7 resultados para calories

em Deakin Research Online - Australia


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There is increasing recognition that the nutrition transition sweeping the world’s cities is multifaceted. Urban food and nutrition systems are beginning to share similar features, including an increase in dietary diversity, a convergence toward “Western-style” diets rich in fat and refined carbohydrate and within-country bifurcation of food supplies and dietary conventions. Unequal access to the available dietary diversity, calories, and gastronomically satisfying eating experience leads to nutritional inequalities and diet-related health inequities in rich and poor cities alike. Understanding the determinants of inequalities in food security and nutritional quality is a precondition for developing preventive policy responses. Finding common solutions to under- and overnutrition is required, the first step of which is poverty eradication through creating livelihood strategies. In many cities, thousands of positions of paid employment could be created through the establishment of sustainable and self-sufficient local food systems, including urban agriculture and food processing initiatives, food distribution centers, healthy food market services, and urban planning that provides for multiple modes of transport to food outlets. Greater engagement with the food supply may dispel many of the food anxieties affluent consumers are experiencing.

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Consumption of a Western diet rich in saturated fats is associated with obesity and insulin resistance. In some insulin-resistant phenotypes this is associated with accumulation of skeletal muscle fatty acids. We examined the effects of diets high in saturated fatty acids (Sat) or n-6 polyunsaturated fatty acids (PUFA) on skeletal muscle fatty acid metabolite accumulation and whole-body insulin sensitivity. Male Sprague-Dawley rats were fed a chow diet (16% calories from fat, Con) or a diet high (53%) in Sat or PUFA for 8 wk. Insulin sensitivity was assessed by fasting plasma glucose and insulin and glucose tolerance via an oral glucose tolerance test. Muscle ceramide and diacylglycerol (DAG) levels and triacylglycerol (TAG) fatty acids were also measured. Both high-fat diets increased plasma free fatty acid levels by 30%. Compared with Con, Sat-fed rats were insulin resistant, whereas PUFA-treated rats showed improved insulin sensitivity. Sat caused a 125% increase in muscle DAG and a small increase in TAG. Although PUFA also resulted in a small increase in DAG, the excess fatty acids were primarily directed toward TAG storage (105% above Con). Ceramide content was unaffected by either high-fat diet. To examine the effects of fatty acids on cellular lipid storage and glucose uptake in vitro, rat L6 myotubes were incubated for 5 h with saturated and polyunsaturated fatty acids. After treatment of L6 myotubes with palmitate (C16:0), the ceramide and DAG content were increased by two- and fivefold, respectively, concomitant with reduced insulin-stimulated glucose uptake. In contrast, treatment of these cells with linoleate (C18:2) did not alter DAG, ceramide levels, and glucose uptake compared with controls (no added fatty acids). Both 16:0 and 18:2 treatments increased myotube TAG levels (C18:2 vs. C16:0, P < 0.05). These results indicate that increasing dietary Sat induces insulin resistance with concomitant increases in muscle DAG. Diets rich in n-6 PUFA appear to prevent insulin resistance by directing fat into TAG, rather than other lipid metabolites.

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Consumption of a high-fat diet (HFD) by rabbits results in increased blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) within 1 wk. Here, we determined how early this activation occurred and whether it was related to changes in cardiovascular and neural 24-h rhythms. Rabbits were meal-fed a HFD for 3 wks, then a normal-fat diet (NFD) for 1 wk. BP, HR, and RSNA were measured daily in the home cage via implanted telemeters. Baseline BP, HR, and RSNA over 24 h were 71 ± 1 mm Hg, 205 ± 4 beats/min and 7 ± 1 normalized units (nu). The 24-h pattern was entrained to the feeding cycle and values increased from preprandial minimum to postprandial maximum by 4 ± 1 mm Hg, 51 ± 6 beats/min, and 1.6 ± .6 nu each day. Feeding of a HFD markedly diminished the preprandial dip after 2 d (79–125% of control; p < 0.05) and this reduction lasted for 3 wks of HFD. Twenty-four-hour BP, HR, and RSNA concurrently increased by 2%, 18%, and 22%, respectively. Loss of preprandial dipping accounted for all of the BP increase and 50% of the RSNA increase over 3 wks and the 24-h rhythm became entrained to the light-dark cycle. Resumption of a NFD did not alter the BP preprandial dip. Thus, elevated BP induced by a HFD and mediated by increased sympathetic nerve activity results from a reduction in preprandial dipping, from the first day. Increased calories, glucose, insulin, and leptin may account for early changes, whereas long-term loss of dipping may be related to increased sensitivity of sympathetic pathways.


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Males often have reduced immune function compared to females but the proximate mechanisms underlying this taxonomically widespread pattern are unclear. Because immune function is resource-dependent and sexes may have different nutritional requirements, we hypothesized that sexual dimorphism in immune function may arise from differential nutrient intake (acquisition hypothesis). To test this hypothesis, we examined patterns of phenoloxidase (PO) activity in relation to nutrient consumption in Queensland fruit flies (Q-flies). In the first experiment, flies were allowed to choose their preferred nutrient intake. Compared with males, female Q-flies had higher PO activity, consumed more calories, and preferred a higher protein:carbohydrate (P:C) diet, suggesting that differential acquisition could explain sex differences. In the second experiment, we restricted flies to one of 12 diets varying in protein and carbohydrate concentrations and mapped PO activity for each sex onto a nutritional landscape. Counter to our hypothesis, females had higher PO activity than males at any given level of nutrient intake. Both carbohydrate and protein intake affected PO activity in females but only protein affected PO activity in males. Our results indicate that sex differences in Q-fly immune function are not solely explained by sex differences in nutrient intake, although nutrition does contribute to the magnitude of these sex differences.

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Caloric restriction (CR) has been widely accepted as a mechanism explaining increased lifespan (LS) in organisms subjected to dietary restriction (DR), but recent studies investigating the role of nutrients have challenged the role of CR in extending longevity. Fuelling this debate is the difficulty in experimentally disentangling CR and nutrient effects due to compensatory feeding (CF) behaviour. We quantified CF by measuring the volume of solution imbibed and determined how calories and nutrients influenced LS and fecundity in unmated females of the Queensland fruit fly, Bactocera tryoni (Diptera: Tephritidae). We restricted flies to one of 28 diets varying in carbohydrate:protein (C:P) ratios and concentrations. On imbalanced diets, flies overcame dietary dilutions, consuming similar caloric intakes for most dilutions. The response surface for LS revealed that increasing C:P ratio while keeping calories constant extended LS, with the maximum LS along C:P ratio of 21:1. In general, LS was reduced as caloric intake decreased. Lifetime egg production was maximized at a C:P ratio of 3:1. When given a choice of separate sucrose and yeast solutions, each at one of five concentrations (yielding 25 choice treatments), flies regulated their nutrient intake to match C:P ratio of 3:1. Our results (i) demonstrate that CF can overcome dietary dilutions; (ii) reveal difficulties with methods presenting fixed amounts of liquid diet; (iii) illustrate the need to measure intake to account for CF in DR studies and (iv) highlight nutrients rather than CR as a dominant influence on LS.

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INTRODUCTION: Menu energy labelling at point of purchase is gaining traction worldwide, yet the potential impact for different socioeconomic groups is unclear. We aimed to summarise evidence on the effectiveness of menu energy labelling by socioeconomic position (SEP). METHODS: A systematic search for papers published to September 2015 was conducted using terms for labelling, food outlets, and SEP. Quality of studies was assessed. Results were summarised across stages of an intervention logic pathway. RESULTS: Eighteen articles were identified. Of twelve studies reporting the effect of menu energy labelling in low SEP populations, six reported on purchase outcomes. All but one of these reported no positive effect of the policy for this population. Two of the five studies that compared purchase outcomes of menu labelling across SEP groups reported that the policy was effective overall. These two studies reported either a significant decline in fast food calories purchased from consumers in high (but not low) SEP neighbourhoods or a significantly greater decline in calories purchased among consumers visiting stores in higher SEP neighbourhoods post policy implementation. Few studies were rated as moderate to high quality. CONCLUSIONS: The current evidence describing the impact of menu energy labelling within or across SEP is limited in quantity and quality. Of the two studies that reported a positive benefit of menu energy labelling overall, both identified a greater effect on fast food purchases among consumers visiting stores in high compared to low SEP neighbourhoods. It is difficult to know whether the absence of effectiveness reported in low SEP populations represents a true lack of effectiveness or is a result of a more general lack of policy effectiveness or the limited quality of the reviewed studies.

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BACKGROUND: Substituting sugar-free for sugar-sweetened beverages reduces weight gain. A possible explanation is that sugar-containing and sugar-free beverages cause the same degree of satiety. However, this has not been tested in long-term trials.

METHODS: We randomized 203 children aged 7-11 years to receive 250 mL per day of an artificially sweetened sugar-free beverage or a similarly looking and tasting sugar-sweetened beverage. We measured satiety on a 5-point scale by questionnaire at 0, 6, 12 and 18 months. We calculated the change in satiety from before intake to 1 minute after intake and 15 minutes after intake. We then calculated the odds ratio that satiety increased by 1 point in the sugar-group versus the sugar-free group. We also investigated how much the children liked and wanted the beverages.

RESULTS: 146 children or 72% completed the study. We found no statistically significant difference in satiety between the sugar-free and sugar-sweetened group; the adjusted odds ratio for a 1 point increase in satiety in the sugar group versus the sugar-free group was 0.77 at 1 minute (95% confidence interval, 0.46 to 1.29), and 1.44 at 15 minutes after intake (95% CI, 0.86 to 2.40). The sugar-group liked and wanted their beverage slightly more than the sugar-free group, adjusted odds ratio 1.63 (95% CI 1.05 to 2.54) and 1.65 (95% CI 1.07 to 2.55), respectively.

CONCLUSIONS: Sugar-sweetened and sugar-free beverages produced similar satiety. Therefore when children are given sugar-free instead of sugar-containing drinks they might not make up the missing calories from other sources. This may explain our previous observation that children in the sugar-free group accumulated less body fat than those in the sugar group.