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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postprandial lipaemia (PL) is associated with the metabolic syndrome, CVD and endothelial dysfunction. Aerobic exercise has been shown to reduce PL. Although resistance exercise is recommended for the improvement of the quality of life, management of body weight and prevention of several disorders, its effect on PL has received little attention. The present study examined the effects of low-volume resistance exercise (LVRE) and high-volume resistance exercise (HVRE) on PL. Ten healthy young men performed three trials, each conducted over 2 d. On the afternoon of day 1, they either refrained from exercise (control), performed LVRE (two sets of eight exercises, twelve repetitions at twelve repetitions maximum (RM) in each set; energy expenditure 0 x 76 MJ), or performed HVRE (four sets of eight exercises, twelve repetitions at 12 RM in each set; energy expenditure 1 x 40 MJ). On the morning of day 2 they consumed a meal containing 67 kJ/kg body weight, of which 65 % energy was from fat. Blood samples were obtained in the fasted state and for 6 h postprandially. The total area under the TAG curve (AUC; mmol/l x h) was lower (P<0 x 05) in HVRE (8 x 76 (sd 3 x 20)) and LVRE (9 x 29 (sd 3 x 64)) compared with control (11 x 60 (sd 4 x 35)). The incremental AUC was lower in HVRE compared with control (3 x 07 (sd 2 x 53) v. 5 x 58 (sd 3 x 72)), but not different between LVRE (3 x 86 (sd 2 x 29)) and control. In conclusion, resistance exercise of 1 x 40 MJ (four sets - eight exercises - twelve RM) or 0 x 76 MJ (two sets - eight exercises - twelve RM) before a high-fat meal reduces the total postprandial lipaemic response.
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PMID:Effects of low- and high-volume resistance exercise on postprandial lipaemia. 1731 8

The metabolic syndrome represents a summation of obesity-driven risk factors for atherosclerotic CVD and type 2 diabetes. Definitions of the syndrome vary but in general agree closely in identifying subjects. The relationships between the metabolic syndrome and atherosclerotic CVD and diabetes also vary, with relative risks of approximately 1.5-3.0 and approximately 3.0-5.0 respectively. Insulin resistance appears to explain much of the pathophysiology of the syndrome. Both increased fatty acid flux and an excess of circulating pro-inflammatory cytokines are likely mediators. With increased waist circumference, increases in fatty acid delivery to the liver result in higher rates of hepatic glucose production and increases in the secretion of apoB-containing lipoproteins. Concomitant changes in HDL ensue, including a replacement of the cholesterol content with TAG, an accelerated clearance from the plasma and thus a reduced number of HDL particles. Typically also present are increases in small dense LDL. Hypertension in part relates to the insulin resistance, but may involve other mechanisms. Impaired fasting glucose often relates to defects in insulin secretion in addition to insulin resistance, and probably more than any other component of the syndrome predicts the increased incidence of type 2 diabetes. Although not included in the diagnostic criteria, increases in pro-inflammatory cytokines and pro-thrombotic factors, in addition to decreases in plasma adiponectin, may also contribute to the increased incidence of atherosclerotic CVD and diabetes. In general, the greater the number of metabolic syndrome components, the greater the risk for these outcomes. The cytokines and pro-thrombotic factors also appear to contribute.
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PMID:Mechanisms of the components of the metabolic syndrome that predispose to diabetes and atherosclerotic CVD. 1734 75

We investigated the effects of a high walnut diet and a high unsalted cashew nut diet on selected markers of the metabolic syndrome. In a randomized, parallel, controlled study design, sixty-four subjects having the metabolic syndrome (twenty-nine men, thirty-five women) with a mean age of 45 (sd 10) years and who met the selection criteria were all fed a 3-week run-in control diet. Hereafter, participants were grouped according to gender and age and then randomized into three groups receiving a controlled feeding diet including walnuts, or unsalted cashew nuts or no nuts for 8 weeks. Subjects were required to have lunch at the metabolic ward of the Nutrition Department of the North-West University (Potchefstroom Campus). Both the walnut and the unsalted cashew nut intervention diets had no significant effect on the HDL-cholesterol, TAG, total cholesterol, LDL-cholesterol, serum fructosamine, serum high-sensitivity C-reactive protein, blood pressure and serum uric acid concentrations when compared to the control diet. Low baseline LDL-cholesterol concentrations in the cashew nut group may have masked a possible nut-related benefit. Plasma glucose concentrations increased significantly (P = 0.04) in the cashew nut group compared to the control group. By contrast, serum fructosamine was unchanged in the cashew nut group while the control group had significantly increased (P = 0.04) concentrations of this short-term marker of glycaemic control. Subjects displayed no improvement in the markers of the metabolic syndrome after following a walnut diet or a cashew nut diet compared to a control diet while maintaining body weight.
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PMID:Effects of a high walnut and high cashew nut diet on selected markers of the metabolic syndrome: a controlled feeding trial. 1738 74

Postprandial hyperlipidaemia is a common metabolic disturbance in atherosclerosis. During the postprandial phase, chylomicrons and their remnants can penetrate the intact endothelium and cause foam cell formation. These particles are highly atherogenic after modification. People in the Western world are non-fasting for most of the day, which consequently leads to a continuous challenge of the endothelium by atherogenic lipoproteins and their remnants. Furthermore, atherosclerosis is considered a low-grade chronic inflammatory disease. Many studies have shown that the process of atherogenesis in part starts with the interaction between the activated leucocytes and activated endothelium. Postprandial lipoproteins can activate leucocytes in the blood and up-regulate the expression of leucocyte adhesion molecules on the endothelium, facilitating adhesion and migration of inflammatory cells into the subendothelial space. Another inflammatory process associated with postprandial lipaemia is the activation of the complement system. Its central component C3 has been associated with obesity, coronary sclerosis, the metabolic syndrome and fasting and postprandial TAGs (triacylglycerols). Moreover, chylomicrons are the strongest stimulators of adipocyte C3 production via activation of the alternative complement cascade. A postprandial C3 increment has been shown in healthy subjects and in patients with CAD (coronary artery disease) and with FCHL (familial combined hyperlipidaemia). Postprandial lipaemia has been related to TAG and free fatty acid metabolism. All of these mechanisms provide an alternative explanation for the atherogenicity of the postprandial period.
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PMID:Postprandial inflammation and endothelial dysfuction. 1751 29

Adiponectin is discussed to regulate energy balance and insulin sensitivity. Several studies indicated an association of fasting adiponectin with parameters of the metabolic syndrome. We investigated postprandial adiponectin release and its relation to traits of the metabolic syndrome. Serum adiponectin concentration after an oral glucose tolerance test and after ingestion of a standardised mixed, fat-containing meal in 110 male non-diabetic subjects was assessed. Fasting and postprandial adiponectin and the decrease of adiponectin were correlated with anthropometric and metabolic parameters. Subjects were genotyped for adiponectin - 11 388 G/A promoter single nucleotide polymorphism. Adiponectin slightly decreased after both test meals. A significant decrease was attained 5 and 6 h after the lipid load and 2 h after the glucose load. Particularly, the mixed meal postprandial adiponectin showed stronger correlations with most traits of the metabolic syndrome than fasting adiponectin: postprandial adiponectin with HDL (r 0.30) v. fasting adiponectin with HDL (r 0.23); with postprandial insulin (area under the curve): r - 0.20 v. r - 0.16; with fasting insulin: r 0.10 v. r 0.14; with BMI: r - 0.23 v. r - 0.20; with waist: r - 0.18 v. - 0.16; with systolic blood pressure: r - 0.14 v. r - 0.12; with diastolic blood pressure: r - 0.18 v. r - 0.15. In multivariate analysis, postprandial TAG were the only independent predictor of adiponectin. There was no significant association of adiponectin, NEFA and TAG with - 11 388 G/A adiponectin promoter polymorphism. Our findings favour the interpretation that postprandial adiponectin has the strongest and independent associations to postprandial TAG metabolism.
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PMID:Postprandial plasma adiponectin decreases after glucose and high fat meal and is independently associated with postprandial triacylglycerols but not with -- 11388 promoter polymorphism. 1766 5

The purpose of the present study was to evaluate the effect of Ramadan fasting on insulin sensitivity in subjects with the metabolic syndrome. Males (n 55; age 34.1 (sd 8.9) years) with the metabolic syndrome were studied. Blood pressure, waist circumference, body weight, HDL-cholesterol (HDL-C), TAG, fasting plasma glucose (FPG), fasting blood insulin and insulin resistance indices (quantitative insulin sensitivity check index (QUICKI), homeostasis model assessment of insulin resistance (HOMA-IR) and reciprocal index of HOMA-IR (1/HOMA-IR)) were evaluated before and after 30 d of Ramadan fasting (two meals at 12 h intervals). The dietary intake was estimated by 24 h recall before and after fasting. The total daily energy intake was decreased by 234.6 (sd 88.2) kJ/d in the fasting period (P = 0.005). 1/HOMA-IR, QUICKI and HDL-C were significantly increased (P = 0.005, P = 0.001 and P = 0.004) and FPG significantly decreased (P < 0.005) after fasting. Simple linear regression analysis demonstrated that HOMA-IR, 1/HOMA-IR and QUICKI were related to waist circumference after intervention (r 0.458, P < 0.001; r - 0.396, P < 0.05; r - 0.342, P < 0.05). In conclusion, the present study showed that the combined change in the number and timing of meals and portioning of the entire intake into only two meals per d may increase insulin sensitivity in subjects with the metabolic syndrome even when the decrease in energy consumption is minimal.
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PMID:Effect of Ramadan fasting on some indices of insulin resistance and components of the metabolic syndrome in healthy male adults. 1805 8

The aim of this study was to examine the responses of uric acid, antioxidant defences and pro-oxidant variables after a high-fat meal. Twenty-five healthy persons without criteria for the metabolic syndrome, underwent a high-fat meal with Supracal (60 g fat). Measurements were made at baseline and 3 h after the meal of TAG, uric acid, HDL-cholesterol, total proteins and oxidative stress. Following the high-fat meal, we detected a significant increase in pro-oxidative variables and a decrease in antioxidative variables. The uric acid concentrations were significantly lower after the high-fat meal and the reduction correlated significantly with the oxidative stress variables. The inverse relation between reduced uric acid and increased carbonylated proteins remained in multiple regression analysis. We conclude that uric acid is a powerful antioxidant and its reduction following a high-fat meal may be related with its acute antioxidative action.
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PMID:Circulating antioxidant defences are decreased in healthy people after a high-fat meal. 1818 52

Naturally-occurring compounds that have been shown to improve insulin sensitivity include Cr and polyphenols found in cinnamon (Cinnamomon cassia). These compounds also have similar effects on insulin signalling and glucose control. The signs of Cr deficiency are similar to those for the metabolic syndrome and supplemental Cr has been shown to improve all these signs in human subjects. In a double-blind placebo-controlled study it has been demonstrated that glucose, insulin, cholesterol and HbA1c are all improved in patients with type 2 diabetes following Cr supplementation. It has also been shown that cinnamon polyphenols improve insulin sensitivity in in vitro, animal and human studies. Cinnamon reduces mean fasting serum glucose (18-29%), TAG (23-30%), total cholesterol (12-26%) and LDL-cholesterol (7-27%) in subjects with type 2 diabetes after 40 d of daily consumption of 1-6 g cinnamon. Subjects with the metabolic syndrome who consume an aqueous extract of cinnamon have been shown to have improved fasting blood glucose, systolic blood pressure, percentage body fat and increased lean body mass compared with the placebo group. Studies utilizing an aqueous extract of cinnamon, high in type A polyphenols, have also demonstrated improvements in fasting glucose, glucose tolerance and insulin sensitivity in women with insulin resistance associated with the polycystic ovary syndrome. For both supplemental Cr and cinnamon not all studies have reported beneficial effects and the responses are related to the duration of the study, form of Cr or cinnamon used and the extent of obesity and glucose intolerance of the subjects.
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PMID:Chromium and polyphenols from cinnamon improve insulin sensitivity. 1823 31

Little is known about the effect of dietary carbohydrate, glycaemic index (GI) and glycaemic load (GL) on the risk of the metabolic syndrome, especially in populations with white rice as the staple food. The study examined the cross-sectional relationship between carbohydrate, GI, GL and risk of the metabolic syndrome. There were a total of 910 middle-aged Korean adults. Dietary carbohydrate, GI and GL were determined by an interview-administered FFQ. The metabolic syndrome was defined using the modified criteria published in the Third Report of the National Cholesterol Education Program Adult Treatment Panel III. The risk of developing the metabolic syndrome was positively related to dietary carbohydrate (P for trend = 0.03), GI (P for trend = 0.03) and GL intakes (P for trend = 0.02) in women after adjusting for potential confounding variables. Among the components of developing the metabolic syndrome, the risk of high TAG and low HDL-cholesterol were positively related to high GI and GL intakes in women. The risk of developing the metabolic syndrome was considerably higher in the highest quintiles of carbohydrate (OR 6.44; 95 % CI 2.16, 19.2), GI (OR 10.4; 95 % CI 3.24, 33.3) and GL intakes (OR 6.68; 95 % CI 2.30, 19.4) than in the lowest quintiles among women with a BMI >/= 25 kg/m2. However, there was no difference in risk across quintiles of carbohydrate, GI and GL among women with a BMI < 25 kg/m2. In conclusion, both the quantity and quality of carbohydrate intake has a positive relationship with the risk of the metabolic syndrome in women but this relationship was dependent on the BMI level.
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PMID:Cross-sectional relationship between dietary carbohydrate, glycaemic index, glycaemic load and risk of the metabolic syndrome in a Korean population. 1832 17

Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.
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PMID:Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women. 1838 5


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