997 resultados para full-fat soybean


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Discusses the Full House Theory, a theory for measuring the demand for new arts centers. Information on the Central Place Theory; Implementation of cultural mapping techniques in assessing the demand for arts centers; Marketing research methodologies.

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Energy conservation directed at accelerating body fat recovery (or catch-up fat) contributes to obesity relapse after slimming and to excess fat gain during catch-up growth after malnutrition. To investigate the mechanisms underlying such thrifty metabolism for catch-up fat, we tested whether during refeeding after caloric restriction rats exhibiting catch-up fat driven by suppressed thermogenesis have diminished skeletal muscle phosphatidylinositol-3-kinase (PI3K) activity or AMP-activated protein kinase (AMPK) signaling—two pathways required for hormone-induced thermogenesis in ex vivo muscle preparations. The results show that during isocaloric refeeding with a low-fat diet, at time points when body fat, circulating free fatty acids, and intramyocellular lipids in refed animals do not exceed those of controls, muscle insulin receptor substrate 1-associated PI3K activity (basal and in vivo insulin-stimulated) is lower than that in controls. Isocaloric refeeding with a high-fat diet, which exacerbates the suppression of thermogenesis, results in further reductions in muscle PI3K activity and in impaired AMPK phosphorylation (basal and in vivo leptin-stimulated). It is proposed that reduced skeletal muscle PI3K/AMPK signaling and suppressed thermogenesis are interdependent. Defective PI3K or AMPK signaling will reduce the rate of substrate cycling between de novo lipogenesis and lipid oxidation, leading to suppressed thermogenesis, which accelerates body fat recovery and furthermore sensitizes skeletal muscle to dietary fat-induced impairments in PI3K/AMPK signaling.—Summermatter, S., Mainieri, D., Russell, A. P., Seydoux, J., Montani, J. P., Buchala, A., Solinas, G., Dulloo, A. G. Thrifty metabolism that favors fat storage after caloric restriction: a role for skeletal muscle phosphatidylinositol-3-kinase activity and AMP-activated protein kinase.

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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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In addition to its role in the storage of fat, adipose tissue acts as an endocrine organ, and it contains a functional renin-angiotensin system (RAS). Angiotensin-converting enzyme (ACE) plays a key role in the RAS by converting angiotensin I to the bioactive peptide angiotensin II (Ang II). In the present study, the effect of targeting the RAS in body energy homeostasis and glucose tolerance was determined in homozygous mice in which the gene for ACE had been deleted (ACE-/-) and compared with wild-type littermates. Compared with wild-type littermates, ACE-/- mice had lower body weight and a lower proportion of body fat, especially in the abdomen. ACE-/- mice had greater fed-state total energy expenditure (TEE) and resting energy expenditure (REE) than wild-type littermates. There were pronounced increases in gene expression of enzymes related to lipolysis and fatty acid oxidation (lipoprotein lipase, carnitine palmitoyl transferase, long-chain acetyl CoA dehydrogenase) in the liver of ACE-/- mice and also lower plasma leptin. In contrast, no differences were detected in daily food intake, activity, fed-state plasma lipids, or proportion of fat excrete in fecal matter. In conclusion, the reduction in ACE activity is associated with a decreased accumulation of body fat, especially in abdominal fat depots. The decreased body fat in ACE-/- mice is independent of food intake and appears to be due to a high energy expenditure related to increased metabolism of fatty acids in the liver, with the additional effect of increased glucose tolerance.

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We measured aerobic metabolism during cold exposure and exercise performance (run duration and oxygen consumption while running at 1 m s−1) in the fat-tailed dunnart Sminthopsis crassicaudata, a dasyurid marsupial, before and after ingestion of 30 mg kg−1 of fenitrothion, an organophosphate (OP) pesticide. Running endurance of OP-exposed animals was less than half that of control animals over the first 3 days after dosing and 55% of control animal endurance on day 5 post-dose. Despite these declines, peak metabolic rate at this running speed (9.3 times basal metabolic rate; BMR) was unaffected by OP exposure. Peak metabolic rate (PMR) and cumulative oxygen consumption during a 1-h exposure to conditions equivalent to −20 °C did not differ between OP-treated and control dunnarts, with PMR averaging 11 times BMR. We conclude that fenitrothion-induced exercise fatigue is not due to limitations in oxygen or substrate delivery to muscle or in their uptake per se, but more likely relates to decreased ability to sustain high-frequency neuromuscular function. The persistence of locomotor impairment following OP exposure in otherwise asymptomatic animals emphasizes the importance of using performance-based measures when characterising sublethal effects of pesticide exposure in an ecological context.

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Unsustainable fishing practices have placed a heavy emphasis on aquaculture to meet the global shortfalls in the supply of fish and seafood, which are commonly accepted as the primary source of health-promoting essential omega-3 (n-3 highly unsaturated fatty acids). However, dietary fish oil is required for the production of omega-3-rich farmed fish and this commodity, in a vicious circle, is at present derived solely from wild fisheries. Decreasing global availability coupled with the highly variable price of this resource has forced the aquaculture industry to investigate the possibilities of alternative dietary lipid sources. This review attempts to compile all principal information available regarding the effects of fish oil replacement for the diets of farmed finfish, analysing the findings using a comparative approach among different cultured fish species. The review initially focuses on the present situation with regard to the production, availability and main nutritional characteristics of fish oil and the principal alternative lipid sources (such as vegetable oils and animal fats). Following this, the effects of fish oil replacement in finfish nutrition on feed quality, fish performance, feed efficiency, fish lipid metabolism, final eating quality and related economic aspects are presented and discussed.

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Background: Knowledge of individual changes in insulin resistance (IR) and longitudinal relationships of IR with lifestyle-associated factors are of important practical significance, but little longitudinal data exist in asymptomatic children. We aimed to determine (a) changes in the homeostatic model of insulin resistance (HOMA-IR) over a 2-yr period and (b) comparisons of longitudinal and cross-sectional relationships between HOMA-IR and lifestyle-related risk factors.

Methods: Our subjects, 241 boys and 257 girls, were assessed at age 8.1 yr (SD 0.35) and again 2 yr later for fasting blood glucose and insulin, dual X-ray absorptiometry-assessed percentage of body fat (%BF), pedometer-assessed physical activity (PA), and cardio-respiratory fitness (CRF) by multistage running test.

Results: HOMA-IR was initially 9% greater in girls than boys and 27% greater 2 yr later. There was no evidence of longitudinal relationships between HOMA-IR and %BF in boys or girls, despite significant cross-sectional relationships (p < 0.001). In boys, there was evidence of a longitudinal relationship between HOMA-IR and both PA (p < 0.001) and CRF (p = 0.05). In girls, we found a cross-sectional relationship between HOMA-IR and CRF (p < 0.001).

Conclusions: HOMA-IR increases between 8 and 10 yr of age and to a greater extent in girls. Longitudinal, unlike cross-sectional, relationships do not support the premise that body fat has any impact on HOMA-IR during this period or that PA or CRF changes affect HOMA-IR in girls. These data draw attention to difficulties in interpreting observational studies in young children.

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Initially, there were three separate strands to the work of the project: a series of forums involving group interviews/discussions with community members; a policy analysis that reviewed policies relating to Aboriginal health at federal and state level; and a literature review. The results of these three separate strands of analysis were then brought together in a fourth strand to the work, a process involving community members to discuss and agree the overall recommendations contained in this report.

Through this structure, the project employed a participatory methodology as the basis for individual and collective empowerment in relation to health outcomes. As mentioned above, the need for the project was identified by Aboriginal people, through their own processes of healing. The need was presented by appropriate figures within their communities, namely community elders. They invited other Aboriginal people to take part through their own communication channels, thus ensuring that responsibility for engagement in the project, and in formulating action for improvement, remained with Aboriginal people and their families. However, the project design also recognised that Aboriginal people exist within broader structural and policy constraints which impact on their ability to manage their own lives successfully or otherwise. Thus the project sought to combine indigenous and non-indigenous knowledge through bringing together the three strands of work in the way described.

A Community Reference Group guided the work of the project at all stages, endorsed the findings and drafted the recommendations. The two elders who had identified the need for the project formed the core of the group, and worked on the project from start to finish. At different times during the project, other community members joined the group to assist in its work, including training Aboriginal researchers, letting others know about the forums, discussing findings and drafting recommendations.
Initially, there were three separate strands to the work of the project: a series of forums involving group interviews/discussions with community members; a policy analysis that reviewed policies relating to Aboriginal health at federal and state level; and a literature review. The results of these three separate strands of analysis were then brought together in a fourth strand to the work, a process involving community members to discuss and agree the overall recommendations contained in this report.

Through this structure, the project employed a participatory methodology as the basis for individual and collective empowerment in relation to health outcomes. As mentioned above, the need for the project was identified by Aboriginal people, through their own processes of healing. The need was presented by appropriate figures within their communities, namely community elders. They invited other Aboriginal people to take part through their own communication channels, thus ensuring that responsibility for engagement in the project, and in formulating action for improvement, remained with Aboriginal people and their families. However, the project design also recognised that Aboriginal people exist within broader structural and policy constraints which impact on their ability to manage their own lives successfully or otherwise. Thus the project sought to combine indigenous and non-indigenous knowledge through bringing together the three strands of work in the way described.


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Objective: To model the health benefits and cost-effectiveness of banning television (TV) advertisements in Australia for energy-dense, nutrient-poor food and beverages during children's peak viewing times.

Methods: Benefits were modelled as changes in body mass index (BMI) and disability-adjusted life years (DALYs) saved. Intervention costs (AUD$) were compared with future health-care cost offsets from reduced prevalence of obesity-related health conditions. Changes in BMI were assumed to be maintained through to adulthood. The comparator was current practice, the reference year was 2001, and the discount rate for costs and benefits was 3%. The impact of the withdrawal of non-core food and beverage advertisements on children's actual food consumption was drawn from the best available evidence (a randomized controlled trial of advertisement exposure and food consumption). Supporting evidence was found in ecological relationships between TV advertising and childhood obesity, and from the effects of marketing bans on other products. A Working Group of stakeholders provided input into decisions surrounding the modelling assumptions and second-stage filters of 'strength of evidence', 'equity', 'acceptability to stakeholders', 'feasibility of implementation', 'sustainability' and 'side-effects'.

Results: The intervention had a gross incremental cost-effectiveness ratio of AUD$ 3.70 (95% uncertainty interval (UI) $2.40, $7.70) per DALY. Total DALYs saved were 37 000 (95% UI 16 000, 59 000). When the present value of potential savings in future health-care costs was considered (AUD$ 300m (95% UI $130m, $480m), the intervention was 'dominant', because it resulted in both a health gain and a cost offset compared with current practice.

Conclusions:
Although recognizing the limitations of the available evidence, restricting TV food advertising to children would be one of the most cost-effective population-based interventions available to governments today. Despite its economic credentials from a public health perspective, the initiative is strongly opposed by food and advertising industries and is under review by the current Australian government.

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The mechanisms of how tea and epigallocatechin-3-gallate (EGCG) lower body fat are not completely understood. This study investigated long-term administration of green tea (GT), black tea (BT), or isolated EGCG (1 mg/kg per day) on body composition, glucose tolerance, and gene expression related to energy metabolism and lipid homeostasis; it was hypothesized that all treatments would improve the indicators of metabolic syndrome. Rats were fed a 15% fat diet for 6 months from 4 weeks of age and were supplied GT, BT, EGCG, or water. GT and BT reduced body fat, whereas GT and EGCG increased lean mass. At 16 weeks GT, BT, and EGCG improved glucose tolerance. In the liver, GT and BT increased the expression of genes involved in fatty acid synthesis (SREBP-1c, FAS, MCD, ACC) and oxidation (PPAR-α, CPT-1, ACO); however, EGCG had no effect. In perirenal fat, genes that mediate adipocyte differentiation were suppressed by GT (Pref-1, C/EBP-β, and PPAR-γ) and BT (C/EBP-β), while decreasing LPL, HSL, and UCP-2 expression; EGCG increased expression of UCP-2 and PPAR-γ genes. Liver triacylglycerol content was unchanged. The results suggest that GT and BT suppressed adipocyte differentiation and fatty acid uptake into adipose tissue, while increasing fat synthesis and oxidation by the liver, without inducing hepatic fat accumulation. In contrast, EGCG increased markers of thermogenesis and differentiation in adipose tissue, while having no effect on liver or muscle tissues at this dose. These results show novel and separate mechanisms by which tea and EGCG may improve glucose tolerance and support a role for these compounds in obesity prevention.