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Shape of snack foods does not predict snack intake in a sample of preschoolers: a cross-over study

Abstract Background In the past decade, the proportion snacking has increased. Snack foods consumed are predominantly not nutritious foods. One potential venue to increase children’s diet quality is to offer healthy snack foods and we explored if shaped snack foods would lead to increased consumption. Methods We investigated the consumption of high-fiber snacks (banana bread, pancakes, and sandwiches) served either in normal (round, square) or shaped (heart, hands, animals) form to preschoolers 2–5 years old attending a local child care center (n = 21). The 9 weeks long, prospective, cross-over intervention study was designed to expose each child repeatedly to each snack in each shape (4 times per snack). Snacks were served as morning or afternoon snack and caretakers’ reports were used to account for the child’s consumption of a meal preceding the study snack (breakfast or lunch). Results There was no significant difference in snack consumption between the shaped and normal snacks. However, the mean energy intake from snacks was significantly greater for Caucasian children compared with Asian children. Further, Asian children consumed much less banana bread than the other two snacks. Overall, children who had not eaten breakfast or lunch prior to the morning or afternoon snack ate significantly more calories from the snacks (84.1 kcal, p-value  Conclusion Findings of this study confirm previous research that the shape of the foods does not affect snack consumption in children. However, we also report two unexpected findings: a) the strong interaction between ethnicity and snack consumption and b) that Asian children consumed much less banana bread than Caucasian children. The role of children’s ethnic background profoundly affects snack preference and must be considered in the study of children’s eating behaviors and in interventions to promote healthy eating habits.</p

Shape of snack foods does not predict snack intake in a sample of preschoolers:a cross-over study

BACKGROUND: In the past decade, the proportion snacking has increased. Snack foods consumed are predominantly not nutritious foods. One potential venue to increase children’s diet quality is to offer healthy snack foods and we explored if shaped snack foods would lead to increased consumption. METHODS: We investigated the consumption of high-fiber snacks (banana bread, pancakes, and sandwiches) served either in normal (round, square) or shaped (heart, hands, animals) form to preschoolers 2–5 years old attending a local child care center (n = 21). The 9 weeks long, prospective, cross-over intervention study was designed to expose each child repeatedly to each snack in each shape (4 times per snack). Snacks were served as morning or afternoon snack and caretakers’ reports were used to account for the child’s consumption of a meal preceding the study snack (breakfast or lunch). RESULTS: There was no significant difference in snack consumption between the shaped and normal snacks. However, the mean energy intake from snacks was significantly greater for Caucasian children compared with Asian children. Further, Asian children consumed much less banana bread than the other two snacks. Overall, children who had not eaten breakfast or lunch prior to the morning or afternoon snack ate significantly more calories from the snacks (84.1 kcal, p-value < 0.0001). CONCLUSION: Findings of this study confirm previous research that the shape of the foods does not affect snack consumption in children. However, we also report two unexpected findings: a) the strong interaction between ethnicity and snack consumption and b) that Asian children consumed much less banana bread than Caucasian children. The role of children’s ethnic background profoundly affects snack preference and must be considered in the study of children’s eating behaviors and in interventions to promote healthy eating habits

Timing of serving dessert but not portion size affects young children's intake at lunchtime

AbstractThe purpose of this repeated exposure, randomized, cross-over quasi-experimental study was to determine the individual and combined impact of (a) the timing of serving dessert and (b) portion size of main course in 2–5year old children (n=23) on energy intake at lunch in a childcare setting. Children were served two study lunches (fish or pasta, each with dessert) twice a week for 12weeks that differed in the timing of dessert (served with or after the main course) and portion size of the main course (reference portion or 50% larger portion). Analyses of variance revealed that serving dessert after the meal resulted in higher energy intakes from both the main course and from dessert, and therefore greater total intake at the meal. Portion size of the main course did not influence total energy intake at the meal. Results indicate that the timing of serving dessert affects children’s energy intake regardless of the portion size of the main course. Specifically, serving dessert with the meal reduces total energy intake regardless of the main course portion size. This suggests that offering dessert with the main course may be an effective strategy for decreasing total energy intake at meals in preschool-aged children

Impacts on Sirtuin Function and Bioavailability of the Dietary Bioactive Compound Dihydrocoumarin

<div><p>The plant secondary metabolite and common food additive dihydrocoumarin (DHC) is an inhibitor of the Sirtuin family of NAD⁺-dependent deacetylases. Sirtuins are key regulators of epigenetic processes that maintain silent chromatin in yeast and have been linked to gene expression, metabolism, apoptosis, tumorogenesis and age-related processes in multiple organisms, including humans. Here we report that exposure to the polyphenol DHC led to defects in several Sirtuin-regulated processes in budding yeast including the establishment and maintenance of Sir2p-dependent silencing by causing disassembly of silent chromatin, Hst1p-dependent repression of meiotic-specific genes during the mitotic cell cycle. As both transient and prolonged exposure to environmental and dietary factors have the potential to lead to heritable alterations in epigenetic states and to modulate additional Sirtuin-dependent phenotypes, we examined the bioavailability and digestive stability of DHC using an <i>in vivo</i> rat model and <i>in vitro</i> digestive simulator. Our analyses revealed that DHC was unstable during digestion and could be converted to melilotic acid (MA), which also caused epigenetic defects, albeit less efficiently. Upon ingestion, DHC was observed primarily in intestinal tissues, but did not accumulate over time and was readily cleared from the animals. MA displayed a wider tissue distribution and, in contrast to DHC, was also detected in the blood plasma, interstitial fluid, and urine, implying that the conversion of DHC to the less bioactive compound, MA, occurred efficiently <i>in vivo</i>.</p></div

DHC prevents Sir spreading and mimics the catalytically inactive <i>sir2-345</i> mutant.

<p><b>a</b> Transcriptional analysis by qRT-PCR of <b><i>a1</i></b> at <i>HMR</i> relative to an internal control (<i>SCR1</i>) was determined for strains with the indicated genotypes grown in rich (YPD) media in the absence or presence of 200 μM DHC, and compared to that observed in <i>sir2-345</i> mutants expressing wild-type H3 and H4, which was set to 100% (AVG ± SD, n = 3). Data was calculated as: 2[(<b><i>a1</i></b>CT − <i>SCR1</i>CT)Indicated strain − (<b><i>a1</i></b>CT − <i>SCR1</i>CT)<i>sir2-345</i> H3/H4]. <b>b</b> Sir3p binding at <i>MAT</i>, <i>HMR E</i> silencer, <b><i>a1</i></b>, and <i>I</i> silencer in the absence or presence of 200 μM DHC was monitored by ChIP using IgG or anti-Sir3p antibodies and qRT-PCR in <i>SIR2</i> and <i>sir2-345</i> strains expressing wild-type or hypoacetylated H3/H4. Efficiency of co-precipitation of each locus is expressed relative to <i>MAT</i> and was calculated as: Locus IP/<i>MAT</i> IP = 2[(<i>MAT</i>CT − LocusCT); See also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0149207#pone.0149207.s002" target="_blank">S2 Fig</a>.</p

DHC and MA are present in intestinal contents.

<p>DHC (<b>a</b>) and MA (<b>b</b>) were extracted from the contents of the stomach, large intestine, and small intestine, and analyzed by HPLC as outlined Materials and methods. *More DHC was present in the stomach contents at 1 hr vs. 6 hr (p = 0.015) and more MA was present in the large intestine contents at 6 hr vs. 1 hr (p = 0.03); <b>a</b> More DHC was present in stomach contents at 1 hr compared to large and small intestine contents at 1 hour (p = 0.0097); <b>b</b> more DHC was present in large intestine contents at 6 hr compared to stomach and small intestine contents at 6 hr (p = 0.014); and <b>c</b> more MA in was present in stomach contents at 1 hr compared to large intestine contents at 1 hr (p = 0.015). AVG ± SE, n = 6.</p

DHC inhibits silencing of reporter genes at <i>HMR</i>.

<p>In reporter strains, <b><i>a1</i></b> and <b><i>a2</i></b> at <i>HMR</i> were replaced by genes encoding A. <i>ADE2</i> or B. <i>TRP1</i>. Logarithmically growing yeast were plated on rich (YPD) media (<b>a</b>) or minimal (YM) media (<b>b</b>) containing or lacking tryptophan plus the indicated amount of DHC and analyzed as outlined in Materials and methods.</p

DHC and MA accumulate in digestive-tract tissues.

<p>For <i>in vivo</i> bioavailability analyses, rats were given 100 mg/kg DHC by gavage. DHC (<b>a</b>) and MA (<b>b</b>) were extracted from flash frozen tissues using ethyl acetate, dried, resuspended in 50% methanol, and analyzed by HPLC. The amount (μmol) of MA or DHC was quantified by determining the area under the peaks and compared to a standard curve. *Significantly more MA (<b>b</b>) was present at 1 hr relative to 6 hr in stomach, small intestine, spleen, and kidney, p = 0.028, 0.027, 0.026, and 0.029, respectively. AVG ± SE, n = 6. See also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0149207#pone.0149207.s003" target="_blank">S3 Fig</a>.</p

DHC inhibits silencing of <i>a1</i> at <i>HMR</i>.

<p>Transcript levels of <b><i>a1</i></b> relative to <i>SCR1</i>, an internal control, were measured by qRT-PCR in logarithmically growing cells in the presence or absence of DHC. The levels of transcripts present in samples treated with 250 μM DHC was set to 1. Data was calculated as: 2[(<b><i>a1</i></b>CT − <i>SCR1</i>CT)DHC − (<b><i>a1</i></b>CT − <i>SCR1</i>CT)No DHC] (AVG ± SD, n = 5).</p