous glucose tolerance test. Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Heart failure patients had similar mean fasting plasma glucose concentration to controls but a significantly greater mean fasting plasma insulin concentration (P = 0.002) and C-peptide concentration (P = 0.02). Plasma glucose response profile was similar in the two groups but the incremental plasma insulin response profile of the heart failure group was significantly greater (P = 0.004). Mean insulin sensitivity was 73% lower in the heart failure patients (P = 0.003). These findings show that patients with severe chronic heart failure are hyperinsulinaemic and insulin resistant compared with a matched health group. This insulin resistance and hyperinsulinaemia may contribute to the progressive deterioration in myocardial function and associated clinical features of fatigue and reduced exercise tolerance seen in heart failure. Interventions designed to overcome or reduce insulin resistance warrant further investigation.

Blood Glucose↗
PubMed1994

Insulin resistance syndrome as a feature of cardiological syndrome X in non-obese men.

OBJECTIVE: To assess the features of the insulin resistance syndrome in patients presenting with cardiological syndrome X, who experience angina despite angiographically normal coronary arteries. PATIENTS AND METHODS: 14 Non-obese male patients with syndrome X and 38 symptom free, apparently healthy, male volunteers were studied. Insulin sensitivity (inversely related to insulin resistance) was measured by minimal modelling analysis of glucose and insulin concentrations during an intravenous glucose tolerance test. Serum lipids, lipoproteins, and apolipoproteins were also measured. RESULTS: Insulin sensitivity was 31% lower in the men with syndrome X (p < 0.05) and fasting insulin concentration was 30% higher (p < 0.05). The patient group also had 64% higher mean triglycerides (p < 0.001) and 20% lower mean high density lipoprotein cholesterol concentration (p < 0.01). Systolic blood pressure was also 10% higher in the syndrome X group (p < 0.01). There were no differences in total cholesterol, low density lipoprotein cholesterol or lipoprotein (a). CONCLUSION: These findings show that non-obese male patients with anginal chest pain but normal coronary arteries (syndrome X) are insulin resistant, hyperinsulinaemic, and have higher concentrations of triglycerides and lower high density lipoprotein cholesterol than healthy men. The insulin resistance syndrome may predispose to a spectrum of arterial disease capable of causing myocardial ischaemia.

Adult↗
PubMed1993

Exercise tolerance in angina is improved by mivazerol--an alpha 2-adrenoceptor agonist.

In a double-blind, placebo-controlled, randomized trial of treadmill exercise tolerance in six patients with chronic stable angina, intravenous mivazerol 1 microgram, 2 micrograms, and 3 micrograms/kg increased the time to onset of angina by 39%, 48%, and 76%; the time to 1-mm ST depression by 36%, 76%, and 104%; and total exercise duration by 15%, 23%, and 30%, respectively. In a subsequent double-blind, placebo-controlled, randomized trial involving a further 12 patients, a single oral dose of mivazerol of 800 micrograms, 1200 micrograms, and 1600 micrograms increased the time to onset of angina by 4%, 11%, and 30%; the time to 1-mm ST depression by 33%, 43%, and 53%; and the total exercise duration by 10%, 18%, and 23%, respectively. Mivazerol is an imidazole derivative with agonist properties at the alpha 2-adrenoceptor and appears to be an effective antianginal. Mivazerol may improve exercise performance by attenuating the effects of exercise-induced sympathetic nervous system activity on the ischemic myocardium.

Administration, Oral↗
PubMed1993

Lowering cholesterol for prevention of coronary heart disease--problems and perspectives.

The evidence for aggressive treatment of severe hypercholesterolemia in men in order to reduce the development on a primary basis of the incidence of coronary heart disease is strong; the main benefit is reduction of morbidity. Extrapolation to women or to the management of mild hypercholesterolemia in either gender is not supported by facts. The value of reducing hypercholesterolemia in the young and in the elderly has not been tested. None of the primary or secondary prevention trials have reduced all-cause mortality. There is an inverse relation between cholesterol levels and noncardiovascular disease. The possibility that reducing mild to moderate elevation of cholesterol might be harmful to some people remains unanswered.

Adolescent↗