78 resultados para Intramuscular triglycerides


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OBJECTIVE--Total sedentary (absence of whole-body movement) time is associated with obesity, abnormal glucose metabolism, and the metabolic syndrome. In addition to the effects of total sedentary time, the manner in which it is accumulated may also be important. We examined the association of breaks in objectively measured sedentary time with biological markers of metabolic risk.

RESEARCH DESIGN AND METHODS--Participants (n = 168, mean age 53.4 years) for this cross-sectional study were recruited from the 2004-2005 Australian Diabetes, Obesity and Lifestyle study. Sedentary time was measured by an accelerometer (counts/[minute-1] < 100) worn during waking hours for seven consecutive days. Each interruption in sedentary time (counts/min [greater than or equal to] 100) was considered a break. Fasting plasma glucose, 2-h plasma glucose, serum triglycerides, HDL cholesterol, weight, height, waist circumference, and resting blood pressure were measured. MatLab was used to derive the breaks variable; SPSS was used for the statistical analysis.

RESULTS--Independent of total sedentary time and moderate-to-vigorous intensity activity time, increased breaks in sedentary time were beneficially associated with waist circumference (standardized ß = -0.16, 95% CI -0.31 to -0.02, P = 0.026), BMI (ß = -0.19, -0.35 to -0.02, P = 0.026), triglycerides (ß = -0.18, -0.34 to -0.02, P = 0.029), and 2-h plasma glucose (ß = -0.18, -0.34 to -0.02, P = 0.025).

CONCLUSIONS--This study provides evidence of the importance of avoiding prolonged uninterrupted periods of sedentary (primarily sitting) time. These findings suggest new public health recommendations regarding breaking up sedentary time that are complementary to those for physical activity.

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OBJECTIVE—We examined the associations of objectively measured sedentary time and physical activity with continuous indexes of metabolic risk in Australian adults without known diabetes.

RESEARCH DESIGN AND METHODS—An accelerometer was used to derive the percentage of monitoring time spent sedentary and in light-intensity and moderate-to-vigorous–intensity activity, as well as mean activity intensity, in 169 Australian Diabetes, Obesity and Lifestyle Study (AusDiab) participants (mean age 53.4 years). Associations with waist circumference, triglycerides, HDL cholesterol, resting blood pressure, fasting plasma glucose, and a clustered metabolic risk score were examined.

RESULTS—Independent of time spent in moderate-to-vigorous–intensity activity, there were significant associations of sedentary time, light-intensity time, and mean activity intensity with waist circumference and clustered metabolic risk. Independent of waist circumference, moderate-to-vigorous–intensity activity time was significantly beneficially associated with triglycerides.

CONCLUSIONS—These findings highlight the importance of decreasing sedentary time, as well as increasing time spent in physical activity, for metabolic health.

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OBJECTIVE—We examined the associations of objectively measured sedentary time and physical activity with continuous indexes of metabolic risk in Australian adults without known diabetes.

RESEARCH DESIGN AND METHODS—An accelerometer was used to derive the percentage of monitoring time spent sedentary and in light-intensity and moderate-to-vigorous–intensity activity, as well as mean activity intensity, in 169 Australian Diabetes, Obesity and Lifestyle Study (AusDiab) participants (mean age 53.4 years). Associations with waist circumference, triglycerides, HDL cholesterol, resting blood pressure, fasting plasma glucose, and a clustered metabolic risk score were examined.

RESULTS—Independent of time spent in moderate-to-vigorous–intensity activity, there were significant associations of sedentary time, light-intensity time, and mean activity intensity with waist circumference and clustered metabolic risk. Independent of waist circumference, moderate-to-vigorous–intensity activity time was significantly beneficially associated with triglycerides.

CONCLUSIONS—These findings highlight the importance of decreasing sedentary time, as well as increasing time spent in physical activity, for metabolic health.

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Aims & rationale/Objectives : Hypercholesterolaemia accounts for 11.6% of total deaths and 6.2% of the disability burden for the Australian population.1 This paper reports population lipid profiles for three rural Australian populations, and assesses evidence-treatment gaps against the most recent (2005-2007) Australian guidelines.

Methods :
Three population surveys were undertaken in the Greater Green Triangle. 3,320 adults aged 25-74 yrs were randomly selected using age/gender stratified electoral roll samples and of these 1563 subjects participated in the survey. Anthropometric, clinical and self-administered questionnaire data relating to chronic disease risk were collected in accordance with the WHO MONICA protocol.2 A detailed investigation of dyslipidaemia was included.

Principal findings : All required data was available for 1255 participants. Age-standardised mean total cholesterol (TC), triglycerides, LDL cholesterol and HDL cholesterol concentrations were 5.36 mmol/l, 1.42 mmol/l, 3.23 mmol/l and 1.48 mmol/l, respectively. Amongst those taking lipid-lowering medication, just 11% categorised as secondary prevention/diabetes, and 39% as primary prevention, achieved all lipid targets. In the 20% of untreated participants at high risk of a primary cardiovascular event, 26% were aware of their hypercholesterolaemia and just 2% achieved all lipid targets (2.8% achieved TC?5.5 mmol, 8.5% achieved LDL<3.5 mmol/l). 11.2% of the overall population used lipid-lowering medication (95% was statin monotherapy).

Implications : Most adults do not achieve their target lipid profile. This paper identifies the subpopulations and lipid components which need to be targeted for future interventions. It also identifies substantial evidence-treatment gaps which should be addressed to help improve lipid profiles at a population level.

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This study evaluated the production of fatty acid ethyl esters from fish oil using ultrasonic energy and alkaline catalysts dissolved in ethanol. The feasibility of fatty acid ethyl ester production was determined using an ultrasonic bath and probe, and between 0.5 and 1% KOH (added to the fish oil). Furthermore, factors such as ultrasonic device (bath and probe), catalyst (KOH and C2H5ONa), temperature (20 and 60 °C), and duration of exposure (10–90 min) were assessed. Sodium ethoxide was found to be a more efficient catalyst than KOH when transesterifying fish oil. Ultrasonic energy applied for greater than 30 min at 60 °C using 0.8% of C2H5ONa as a catalyst transesterified over 98% fish oil triglycerides to fatty acid ethyl esters. It is reasonable to conclude that the yield of fatty acid ethyl esters produced by applying ultrasonic energy to fish oil is related to the sonication time. Due to increases in the surface area contact between the reactants and the catalyst, ultrasonic energy has the potential to reduce the production time required by a conventional large-scale commercial transesterification method that uses agitation as a way of mixing.

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Context: Chemerin is a novel adipokine previously associated with metabolic syndrome phenotypes in a small sample of subjects from Mauritius. Objective: The aim of the study was to determine whether plasma chemerin levels were associated with metabolic syndrome phenotypes in a larger sample from a second, unrelated human population. Design, Setting, Patients, and Intervention: Plasma samples were obtained from the San Antonio Family Heart Study (SAFHS), a large family-based genetic epidemiological study including 1431 Mexican-American individuals. Individuals were randomly sampled without regard to phenotype or disease status. This sample is well-characterized for a variety of phenotypes related to the metabolic syndrome. Main Outcomes: Plasma chemerin levels were measured by sandwich ELISA. Linear regression and correlation analyses were used to determine associations between plasma chemerin levels and metabolic syndrome phenotypes. Results: Circulating chemerin levels were significantly higher in nondiabetic subjects with body mass index (BMI) greater than 30 kg/m2 compared with those with a BMI below 25 kg/m2 (P < 0.0001). Plasma chemerin levels were significantly associated with metabolic syndrome-related parameters, including BMI (P < 0.0001), fasting serum insulin (P < 0.0001), triglycerides (P < 0.0001), and high-density lipoprotein cholesterol (P = 0.00014), independent of age and sex in nondiabetic subjects. Conclusion: Circulating chemerin levels were associated with metabolic syndrome phenotypes in a second, unrelated human population. This replicated result using a large human sample suggests that chemerin may be involved in the development of the metabolic syndrome.

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The purpose of this study was to examine the reliability of normalisation methods used in the study of the posterior and posterolateral neck muscles in a group of healthy controls. Six asymptomatic male subjects performed a total of 12 maximum voluntary isometric contractions (MVIC) and 60%-submaximal isometric contractions (60%-MVIC) against the torque arm of an isokinetic dynamometer whilst surface and intramuscular electromyography (EMG) was recorded unilaterally from representative posterior and posterolateral locations. Reliability was calculated using intra-class correlation coefficient (ICC), relative standard error of measurement (%SEM) and relative coefficient of variation (%CV). Maximal torque output was found to be highly reliable in the directions of extension and right lateral bending when the first of three MVIC contractions was excluded. When averaged across contraction direction, high reliability was found for both surface (MVIC: ICC = 0.986, %SEM = 7.5, %CV = 9.2; 60%-MVIC: ICC = 0.975, %SEM = 10, %CV = 13.7) and intramuscular (MVIC: ICC = 0.910, %SEM = 20, %CV = 19.1; 60%-MVIC: ICC = 0.952, %SEM = 16.5, %CV = 13.5) electrodes. Intramuscular electrodes displayed the least reliability in right lateral bending. The use of visual feedback markedly increased the reliability of 60%-MVIC contractions.

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Evidence from epidemiologic studies that central obesity precedes future metabolic change and does not occur concurrently with the appearance of the blood pressure, glucose, and lipid abnormalities that characterize the metabolic syndrome (MetS) has been lacking. Longitudinal surveys were conducted in Mauritius in 1987, 1992, and 1998, and in Australia in 2000 and 2005 (AusDiab). This analysis included men and women (aged 25 years) in three cohorts: AusDiab 2000–2005 (n = 5,039), Mauritius 1987–1992 (n = 2,849), and Mauritius 1987–1998 (n = 1,999). MetS components included waist circumference, systolic blood pressure, fasting and 2-h postload plasma glucose, high-density lipoprotein (HDL) cholesterol, triglycerides, and homeostasis model assessment of insulin sensitivity (HOMA-S) (representing insulin sensitivity). Linear regression was used to determine which baseline components predicted deterioration in other MetS components over 5 years in AusDiab and 5 and 11 years in Mauritius, adjusted for age, sex, and ethnic group. Baseline waist circumference predicted deterioration (P < 0.01) in four of the other six MetS variables tested in AusDiab, five of six in Mauritius 1987–1992, and four of six in Mauritius 1987–1998. In contrast, an increase in waist circumference between baseline and follow-up was only predicted by insulin sensitivity (HOMA-S) at baseline, and only in one of the three cohorts. These results suggest that central obesity plays a central role in the development of the MetS and appears to precede the appearance of the other MetS components.

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OBJECTIVE--We examined the associations of objectively measured sedentary time and physical activity with continuous indexes of metabolic risk in Australian adults without known diabetes.

RESEARCH DESIGN AND METHODS--An accelerometer was used to derive the percentage of monitoring time spent sedentary and in light-intensity and moderate-to-vigorous-intensity activity, as well as mean activity intensity, in 169 Australian Diabetes, Obesity and Lifestyle Study (AusDiab) participants (mean age 53.4 years). Associations with waist circumference, triglycerides, HDL cholesterol, resting blood pressure, fasting plasma glucose, and a clustered metabolic risk score were examined.

RESULTS--Independent of time spent in moderate-to-vigorous-intensity activity, there were significant associations of sedentary time, light-intensity time, and mean activity intensity with waist circumference and clustered metabolic risk. Independent of waist circumference, moderate-to-vigorous-intensity activity time was significantly beneficially associated with triglycerides.

CONCLUSIONS--These findings highlight the importance of decreasing sedentary time, as well as increasing time spent in physical activity, for metabolic health.

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Objective: To examine gender differences in the characteristics and prevalence of various categories of glucose tolerance in a population study in Mauritius.

Research design and methods: In 1998, a community-based cross-sectional survey was conducted in Mauritius. Categories of glucose metabolism were determined in 5388 adults, with an oral glucose tolerance test given to those who did not have previously diagnosed diabetes (n = 4036). Other cardiovascular risk factors were assessed among those without known diabetes.

Results
: For men and women the prevalence of diabetes (22.0 vs. 21.8%, respectively) and the prevalence of coexisting impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) (3.2 vs. 2.9%) were similar. However, men were twice as likely as women to have isolated IFG [5.1% (4.2–6.0) vs. 2.9% (2.3–3.5)], despite being younger, thinner and with lower plasma insulin but higher lipids. Conversely, the prevalence of isolated IGT was lower in men [9.0% (7.9–10.2) vs. 13.9% (12.6–15.1)]. Among non-diabetic individuals, fasting glucose was higher in men than women, whereas 2-h glucose was higher in women. In people without diabetes, women had significantly higher body mass index, beta cell function (HOMA-B), fasting and 2-h insulin than men and significantly lower waist-hip ratios, waist circumference, insulin sensitivity (HOMA-S) and triglycerides.

Conclusion: In Mauritius, the distribution of impaired glucose metabolism differs by sex. The observation that IFG is more prevalent in men and IGT more prevalent in women raises important questions about their underlying aetiology and the ability of the current glucose thresholds to equally identify men and women at high-risk of developing diabetes. IFG should be seen as a complimentary category of abnormal glucose tolerance, rather than a replacement for IGT.

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Metabolic syndrome (MetS), also previously known by a variety of other names, including insulin resistance syndrome and the deadly quartet, is characterized by clustering of abdominal (visceral and retroperitoneal) obesity and other cardiovascular risk factors, including impaired glucose regulation, raised triglycerides, decreased high-density lipoprotein cholesterol (HDL-C), elevated blood pressure (BP).

Associated with increased risk of both type 2 diabetes and cardiovascular disease (CVD), MetS is believed to be a contributor to the modern-day epidemics of diabetes and CVD and has become a major public health challenge around the world [I]. Currently, there are five different sets of criteria which have been developed to characterize the syndrome. These definitions differ in the components included and the cut-points used for each component. The prevalence of MetS in the westernized world is significant (10-50%) and believed to be increasing over time. The pathophysiology of the syndrome is unclear, but it is thought that obesity and/or insulin resistance are key underlying components. Genetics, lifestyle and environment factors are also important causes of MetS.

This chapter provides:

• a historical overview of the evolution of MetS;
• a summary of the value of the different definitions used to characterize the syndrome;
• a summary of the underlying pathophysiology, the causes and other important risk factors of MetS;
• a summary of the evidence describing the association of MetS with CVD and diabetes;
• a summary of the prevalence of MetS using the various definitions in different countries.

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Several observational studies have shown that the chronic consumption of high glycaemic index diet is associated with an increased risk of developing metabolic syndrome.  This study was performed to identify the direct influences on the lipid profile and the adipose tissue deposition and the subsequent development of the risk of metabolic syndrome in rats by feeding diets of low glycaemic index (LGI) and high glycaemic index (HGI). Fifty rat weanlings (three weeks old) were equally divided into two groups and fed on either low glycaemic index diet based on high amylose, or isocaloric high glycacmic index diet for 12 weeks. Postprandial blood and tissue samples were collected at the end of the 12 weeks of feeding. The total white adipose tissue weights of the HGl fed rats (24.74 ± 0.53 glrat) were significantly higher than the LGl fed rats (15.37 ± 0.36 gh·at). The HO! led rats had higher postprandial leptin concentrations (1.86 ± 0.17 ng/ml) than LGI fed rats (1.34 ± 0.12 ng/ml). The postprandial insulin, and postprandial insulin glucose ratio were higher in the HGI fed rats (7.06 ± 0.90 ng/ml and 0.67 ± 0.01 ng/mlxmM) compared to the LGl fed rats (3.91 ± 0.4 ng/ml and 0.44 ± 0.01 ng/mlxmM). Triglycerides of the l-IGI fed rats showed higher values (I .56 ± 0.10 mM) than the LO! fed rats (l.07 ± 0.08 mM). The results indicated that LGI feeding was beneficial in preventing the conditions enhancing the cardio vascular disease whereas long-term feeding of HGI diet may increase the risk of developing metabolic syndrome in rats.

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Recovery after prolonged or high-intensity exercise is characterised by a substantial increase in adipose tissue lipolysis, resulting in elevated rates of plasma-derived fat oxidation. Despite the large increase in circulating fatty acids (FAs) after exercise, only a small fraction of this is taken up by exercised muscle in the lower extremities. Indeed, the predominant fate of non-oxidised FAs derived from post-exercise lipolysis is reesteriflcation hi the liver. During recovery from endurance exercise, a number of changes also occur hi skeletal muscle that allow for a high metabolic priority towards glycogen resynthesis. Reducing muscle glycogen during exercise potentiates these effects, however the cellular and molecular mechanisms regulating substrate oxidation following exercise remain poorly defined. The broad arm of this thesis was to examine the regulation of fat metabolism during recovery from glycogen-lowering exercise hi the presence of altered fat and glucose availability. In study I, eight endurance-trained males completed a bout of exhaustive exercise followed by ingestion of carbohydrate (CHO)-rich meals (64-70% of energy from CHO) at 1, 4, and 7 h of recovery. Duplicate muscle biopsies were obtained at exhaustion and 3, 6 and 18 h of recovery. Despite the large intake of CHO during recovery (491 ± 28 g or 6.8 + 0.3 g • kg-1), respiratory exchange ratio values of 0.77 to 0.84 indicated a greater reliance on fat as an oxidative fuel. Intramuscular triacylglycerol (IMTG) content remained unchanged in the presence of elevated glucose and insulin levels during recovery , suggesting IMTG has a negligible role in contributing to the enhanced fat oxidation after exhaustive exercise. It appears that the partitioning of exogenous glucose towards glycogen resynthesis is of high metabolic priority during immediate post-exercise recovery, supported by the trend towards reduced pyruvate dehydrogenase (PDH) activity and increased fat oxidation. The effect of altering plasma FA availability during post-exercise recovery was examined in study II. Eight endurance-trained males performed three trials consisting of glycogen-lowering exercise, followed by infusion of either saline (CON), saline + nicotinic acid (NA) (LFA) or Intralipid and heparin (HFA). Muscle biopsies were obtained at the end of exercise (0 h) and at 3 and 6 h in recovery. Altering the availability of plasma FAs during recovery induced changes in whole-body fat oxidation that were unrelated to differences in skeletal muscle malonyl-CoA. Furthermore, fat oxidation and acetyl-CoA carboxylase (ACC) phosphorylation appear to be dissociated after exercise, suggesting mechanisms other than phosphorylation-mediated changes in ACC activity have an important role in regulating malonyl-CoA and fat metabolism in human skeletal muscle after exercise. Alternative mechanisms include citrate and long-chain fatty acyl-CoA mediated changes in ACC activity, or differences in malonyl-CoA decarboxylase (MCD) activity. Reducing plasma FA concentrations with NA attenuated the post-exercise increase in MCD and pyruvate dehydrogenase kinase 4 (PDK4) gene expression, suggesting that FAs and/or other factors induced by NA are involved hi the regulation of these genes. Despite marked changes hi plasma FA availability, no significant changes in IMTG concentration were detected, providing further evidence that plasma-derived FAs are the preferential fuel source contributing to the enhanced fat oxidation post-exercise during recovery. To further examine the effect of substrate availability after exercise, Study III investigated the regulation of fat metabolism during a 6 h recovery period with or without glucose infusion. Enhanced glucose availability significantly increased CHO oxidation compared with the fasted state, although no differences in whole-body fat oxidation were apparent. Consistent with the similar rates of fat metabolism, no difference hi AMPK or ACCβ phosphorylation were observed between trials. In addition, no significant treatment or time effects for IMTG concentration were detected during recovery. The large exercise-induced PDK4 gene expression was attenuated when plasma FAs were reduced during glucose infusion, supporting the hypothesis that PDK4 is responsive to sustained changes in lipid availability and/or changes in plasma insulin. Furthermore, the possibility exists that the suppression of PDK4 mRNA also reduced PDK activity and thus maintained PDH activity to account for the higher rates of CHO oxidation observed during glucose infusion compared with the control trial.

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Objective : To compare the effects of a modified-fat diet high in monounsaturated fat, and a low-fat/high-carbohydrate diet on arterial elasticity.
Design : Randomized crossover design; each diet period was 1 month and a 2-week wash out period occurred in between.
Subjects/setting : Thirty healthy, free-living, nonsmoking men and women were recruited from the Melbourne, Australia, metropolitan region of Australia. Men were aged 35 to 55 years and postmenopausal women were aged 50 to 60 years and were not taking hormone replacement therapy. Twenty-eight subjects completed the study.
Intervention : Two diets of equal energy value: a modified-fat diet and a low-fat/high-carbohydrate diet; the modified-fat diet had 3 times more energy from monounsaturated fat.
Main outcome measures : Arterial elasticity and serum lipoprotein concentrations.
Statistical analysis : The general linear model was used to investigate overall effect and any carryover or order effects. Paired t test and the general linear model were used to compare the results from the 2 diet periods.
Results : High-density lipoprotein cholesterol concentration was significantly higher on the modified-fat diet than on the low-fat/low-carbohydrate diet. Arterial elasticity and concentrations of total cholesterol, low-density lipoprotein cholesterol, and triglycerides were not significantly different on the 2 diets.
Applications/conclusions : There is no evidence to favor a diet high in monounsaturated fat over a low-fat/high-carbohydrate diet because of an effect on arterial elasticity. Other changes in diet may be needed to cause a beneficial effect on arterial elasticity.

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Several soluble polysaccharides have been shown to have cholesterol-lowering properties and to have a role in prevention of heart disease. Major sources of one such polysaccharide (beta-glucan) are oats and barley. The aim of this study was to examine the effects on plasma lipid concentrations when beta-glucan derived from a fractionated oat preparation was consumed by people with elevated plasma lipids. A single-blind, crossover design compared plasma cholesterol, triglycerides, high density lipoproteins and low density lipoproteins (LDLs) in 14 people; in the order of low, high and low beta-glucan supplemented diets, each of three weeks duration. For the high beta-glucan diet, an average intake of 7 g per day was consumed from cereal, muffins and bread. The background diet remained relatively constant over the three test periods. Differences during the interventions were calculated by one-way repeated measures analysis of variance. Where treatments were found to be significantly different, pairwise multiple comparison procedures (Tukey Test) were carried out between the high beta-glucan and each of the low beta-glucan phases and there was a highly significant difference between treatments for plasma cholesterol (P = 0.009) and for LDL-cholesterol concentrations (P < 0.001). The differences in plasma cholesterol (6.42 +/- 0.7, 6.14 +/- 0.53, 6.44 +/- 0.67 mmol/L) and LDL-cholesterol (4.59 +/- 0.59, 4.17 +/0.58, 4.52 +/- 0.65 mmol/L) between high beta-glucan and each of the low beta-glucan treatments were significant (P < 0.05). The effect on LDLs (9% lower) is among the highest reported. The results of this study confirm that beneficial reductions in plasma cholesterol and LDL-cholesterol concentrations can be obtained with beta-glucan incorporated into a variety of foods.