91 resultados para Fat-free mass

em Deakin Research Online - Australia


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Background
Bioelectrical impedance (BIA) represents a simple, inexpensive and non-invasive method that is often used to assess fat-mass (FM) and fat-free mass (FFM) in large population-based cohorts.

Objective

The aim of this study was to describe the reference ranges and examine the influence of age and gender on FM, FFM and skeletal muscle mass (SMM) as well as height-adjusted estimates of FM [fat mass index (FMI)], FFM [fat-free mass index (FFMI)] and SMM [SMM index (SMI)] in a national, population-based cohort of Australian adults.

Design and Participants

The analytical sample included a total of 8,582 adults aged 25–91 years of Europid origin with complete data involved in the cross-sectional 1999–2000 Australian, Diabetes, Obesity and Lifestyle (AusDiab) Study.

Measurements

Bioelectrical impedance analysis was used to examine components of body composition. Demographic information was derived from a household interview.

Results

For both genders, FFM, SMM and SMI decreased linearly from the age of 25 years, with the exception that in men SMI was not related to age and FFM peaked at age 38 years before declining thereafter. The relative loss from peak values to ≥75 years in FFM (6–8%) and SMM (11–15%) was similar between men and women. For FM and FMI, there was a curvilinear relationship with age in both genders, but peak values were detected 6–7 years later in women with a similar relative loss thereafter. For FFMI there was no change with age in men and a modest increase in women.

Conclusion

In Australian adults there is heterogeneity in the age of onset, pattern and magnitude of changes in the different measures of muscle and fat mass derived from BIA, but overall the agerelated losses were similar between men and women.

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Objective: There is emerging evidence that angiotensin stimulates adipocyte differentiation and lipogenesis. This study tested the hypothesis that inhibition of angiotensin II by treatment with an angiotensin-converting enzyme inhibitor, perindopril, would reduce fat mass in rats. Design: After a 12-day baseline, rats were divided into two groups: one was untreated and the other received perindopril (1.2 mg kg−1 per day) in drinking water for 26 days.Subjects: In total, 16 male Sprague–Dawley rats aged 10 weeks at the start of the study. Measurements: Plasma leptin was measured in samples collected at baseline, half-way through and at the end of treatment. Body weight, food and water intake were measured daily throughout the experiment. Body fat mass, bone and lean mass were determined by dual energy X-ray absorptiometry (DEXA) at the end of the treatment period. Results: Daily food intake was the same in both groups throughout the study. By the end of treatment, animals receiving perindopril showed a modest reduction in weight gain relative to the untreated animals (62.4±5.0 g vs 73.0±4.0 g; P<0.05). DEXA analysis showed that body composition was greatly altered and the perindopril-treated group had 26% less body fat mass than the untreated group (61.0±5.2 g vs 44.4±4.2 g; P<0.01). The reduction in body fat mass was correlated with reductions in the weight of both the epididymal and retroperitoneal fat pads (P<0.001). Similarly, plasma leptin was reduced by perindopril treatment (4.64±0.56 ng ml−1) compared to the untreated group (8.27±1.03 ng ml−1; P<0.001). In contrast, there were no differences in lean or bone mass between the two groups.Conclusion: Oral treatment with perindopril selectively reduced body fat mass without influencing daily food intake. In contrast, there were no differences in lean or bone mass between the two groups

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OBJECTIVE: Foot pain is a common complaint in adults. Evidence suggests that body composition is involved in the development of foot pain. However, whether this is the case in men remains unclear because previous studies mainly examined women. The aim of this cross-sectional study was to determine the relationship between body composition and foot pain in men while accounting for important risk factors. METHODS: Among 978 men (median age 60 yrs, range 24-98) from the Geelong Osteoporosis Study who participated in a followup study in 2006 to 2011, 796 provided responses to questions on health status and foot pain. Foot pain was determined using the Manchester Foot Pain and Disability Index, and body composition was measured using dual-energy x-ray absorptiometry. RESULTS: Of the 796 respondents, 177 (22%) had foot pain. Risk factors for foot pain were age (OR 1.03, 95% CI 1.02-1.04), self-reported depression (OR 2.05, 95% CI 1.30-3.20), decreased mobility (OR 1.54, 95% CI 1.05-2.24), and lower education (OR 1.47, 95% CI 1.03-2.09). Foot pain was associated with body mass index (OR 1.05, 95% CI 1.00-1.10), fat mass (OR 1.02, 95% CI 1.03-1.05), and fat mass index (OR 1.08, 95% CI 1.01-1.15), but not fat-free mass (OR 1.01, 95% CI 0.98-1.04) or fat-free mass index (OR 1.05, 95% CI 0.95-1.15) after appropriate adjustments were made. CONCLUSION: Fat mass is associated with foot pain in men. These findings complement those in studies that have mainly examined women, and provide further evidence for the relationship between obesity and foot pain.

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Aims To investigate body size and body fat relationships and fat distribution in young healthy men drawn from New Zealand European, Pacific Island, and Asian Indian populations.
Method A total of 114 healthy men (64 European, 31 Pacific Island, 19 Asian Indian) aged 17–30 years underwent measurements of height, weight, and body composition by total body dual-energy X-ray absorptiometry (DXA). Body mass index (BMI) was then calculated. Percent body fat (%BF), fat-free mass, bone mineral content, bone mineral density, abdominal fat, thigh fat, and appendicular skeletal muscle mass (ASMM) were obtained from the DXA scans.
Results For the same BMI, %BF for Pacific Island men was 4% points lower and for Asian Indian men was 7–8% points higher compared to Europeans. Compared to European men for the same %BF, BMI was 2–3 units higher for Pacific Island, and 3–6 units lower for Asian Indian. The ratio of abdominal fat to thigh fat, adjusted for height, weight, and %BF, was significantly higher for Asian Indian men than European (p=0.022) and Pacific Island (p=0.002) men. ASMM, adjusted for height and weight, was highest in Pacific Island and lowest in Asian Indian men.
Conclusions The relationship between %BF and BMI is different for European, Pacific Island, and Asian Indian men which may, at least in part, be due to differences in muscularity. Asian Indians have more abdominal fat deposition than their European and Pacific Island counterparts. Use of universal BMI cut-off points are not appropriate for comparison of obesity prevalence between these ethnic groups.

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Objective: Our objective was to delineate the potential role of adipogenesis in insulin resistance and type 2 diabetes. Obesity is characterized by an increase in adipose tissue mass resulting from enlargement of existing fat cells (hypertrophy) and/or from increased number of adipocytes (hyperplasia). The inability of the adipose tissue to recruit new fat cells may cause ectopic fat deposition and insulin resistance.

Research Methods and Procedures: We examined the expression of candidate genes involved in adipocyte proliferation and/or differentiation [ CCAAT/enhancer-binding protein (C/EBP) alpha, C/EBPdelta, GATA domain-binding protein 3 (GATA3), C/EBPbeta, peroxisome proliferator-activated receptor (PPAR) gamma2, signal transducer and activator of transcription 5A (STAT5A), Wnt-10b, tumor necrosis factor alpha, sterol regulatory element-binding protein 1c (SREBP1c), 11 beta-hydroxysteroid dehydrogenase, PPARG angiopoietin-related protein (PGAR), insulin-like growth factor 1, PPARitalic gamma coactivator 1alpha, PPARitalic gamma coactivator 1beta, and PPARdelta] in subcutaneous adipose tissue from 42 obese individuals with type 2 diabetes and 25 non-diabetic subjects matched for age and obesity.

Results: Insulin sensitivity was measured by a 3-hour 80 mU/m2 per minute hyperinsulinemic glucose clamp (100 mg/dL). As expected, subjects with type 2 diabetes had lower glucose disposal (4.9 plusminus 1.9 vs. 7.5 plusminus 2.8 mg/min per kilogram fat-free mass; p < 0.001) and larger fat cells (0.90 plusminus 0.26 vs. 0.78 plusminus 0.17 mum; p = 0.04) as compared with obese control subjects. Three genes (SREBP1c, p < 0.01; STAT5A, p = 0.02; and PPARitalic gamma2, p = 0.02) had significantly lower expression in obese type 2 diabetics, whereas C/EBPbeta only tended to be lower (p = 0.07).

Discussion: This cross-sectional study supports the hypothesis that impaired expression of adipogenic genes may result in impaired adipogenesis, potentially leading to larger fat cells in subcutaneous adipose tissue and insulin resistance.

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Most research on creatine has focused on short-term creatine loading and its effect on high-intensity performance capacity. Some studies have investigated the effect of prolonged creatine use during strength training. However, studies on the effects of prolonged creatine supplementation are lacking. In the present study, we have assessed the effects of both creatine loading and prolonged supplementation on muscle creatine content, body composition, muscle and whole-body oxidative capacity, substrate utilization during submaximal exercise, and on repeated supramaximal sprint, as well as endurance-type time-trial performance on a cycle ergometer. Twenty subjects ingested creatine or a placebo during a 5-day loading period (20g·day-1) after which supplementation was continued for up to 6 weeks (2g·day-1). Creatine loading increased muscle free creatine, creatine phosphate (CrP) and total creatine content (P<0.05). The subsequent use of a 2g·day-1 maintenance dose, as suggested by an American College of Sports Medicine Roundtable, resulted in a decline in both the elevated CrP and total creatine content and maintenance of the free creatine concentration. Both short- and long-term creatine supplementation improved performance during repeated supramaximal sprints on a cycle ergometer. However, whole-body and muscle oxidative capacity, substrate utilization and time-trial performance were not affected. The increase in body mass following creatine loading was maintained after 6 weeks of continued supplementation and accounted for by a corresponding increase in fat-free mass. This study provides definite evidence that prolonged creatine supplementation in humans does not increase muscle or whole-body oxidative capacity and, as such, does not influence substrate utilization or performance during endurance cycling exercise. In addition, our findings suggest that prolonged creatine ingestion induces an increase in fat-free mass.

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Creatine monohydrate (CrM) supplementation has been shown to increase fat-free mass and muscle power output possibly via cell swelling. Little is known about the cellular response to CrM. We investigated the effect of short-term CrM supplementation on global and targeted mRNA expression and protein content in human skeletal muscle. In a randomized, placebo-controlled, crossover, double-blind design, 12 young, healthy, nonobese men were supplemented with either a placebo (PL) or CrM (loading phase, 20 g/day x 3 days; maintenance phase, 5 g/day x 7 days) for 10 days. Following a 28-day washout period, subjects were put on the alternate supplementation for 10 days. Muscle biopsies of the vastus lateralis were obtained and were assessed for mRNA expression (cDNA microarrays + real-time PCR) and protein content (Kinetworks KPKS 1.0 Protein Kinase screen). CrM supplementation significantly increased fat-free mass, total body water, and body weight of the participants (P < 0.05). Also, CrM supplementation significantly upregulated (1.3- to 5.0-fold) the mRNA content of genes and protein content of kinases involved in osmosensing and signal transduction, cytoskeleton remodeling, protein and glycogen synthesis regulation, satellite cell proliferation and differentiation, DNA replication and repair, RNA transcription control, and cell survival. We are the first to report this large-scale gene expression in the skeletal muscle with short-term CrM supplementation, a response that suggests changes in cellular osmolarity.

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To examine whether genes associated with cellular defense against oxidative stress are associated with insulin sensitivity, patients with type 2 diabetes (n = 7) and age-matched (n = 5) and young (n = 9) control subjects underwent a euglycemic-hyperinsulinemic clamp for 120 min. Muscle samples were obtained before and after the clamp and analyzed for heat shock protein (HSP)72 and heme oxygenase (HO)-1 mRNA, intramuscular triglyceride content, and the maximal activities of β-hyroxyacyl-CoA dehydrogenase (β-HAD) and citrate synthase (CS). Basal expression of both HSP72 and HO-1 mRNA were lower (P < 0.05) by 33 and 55%, respectively, when comparing diabetic patients with age-matched and young control subjects, with no differences between the latter groups. Both basal HSP72 (r = 0.75, P < 0.001) and HO-1 (r = 0.50, P < 0.05) mRNA expression correlated with the glucose infusion rate during the clamp. Significant correlations were also observed between HSP72 mRNA and both β-HAD (r = 0.61, P < 0.01) and CS (r = 0.65, P < 0.01). HSP72 mRNA was induced (P < 0.05) by the clamp in all groups. Although HO-1 mRNA was unaffected by the clamp in both the young and age-matched control subjects, it was increased (P < 0.05) ∼70-fold in the diabetic patients after the clamp. These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. The data provide new evidence that the pathogenesis of type 2 diabetes involves perturbations to the antioxidant defense mechanism within skeletal muscle.

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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: Clinical practice guidelines globally recommend lifestyle modification including diet and exercise training as first-line treatment for obesity. The clinical benefits of exercise training in adults with obesity is well-documented; however, there is no strong evidence for the effectiveness of exercise training for weight loss in class II and class III obesity. The purpose of the randomised controlled trial described in this protocol article is to examine the effect of exercise training, in addition to a very low energy diet (VLED), in clinically severe obese women for changes in body composition, physical function, quality of life, and markers of cardiometabolic risk.

METHODS/DESIGN: Sixty women, aged 18-50 years with a body mass index (BMI) greater than 34.9 kg.m(2) and at least one obesity-related co-morbidity, will be recruited for this 12-month study. Participants will be randomised to either exercise plus energy restriction (n = 30), or energy restriction alone (n = 30). All participants will follow an energy-restricted individualised diet incorporating a VLED component. The exercise intervention group will also receive exercise by supervised aerobic and resistance training and a home-based exercise programme totalling 300 minutes per week. Primary outcome measures include body composition and aerobic fitness. Secondary outcome measures include: physical function, cardiometabolic risk factors, quality of life, physical activity, and mental health. All outcome measures will be conducted at baseline, 3, 6 and 12 months.

DISCUSSION: Previous research demonstrates various health benefits of including exercise training as part of a healthy lifestyle at all BMI ranges. Although clinical practice guidelines recommend exercise training as part of first-line treatment for overweight and obesity, there are few studies that demonstrate the effectiveness of exercise in class II and class III obesity. The study aims to determine whether the addition of exercise training to a VLED provides more favourable improvements in body composition, physical function, quality of life, and markers of cardiometabolic risk for women with clinically severe obesity, compared to VLED alone.

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Estimates of body fat based on anthropometric measurements were compared in two groups of females, one from the local community and the other from the 1984 Australian Olympic Team. Estimates of body fat based on electrical impedance measurements were also made for the community group. For estimates of total body fat based on skinfold measurements, a significant difference of approximately 1 kg fat/m2 was observed between athletes and non-athletes. In the group of non-athletes estimates of fat based on skinfold measurements were significantly higher than those based on body mass index, with estimates from electrical impedance falling between. Electrical impedance measurements may provide a means of estimating body fat which takes into account differences in fat distribution and in the ratio of fat to fat-free tissue and may thus overcome the problems associated with estimates based on measurements of subcutaneous fat (skinfolds) or body size which do not allow for these differences.

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Objective: To assess the influence of body build on the bias and limits of agreement for estimates of body fat obtained from anthropometric prediction equations when compared with the same data obtained by dual energy X-ray absorptiometry (DEXA).

Survey design and subjects:
Ninety-one premenopausal women, aged between 20 and 54 years, were chosen to represent a range of skeletal body build (relative silting height 0.50-0.56) and body fatness [body mass index (BMI) 18-34 kg/m2]. Measurements of weight, sitting height, stature, skinfold thickness, waist, umbilical and hip circumference and total body resistance and reactance were made on all subjects by standard techniques after an overnight fast. A DEXA measurement of total body fat, fat-free soft tissue and total body bone mineral mass was also obtained within 2 weeks of the anthropometric assessment.

Results:
At the group level the mean difference (bias) between DEXA and the anthropometric estimates of body fat was similar for all three anthropometric estimates ranging from 2.7 kg with impedance to 1.8 kg with skinfold thickness. The 95% limits of agreement were also similar, ranging from ±5.3 kg with body mass index to ±4.1 kg with impedance. Umbilical circumference, BMI and the amount of bone mineral expressed as a proportion of the fat-free soft-tissue mass were all significantly (P < 0.01) correlated with the level of bias between DEXA and the anthropometric estimates of body fat. This was not the case for relative sitting height or measures of body fat distribution. Regression equations which included BMI or umbilical circumference in combination with the predicted estimates of body fat essentially eliminated the association between the level of bias in predicted body fat and the level of body fatness. They also reduced the 95% limits of agreement between DEXA and the anthropometric estimates of body fat.

Conclusions:
Using DEXA estimates of body fat as the standard of reference our results suggest that the comparability and precision of body fat estimates derived from age- and/or sex-specific anthropometric prediction equations based on skinfolds and BMI, but not impedance, can be improved by adjusting for differences in BMI and umbilical circumference respectively.

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We tested whether mild adiposity alters responsiveness of the kidney to activation of the renal sympathetic nerves. After rabbits were fed a high-fat or control diet for 9 wk, responses to reflex activation of renal sympathetic nerve activity (RSNA) with hypoxia and electrical stimulation of the renal nerves (RNS) were examined under pentobarbital anesthesia. Fat pad mass and body weight were, respectively, 74% and 6% greater in fat-fed rabbits than controls. RNS produced frequency-dependent reductions in renal blood flow, cortical and medullary perfusion, glomerular filtration rate, urine flow, and sodium excretion and increased renal plasma renin activity (PRA) overflow. Responses of sodium excretion and medullary perfusion were significantly enhanced by fat feeding. For example, 1 Hz RNS reduced sodium excretion by 79 ± 4% in fat-fed rabbits and 46 ± 13% in controls. RNS (2 Hz) reduced medullary perfusion by 38 ± 11% in fat-fed rabbits and 9 ± 4% in controls. Hypoxia doubled RSNA, increased renal PRA overflow and medullary perfusion, and reduced urine flow and sodium excretion, without significantly altering mean arterial pressure (MAP) or cortical perfusion. These effects were indistinguishable in fat-fed and control rabbits. Neither MAP nor PRA were significantly greater in conscious fat-fed than control rabbits. These observations suggest that mild excess adiposity can augment the antinatriuretic response to renal nerve activation by RNS, possibly through altered neural control of medullary perfusion. Thus, sodium retention in obesity might be driven not only by increased RSNA, but also by increased responsiveness of the kidney to RSNA.

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Dietary polyunsaturated fatty acids (PUFA) play a key role in regulating delta-6 desaturase (D6D), the key enzyme for long-chain PUFA biosynthesis. Nevertheless, the extent of their effects on this enzyme remains controversial and difficult to assess. It has been generally admitted that C18 unsaturated fatty acids (UFAs) regulate negatively delta-6 desaturase (D6D). This inhibition has been evidenced in regard to a high glucose/fat free (HG/FF) diet used in reference. However, several nutritional investigations did not evidence any inhibition of desaturases when feeding fatty acids.

Because the choice of the basal diet appeared to be of primary importance in such experiments, our goal was to reconsider the specific role of dietary UFAs on D6D regulation, depending on nutritional conditions. For that, sixteen adult Wistar rats were fed purified linoleic acid, α-linolenic acid or oleic acid, included in one of two diets at 4% by weight: an HG/FF or a high starch base (HS) where the pure UFAs replaced a mixed vegetable oil. Our results showed first that D6D specific activity was significantly greater when measured in presence of an HG/FF than with an HS/4% vegetable oil diet. Secondly, we found that linoleic and alpha-linolenic acids added to HG/FF reduced the specific activity of D6D. In contrast, when pure UFAs were added to an HS base, D6D specific activities remained unchanged or increased. Concordant results were obtained on D6D mRNA expression.

Altogether, this study evidenced the importance of the nutritional status in D6D regulation by C18 UFAs: when used as control, HG/FF diet stimulates D6D compared with a standard control diet containing starch and 4% fats, leading to an overestimation of the D6D regulation by UFAs. Then, UFAs should be considered as repressors for unsaturated fatty acid biosynthesis only in very specific nutritional conditions.

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This thesis deals with two electrical methods designed to enable rapid, safe and noninvasive measurement of body composition, both for clinical and community use. The first section provides a review of the literature related to measurement of body composition in humans and outlines the approach of the research project. The second section deals with established methods of determining body composition, the two most important being hydrostatic densitometry and deuterium oxide dilution. In this part of the report, a novel method for measuring lung volume by hydrogen dilution at the time of underwater weighing is described. The main findings of the thesis are contained in the third section which deals with the assessment of body opposition by electrical means. There are two components to this part of the study. The first involved the testing of a commercially available bioelectric impedance analyser (BIA) which measures impedance to a flow of current through the body. Studies on the reproducibility and reliability of measurements were performed. Results showed the importance of correct electrode placement and revealed that subjects can consume a light meal and a drink before being measured with the BIA without adversely affecting impedance readings. Results suggested, however, that subjects empty their bladders before measurements are made. Strong correlations were found between height 2/ resistance and measurements of total body water (r = 0.839) and fat-free weight derived from densitometry (r = 0.821), Moderate correlations (r = 0.6 to 0.7) were also found when height /resistance was related to fat-free weight derived from anthropometric measurements. The second and major consonant of the third section deals with the development of a method based on the absorption of energy from a weak electromagnetic field established in a capacitor or chamber large enough to accommodate an adult human subject. The method involves measurement of the effect of the body on the electromagnetic field, and is based on differential absorption of energy by body fat and fat-free tissues. Regression equations were developed for predicting the weight of fat and fat-free tissue in the body from measurement of electromagnetic field effects in a test capacitor and in a resonating chamber. The test capacitor comprised a large aluminum cylinder with a copper rod as a central conductor. The following equation was derived for the relationship of fat-free weight (FEW) based on body density, with measurements of change in resonant frequency (ΔfR), height (H) and weight (W) : FFW = -4.39 + 0.690 W + 19.9 H + 37.6 ΔfR In a study of 17 subjects, a value of 0.891 was found for R2, and S.E.E. was 1.63. The resonating chamber consisted of a large enclosed aluminium cylinder with a copper rod as a central conductor. The following equation was derived for the relationship of fat weight (FW) based on the mean of estimates from body density and total body water, with measurements of change in signal attenuation (ΔA), change in resonant frequency (ΔfR), and height (H) and weight (W) : FW = 73.48 + 0.291 (W/√(ΔA) - 49.2 H - 0.53 ΔfR In a study of 27 subjects, a value of 0.956 was found for R2, and S.E.E. was 1.97. In these equations, variables were measured in the following units : FEW, FW and W (kg), ΔfR (MHz) and H (m).