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Biomedical subjects

P Marckmann

Publications and source records attributed to P Marckmann.

At least 19 recordsLinked to original sources
PubMed2005

Effect of red wine and red grape extract on blood lipids, haemostatic factors, and other risk factors for cardiovascular disease.

OBJECTIVE: Some epidemiological studies found a lower risk of cardiovascular disease among wine drinkers than among drinkers of other types of ethanol. This difference might be due to an effect of nonalcohol compounds in wine on important cardiovascular risk factors. The objective of this study was to compare the effect of red wine, nonalcohol compounds of red wine and placebo on established cardiovascular risk factors. DESIGN: A parallel, four-armed intervention study. SUBJECTS: A total of 69 healthy 38-74-y-old men and women. INTERVENTIONS: Subjects were randomised to either 1: red wine (males: 300 ml/day, 38.3 g alcohol/day, female subjects: 200 ml/day, 25.5 g alcohol/day), 2: water + red grape extract tablets (wine-equivalent dose), 3: water + red grape extract tablets (half dose), or 4: water + placebo tablets for a period of 4 weeks. No other sources of alcohol or anthocyanin were allowed. Plasma high-density lipoprotein (HDL)-cholesterol (HDL-C), low-density lipoprotein (LDL)-cholesterol (LDL-C), HDL-C/LDL-C-ratio, very-low-density lipoprotein (VLDL)-triacylglycerol, total cholesterol, fibrinogen, factor VII coagulant activity (FVIIc), blood pressure, and body weight were determined before and after intervention. RESULTS: Wine consumption was associated with a significant 11-16% increase in fasting HDL-C and 8-15% decrease in fasting fibrinogen relative to not drinking wine. There were no significant treatment effects on fasting LDL-C, HDL-C/LDL-C-ratio, VLDL-triacylglycerol, total cholesterol, FVIIc, or blood pressure. Drinking wine was associated with relative body weight increments closely corresponding to the energy contributed by the alcohol component. CONCLUSION: Moderate red wine consumption for 4 weeks is associated with desirable changes in HDL-C and fibrinogen compared with drinking water with or without red grape extract. The impact of wine on the measured cardiovascular risk factors thus seems primarily explained by an alcohol effect. Our finding suggests that the putative difference in cardiac risk associated with wine vs other alcoholic beverages might be rather explained by other life-style confounders than by red wine contents of nonalcohol components.

Adult↗
PubMed2003

Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes.

OBJECTIVE: Fish oil supplement has been proposed as a non-pharmacological strategy to correct the atherogenic lipid profile associated with type 2 diabetes mellitus. However, fish oil may have deleterious effects on lipid peroxidation and glycemic control. DESIGN: In this study, 44 type 2 diabetic patients were randomized to vitamin E standardized (53.6 mg/day) supplementation (capsules) with 4 g daily of either fish oil (n=23) or corn oil (n=21) for 8 weeks preceded by a 4 week run-in period of corn oil supplementation. LDL was isolated by density gradient ultracentrifugation and oxidized in vitro with Cu(2+). As a marker of in vivo oxidation malondialdehyde concentration in LDL (LDL-MDA) was measured. RESULTS: Fish oil reduced both mean lag time (before, 57.8; after, 48.8 min, P<0.001) and mean propagation rate (before, 0.018 DeltaOD/min; after, 0.015 DeltaOD/min, P<0.001), whereas corn oil had no influence on lag time and propagation rate. The changes in lag time and propagation rate differed significantly between fish oil and corn oil treatment. LDL-MDA changes differed borderline significantly between groups (FO, 110.4 pmol/mg protein; CO, 6.7 pmol/mg protein; P=0.057). Fish oil supplementation had no influence on glycemic control as assessed from HbA(1c) and fasting blood glucose. CONCLUSION: According to our findings, fish oil supplementation leads to increased in vivo oxidation and increased in vitro oxidation susceptibility of LDL particles. More studies are needed to clarify the clinical importance of this finding.

Adult↗
PubMed2003

Fish oil feeding is associated with an increased accumulation of dietary lipids in enterocytes: results from an in vivo study in rats.

BACKGROUND: Chronic fish oil consumption is associated with reduced postprandial lipaemia, but the mechanism behind this effect is not fully understood. We studied whether lipid absorption might be altered in rats fed fish oil. METHODS: Male Wistar rats were fed fish oil enriched chow (n = 6) or control oil enriched chow (n = 6). After 4 weeks, 61 mg 3H-triolein was instilled into duodenal tied-off loops. Intestinal segments were removed after 15, 30, 45, 60 and 90 min. Enterocytes were then isolated by calcium chelation and quantified by DNA determination. Non-absorbed 3H-lipid and 3H-lipid contents of enterocytes were determined by liquid scintillation counting. Two other groups of rats (2 x 6) fed the experimental diets were given an oral fat load and fasting and postprandial blood samples were taken. RESULTS: The accumulation of 3H-lipids in enterocytes was higher in rats fed fish oil than in controls (area under the 3H-lipid time curve: 1041.3 versus 670.3 nmol oleic acid x min/microg DNA, P < 0.05). Separation of lipids showed that an accumulation of triglycerides and free fatty acids occurred in rats fed fish oil. The amount of non-absorbed 3H-lipid tended to be higher in the fish oil fed rats (P > 0.1). It was confirmed that the fish oil enriched chow caused lower postprandial lipaemia (34% reduction in serum triglyceride concentrations, P < 0.05). CONCLUSION: Attenuated postprandial lipaemia following fish oil feeding is explained, at least partly, by a transient lipid accumulation in enterocytes which may result in a delayed triglyceride efflux from the enterocytes into the circulation.

Animals↗
PubMed2002

The Göttingen minipig as a model for postprandial hyperlipidaemia in man: experimental observations.

Postprandial hyperlipidaemia is believed to be atherogenic. This study aimed to establish a minipig model to investigate determinants of postprandial lipid metabolism. In a randomized cross-over design seven minipigs were subjected to six different feeding regimens: intragastric fat loads of 1, 2, and 4 g fat (Intralipid, 20%) kg(-1) in two fractions 1.5 h apart (1/3 first, 2/3 second), 2 g fat (Intralipid kg(-1) in one fraction, and 2 g olive oil kg(-1) in two fractions, all after pre-feeding with standard diet, and finally 2 g fat (Intralipid kg(-1) in two fractions without pre-feeding. Blood was sampled before and hourly for 7 h after gavaging, and plasma triglycerides were measured. Triglycerides increased significantly in all the feeding regimens (P < 0.001), except when olive oil was used as the fat source. A borderline significant dose-response effect of the Intralipid dose on the triglyceride response was observed. We found no significant differences in triglyceride response whether 2 g fat (Intralipid kg(-1) was given in one or two fractions, with or without pre-feeding. We conclude that postprandial hyperlipidaemia in minipigs can be induced by gavaging an emulgated lipid solution (1-4 g fat/kg, Intralipid, while olive oil is not applicable. There is no need to administer the fat fractionated or to withhold food prior to administration.

Administration, Oral↗
PubMed2001

[The effect of dietary oils on blood lipids and the risk of ischemic heart disease with special emphasis on olive oil. A literature review].

INTRODUCTION: The European Union is financing a large-scale campaign, in which olive oil is represented as the optimal fat for dietetic prevention of coronary heart disease. METHOD: We reviewed all controlled dietary studies comparing the effect on blood lipids of olive oil and alternative vegetable oils. Fifteen studies were identified. RESULTS: Consumption of olive oil was associated with significantly raised plasma concentrations of low density lipoprotein cholesterol (+6.5%), high density lipoprotein cholesterol (), and triglycerides (+7%) as compared with an average of the alternative oils. In the light of these differences in blood lipids and the risk coefficients published earlier, we calculated that the consumption of olive oil was associated with a 7% increase in the risk of coronary heart disease. CONCLUSION: We conclude that olive oil cannot be considered more cardioprotective than other unsaturated vegetable oils as judged from its effects on blood lipids.

Adult↗
PubMed2001

A high-fat meal does not activate blood coagulation factor VII in minipigs.

It is a matter of debate whether postprandial activation of blood coagulation factor VII (FVII) is associated with an increased risk of thrombosis. To clarify this question, an animal model in which consequences of dietary FVII activation can be studied in a more detailed way would be an important tool. We studied postprandial FVII activation in seven non-fasting Göttingen minipigs. Intralipid (4 g/kg) was administered through a gastric tube in two fractions at 9.00 a.m. (one-third of total dose) and 10.30 a.m. (two-thirds of total dose). Blood samples were drawn 0.5 h before (baseline) and 2, 3, 3.5, 4, 5, and 6 h after the first fat load. Triglycerides, activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII amidolytic activity (FVIIam) and prothrombin fragment I + 2 (F1 + 2) were analysed in plasma samples. Median plasma triglycerides were significantly raised from 0.67 mmol/l (baseline) to 2.56 mmol/l 5 h postprandially (P < 0.001). There were no significant changes in FVIIa (9.6 U/l at baseline), FVIIam (142% at baseline) and F1 + 2 (0.13 nmol/l at baseline). FVIIc decreased from 141% at baseline to 114% 6 h postprandially (P < 0.001). As a high-fat meal does not seem to activate blood coagulation FVII in minipigs, the pig is apparently not a relevant model for the study of dietary FVII activation and thrombin generation.

Animals↗
PubMed2000

[A quantitative assessment of the impact of diet on the mortality of heart disease in Denmark. Estimation of etiologic fraction].

INTRODUCTION: The aim of the present study was to quantify the impact of different dietary factors on the mortality from ischaemic heart disease in Denmark. METHODS: Relative risks and knowledge on the distribution of different dietary factors were used to estimate etiological fractions. RESULTS: It is estimated that an intake of fruit and vegetables and saturated fat as recommended would prevent 12 and 22%, respectively, of deaths from ischaemic heart disease in Denmark. An intake of fish among those at high risk for ischaemic heart disease, would lead to a 26% lower mortality, while alcohol intake among abstainers would have no significant quantitative effect. DISCUSSION: These results suggest that changes in dietary habits according to current recommendations would have an impact on public health in Denmark.

Alcohol Drinking↗
PubMed2000

Dietary treatment of thrombogenic disorders related to the metabolic syndrome.

The increased risk of coronary heart disease associated with the metabolic syndrome may be partially explained by prothrombotic deviations of the haemostatic system. Individuals with insulin resistance, dyslipidaemia and obesity are characterized by elevated plasma fibrinogen and factor VII coagulant activity levels and raised concentrations of plasminogen-activator inhibitor, the main inhibitor of endogenous fibrinolysis. These haemostatic abnormalities may be corrected with dietary treatment of the underlying clinical disorder. Dietary trials of diseased and healthy volunteers suggest that the optimal antithrombotic diet is a low-fat diet with a high content of foods rich in complex carbohydrates and dietary fibre. The dietary fatty acid composition has a profound effect on blood lipids, but seems of minor importance for the haemostatic system.

Coronary Disease↗
PubMed2000

Ad libitum intake of low-fat diets rich in either starchy foods or sucrose: effects on blood lipids, factor VII coagulant activity, and fibrinogen.

People are advised to reduce their intake of saturated fat and replace it by carbohydrate to avoid coronary heart disease. It is unknown whether sucrose and starchy foods, two major sources of carbohydrates, have similar effects on cardiovascular risk markers if incorporated as a replacement for saturated fat into diets eaten ad libitum. We served 20 healthy, normal-weight women aged 21 to 52 years three strictly controlled diets ad libitum: FAT, high in total fat (46% of total energy [E%]) and saturated fat (21 E%); STARCH, high in total carbohydrates (59 E%) and low in sucrose (2.5 E%); and SUCROSE, high in total carbohydrates (59 E%) and sucrose (23.2 E%). The diets were eaten in randomized order for a period of 2 weeks. Blood lipids, factor VII coagulant activity (FVIIc), and fibrinogen concentrations were measured with subjects in the fasted state (9:45 AM) and the postabsorptive state (6:00 PM). STARCH was associated with lower total cholesterol (mean difference, 0.34 mmol/L; 95% confidence interval [CI], 0.18 to 0.50), low-density lipoprotein (LDL) cholesterol (0.25 mmol/L; 95% CI, 0.13 to 0.37), fasting triglycerides (0.15 mmol/L; 95% CI, 0.07 to 0.23), nonfasting triglycerides (0.44 mmol/L; 95% CI, 0.30 to 0.58), and nonfasting FVIIc (9.8%; 95% CI, 3.8 to 15.8) than SUCROSE. Compared with FAT, STARCH resulted in a desirable decrease of LDL cholesterol and nonfasting FVIIc. STARCH was also associated with a minor weight loss (0.7 kg) that was not found on the other 2 diets. We conclude that starchy foods with a natural content of dietary fiber can be recommended as substitutes for saturated fat in the dietary prevention of coronary heart disease. According to the present short-term findings in healthy females, substitution with sucrose is not advisable.

Adult↗
PubMed2000

The link between high-fat meals and postprandial activation of blood coagulation factor VII possibly involves kallikrein.

Contrary to low-fat meals, high-fat meals are known to cause postprandial factor VII (FVII) activation, but the mechanism is unknown. To study the postprandial FVII activation in detail, 18 young men consumed in randomized order high-fat or low-fat test meals. Fasting and non-fasting blood samples were collected. The high-fat test was associated with an increase in plasma triglyceride and kallikrein concentrations and postprandial FVII activation (p<0.001). Plasma kallikrein was strongly associated with triglycerides in fasting and non-fasting samples (r2=0.74-0.87, p<0.0001), suggesting that triglyceride-rich lipoproteins may activate prokallikrein. Neither plasma triglycerides nor kallikrein and activated FVII were statistically associated. This may suggest that additional factors are involved in the postprandial FVII activation. No clear evidence for a role of tissue factor expression by monocytes, factor XII or insulin in postprandial FVII activation was observed. Tissue factor pathway inhibitor and prothrombin fragment 1+2, a marker of thrombin generation, were not affected postprandially after either the high-fat or the low-fat meals. Our findings indicate that triglyceride-rich lipoproteins activate prokallikrein postprandially, which might form an important initial event in FVII activation after consumption of high-fat meals.

Adult↗
PubMed2000

Dietary factor VII activation does not increase plasma concentrations of prothrombin fragment 1+2 in patients with stable angina pectoris and coronary atherosclerosis.

Studies in healthy subjects showed that blood coagulation factor VII (FVII) is activated postprandially after consumption of high-fat meals, but accompanying thrombin formation has not been demonstrated. In patients with coronary atherosclerosis, the arterial intima is supposed to present more tissue factor, the cofactor of FVII, to circulating blood; therefore, thrombin formation in response to FVII activation is more likely to occur in such patients. This hypothesis was tested in a randomized crossover study of 30 patients (aged 43 to 70 years) with stable angina pectoris and angiographically verified coronary atherosclerosis. They were served a low-fat (5% of energy from fat) breakfast and lunch and a high-fat (40% of energy from fat) breakfast and lunch on 2 different days. Venous blood samples were collected at 8:15 AM (fasting), 12:30 PM, 2:00 PM, 3:30 PM, and 4:45 PM and analyzed for triglycerides, activated FVII (FVIIa), FVII protein concentration (FVII:Ag), prothrombin fragment 1+2 (F1+2), and soluble fibrin. Triglyceride levels increased from fasting levels on both diets, but they increased most markedly on the high-fat diet. FVIIa and FVIIa/FVII:Ag increased with the high-fat diet and decreased with the low-fat diet. For both diets, FVII:Ag and F1+2 decreased slightly. No postprandial changes were observed for soluble fibrin. Postprandial mean values of triglycerides, FVIIa, FVII:Ag, and FVIIa/FVII:Ag were significantly higher for the high-fat diet than for the low-fat diet. Our findings confirm that high-fat meals cause immediate activation of FVII. The clinical implication is debatable because FVII activation was not accompanied by an increase in plasma F1+2 concentrations in patients with severe atherosclerosis. However, a local thrombin generation on the plaque surface cannot be excluded.

Adult↗