127 resultados para adiposity


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To determine the effect of adiposity in males aged 50-70 years on cardiovascular responses to acute psychological stress.

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Excessive daytime sleepiness (EDS) is often associated with increased adiposity, particularly when assessed in the context of samples of sleep-disordered patients; however, it is unclear if this relationship is sustained among non-clinical, population-based cohorts. This study aimed to investigate the relationship between EDS and a number of body composition markers among a population-based sample of men and women.

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Few studies of media use and adiposity explore the influence of parenting on children’s lifestyle behaviors. Screen media access, bedroom television, lack of physical activity, and snacking on energy-dense foods have long been implicated in child overweight. This research used data from the first three waves of the Longitudinal Study of Australian Children to investigate, prospectively, the associations between parental practices in early to middle childhood and children’s behaviors and weight in late childhood. A path model was used to investigate whether consistent parentingpredicted setting of boundaries for access to and use of media, and was indirectly associated with children’s lifestyle behaviors that increase the likelihood of healthy weight maintenance. The findings demonstrated that children’s lifestyles pertinent to weight maintenance and media use cluster together and involve both old and newer screen media, but are also predicted by parenting practices and the family environment.

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Although the association between obesity and hypertension is well known, the underlying mechanism remains elusive. Previously, we have shown that 3 week fat feeding in rabbits produces greater visceral adiposity, hypertension, tachycardia and elevated renal sympathetic nerve activity compared to rabbits on a normal diet. Because hyperinsulinaemia, hyperleptinemia and dyslipidaemia are independent cardiovascular risk factors associated with hypertension we compared plasma insulin, leptin and lipid profiles in male New Zealand White rabbits fed a normal fat diet (NFD 4.3% fat, n = 11) or high fat diet (HFD 13.4% fat, n = 13) at days 1, 2, 3 and weeks 1, 2, 3 of the diet. Plasma concentrations of diacylglyceride (DG), triacylglyceride (TG), ceramide and cholesteryl esters (CE) were obtained after analysis by liquid chromatography mass spectrometry. Plasma insulin and glucose increased within the first 3 days of the diet in HFD rabbits (P <0.05) and remained elevated at week 1 (P <0.05). Blood pressure and heart rate followed a similar pattern. By contrast, in both groups, plasma leptin levels remained unchanged during the first few days (P >0.05), increasing by week 3 in fat fed animals alone (P <0.05). Concentrations of total DG, TG, CE and Ceramide at week 3 did not differ between groups (P >0.05). Our data show plasma insulin increases rapidly following consumption of a HFD and suggests that it may play a role in the rapid rise of blood pressure. Dyslipidaemia does not appear to contribute to the hypertension in this animal model.

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Defective control of lipid metabolism leading to lipotoxicity causes insulin resistance in skeletal muscle, a major factor leading to diabetes. Here, we demonstrate that perilipin (PLIN) 5 is required to couple intramyocellular triacylglycerol lipolysis with the metabolic demand for fatty acids. PLIN5 ablation depleted triacylglycerol stores but increased sphingolipids including ceramide, hydroxylceramides and sphingomyelin. We generated perilipin 5 (Plin5)-/- mice to determine the functional significance of PLIN5 in metabolic control and insulin action. Loss of PLIN5 had no effect on body weight, feeding or adiposity but increased whole-body carbohydrate oxidation. Plin5-/- mice developed skeletal muscle insulin resistance, which was associated with ceramide accumulation. Liver insulin sensitivity was improved in Plin5-/- mice, indicating tissue-specific effects of PLIN5 on insulin action. We conclude that PLIN5 plays a critical role in coordinating skeletal muscle triacylglycerol metabolism, which impacts sphingolipid metabolism, and is requisite for the maintenance of skeletal muscle insulin action. © 2014 The Authors.

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Sedentary behaviour is associated with increased risk for all-cause and cardiovascular mortality. Plasma fibrinogen and C reactive protein (CRP)-key inflammatory and/or haemostatic markers-may contribute to this association; however, few studies have examined their relationships with sedentary behaviours. We examined associations of overall sitting and TV viewing time with fibrinogen and high-sensitivity CRP (hsCRP).

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Childhood cardiovascular risk factors affect vascular function long before overt cardiovascular disease. Twin studies provide a unique opportunity to examine the influence of shared genetic and environmental influences on childhood cardiovascular function. We examined the relationship between birth parameters, markers of adiposity, insulin resistance, lipid profile and blood pressure and carotid-femoral pulse wave velocity (PWV), a validated non-invasive measure of arterial stiffness in a healthy cohort of school-aged twin children. PWV was performed on a population-based birth cohort of 147 twin pairs aged 7-11 years. Fasting blood samples, blood pressure and adiposity measures were collected concurrently. Mixed linear regression models were used to account for twin clustering, within- and between-twin pair associations. There were positive associations between both markers of higher adiposity, insulin resistance, elevated triglycerides and PWV, which remained significant after accounting for twin birth-set clustering. There was a positive association between both diastolic and mean arterial blood pressure and PWV in within-pair analysis in dizygotic, but not monozygotic twins, indicating genetic differences evident in dizygotic not monozygotic twins may affect these associations. Increased blood pressure, triglycerides and other metabolic markers are associated with increased PWV in school-aged twins. These results support both the genetic and environmental contribution to higher PWV, as a marker of arterial stiffness, and reiterate the importance of preventing metabolic syndrome from childhood.

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Body mass index (BMI) (kg/m(2)) is used internationally to assess body mass or adiposity. However, BMI does not discriminate body fat content or distribution and may vary among ethnicities. Many women with normal BMI are considered healthy, but may have an unidentified "hidden fat" profile associated with higher metabolic disease risk. If only BMI is used to indicate healthy body size, it may fail to predict underlying risks of diseases of lifestyle among population subgroups with normal BMI and different adiposity levels or distributions. Higher body fat levels are often attributed to excessive dietary intake and/or inadequate physical activity. These environmental influences regulate genes and proteins that alter energy expenditure/storage. Micro ribonucleic acid (miRNAs) can influence these genes and proteins, are sensitive to diet and exercise and may influence the varied metabolic responses observed between individuals. The study aims are to investigate associations between different body fat profiles and metabolic disease risk; dietary and physical activity patterns as predictors of body fat profiles; and whether these risk factors are associated with the expression of microRNAs related to energy expenditure or fat storage in young New Zealand women. Given the rising prevalence of obesity globally, this research will address a unique gap of knowledge in obesity research.

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BACKGROUND: Evidence relating childhood cancer to high birthweight is derived primarily from registry and case-control studies. We aimed to investigate this association, exploring the potential modifying roles of age at diagnosis and maternal anthropometrics, using prospectively collected data from the International Childhood Cancer Cohort Consortium.

METHODS: We pooled data on infant and parental characteristics and cancer incidence from six geographically and temporally diverse member cohorts [the Avon Longitudinal Study of Parents and Children (UK), the Collaborative Perinatal Project (USA), the Danish National Birth Cohort (Denmark), the Jerusalem Perinatal Study (Israel), the Norwegian Mother and Child Cohort Study (Norway), and the Tasmanian Infant Health Survey (Australia)]. Birthweight metrics included a continuous measure, deciles, and categories (≥4.0 vs. <4.0 kilogram). Childhood cancer (377 cases diagnosed prior to age 15 years) risk was analysed by type (all sites, leukaemia, acute lymphoblastic leukaemia, and non-leukaemia) and age at diagnosis. We estimated hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional hazards models stratified by cohort.

RESULTS: A linear relationship was noted for each kilogram increment in birthweight adjusted for gender and gestational age for all cancers [HR = 1.26; 95% CI 1.02, 1.54]. Similar trends were observed for leukaemia. There were no significant interactions with maternal pre-pregnancy overweight or pregnancy weight gain. Birthweight ≥4.0 kg was associated with non-leukaemia cancer among children diagnosed at age ≥3 years [HR = 1.62; 95% CI 1.06, 2.46], but not at younger ages [HR = 0.7; 95% CI 0.45, 1.24, P for difference = 0.02].

CONCLUSION: Childhood cancer incidence rises with increasing birthweight. In older children, cancers other than leukaemia are particularly related to high birthweight. Maternal adiposity, currently widespread, was not demonstrated to substantially modify these associations. Common factors underlying foetal growth and carcinogenesis need to be further explored.

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Abstract
Background:
To identify longitudinal individual, social and environmental predictors of adiposity (BMI z-score),
and of resilience to unhealthy weight gain, in healthy weight children and adolescents.
Methods:
Two hundred healthy weight children aged 5–12 years at baseline and their parents living in socio-economically disadvantaged neighborhoods were surveyed at baseline and three years later. Children’s height and weight were objectively measured, parents completed a detailed questionnaire that examined the home, social and neighborhood environments, and objective measures of the neighborhood environment were assessed using geographic information system data. Ch
ildren classified as healthy weight at baseline who had
small or medium increases in their BMI z-score between baseline and three year follow up (those in the bottom
and middle tertiles) were categorized as‘ resilient to unhealthy weight gain’. Where applicable, fully adjusted
multivariable regression models were employed to determine baseline intrapersonal, social and environmental predictors of child BMI z-scores at follow-up, and resilience to unhealthy weight gain at
follow-up.
Results:
Maternal efficacy for preventing their child from engaging in sedentary behaviors (B = − 0.03, 95 % CI: 0.06, 0.00) was associated with lower child BMI z-score at follow up. Rules to limit sedentary behaviors (OR = 1.14, 95 % CI: 1.03, 1.25) was a predictor of being resilient to unhealthy weight gain.
Conclusion:
The findings suggest that strategies to support parents to limit their children ’s sedentary behavior may be important in preventing unhealthy weight gain in socioeconomically disadvantaged communities.

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OBJECTIVES: To investigate the sociodemographic and behavioural factors associated with incidence, persistence or remission of obesity in a longitudinal sample of Australian children aged 4-10 years. SETTING: Nationally representative Longitudinal Study of Australian Children (LSAC). PARTICIPANTS: The sample for this analysis included all children in the Kinder cohort (aged 4-5 years at wave 1) who participated in all four waves of LSAC (wave 1, 2004, aged 4-5 years; wave 2, 2006, aged 6-7 years; wave 3, 2008, aged 8-9 years and wave 4, 2010, aged 10-11 years). Of the 4983 children who participated in the baseline (wave 1) survey, 4169 (83.7%) children completed all four waves of data collection. PRIMARY AND SECONDARY OUTCOME MEASURES: Movement of children between weight status categories over time and individual-level predictors of weight status change (sociodemographic characteristics, selected dietary and activity behaviours). RESULTS: The study found tracking of weight status across this period of childhood. There was an inverse association observed between socioeconomic position and persistence of overweight/obesity. Sugar-sweetened beverages and fruit and vegetable intake and screen time appeared to be important predictors of stronger tracking. CONCLUSIONS: Overweight and obesity established early in childhood tracks strongly to the middle childhood years in Australia, particularly among children of lower socioeconomic position and children participating in some unhealthy behaviour patterns.

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Due to their differing etiologies and consequences, it has been proposed that the term "sarcopenia" should revert to its original definition of age-related muscle mass declines, with a separate term, "dynapenia", describing muscle strength and function declines. There is increasing interest in the interactions of sarcopenia and dynapenia with obesity. Despite an apparent protective effect of obesity on fracture, increased adiposity may compromise bone health, and the presence of sarcopenia and/or dynapenia ("sarcopenic obesity" and "dynapenic obesity") may exacerbate the risk of falls and fracture in obese older adults. Weight loss interventions are likely to be beneficial for older adults with sarcopenic and dynapenic obesity but may result in further reductions in muscle and bone health. The addition of exercise including progressive resistance training and nutritional strategies, including protein and vitamin D supplementation, may optimise body composition and muscle function outcomes thereby reducing falls and fracture risk in this population.

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BACKGROUND: Obesity in early childhood is a robust predictor of obesity later in life. Schools provide unparalleled access to children and have subsequently become major intervention sites. However, empirical evidence supporting the effectiveness of school-based interventions against childhood obesity is of limited scope and unknown quality. The aim of this systematic review is to critically assess how researchers have characterized the school environment in determining its effect on childhood weight status in order to improve the quality and consistency of research in this area. We conducted a narrative review with a systematic search of the literature in line with PRISMA guidelines (2009). Original peer-reviewed research articles in English were searched from Medline, EMBASE, CENTRAL, CINAHL and PsycINFO databases from earliest record to January 2014. We included empirical research that reported at least one measure of the primary/elementary school environment and its relationship with at least one objective adiposity-related variable for students aged 4-12 years. Two authors independently extracted data on study design, school-level factors, student weight status, type of analysis and effect. RESULTS: Five studies met the inclusion criteria. Each study targeted different parts of the school environment and findings across the studies were not comparable. The instruments used to collect school-level data report no validity or reliability testing. CONCLUSIONS: Our review shows that researchers have used instruments of unknown quality to test if the school environment is a determinant of childhood obesity, which raises broader questions about the impact that schools can play in obesity prevention.

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Obesity is a risk factor for cancer. However, it is not known if general adiposity, as measured by body mass index (BMI) or central adiposity [e.g., waist circumference (WC)] have stronger associations with cancer, or which anthropometric measure best predicts cancer risk. We included 79,458 men and women from the Australian and New Zealand Diabetes and Cancer Collaboration with complete data on anthropometry [BMI, WC, Hip Circumference (HC), WHR, waist to height ratio (WtHR), A Body Shape Index (ABSI)], linked to the Australian Cancer Database. Cox proportional hazards models assessed the association between each anthropometric marker, per standard deviation and the risk of overall, colorectal, post-menopausal (PM) breast, prostate and obesity-related cancers. We assessed the discriminative ability of models using Harrell's c-statistic. All anthropometric markers were associated with overall, colorectal and obesity-related cancers. BMI, WC and HC were associated with PM breast cancer and no significant associations were seen for prostate cancer. Strongest associations were observed for WC across all outcomes, excluding PM breast cancer for which HC was strongest. WC had greater discrimination compared to BMI for overall and colorectal cancer in men and women with c-statistics ranging from 0.70 to 0.71. We show all anthropometric measures are associated with the overall, colorectal, PM breast and obesity-related cancer in men and women, but not prostate cancer. WC discriminated marginally better than BMI. However, all anthropometric measures were similarly moderately predictive of cancer risk. We do not recommend one anthropometric marker over another for assessing an individuals' risk of cancer.

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Background: Previous studies exploring the association between obesity and hypertension generally used a single baseline measurement of obesity. The effect of accumulating excess adiposity over time on the risk of hypertension is uncertain. This study aimed to examine the relationship between duration of obesity and incident hypertension using the Framingham Heart Study.

Methods: Two thousand, nine hundred and fifty-three participants aged 30–62 years without baseline hypertension were included. Blood pressure, height and weight were measured biennially. Duration of obesity was calculated. Time to incident hypertension was analysed using time-varying Cox proportional hazards regression with age as the time scale and censoring at time of death or end of follow-up.

Results: Eighty percent of participants developed hypertension (median follow-up 15.9 years). A positive association between obesity duration and incident hypertension was observed in women. There was no longer an association when time-varying BMI was adjusted for (hazard ratio 0.95; (95% confidence interval 0.85–1.05)).

Conclusion: These findings suggest that the mechanism by which excess adiposity may increase blood pressure is primarily immediate and that long-term exposure to obesity does not further increase the risk of developing hypertension beyond the level of BMI attained.