The Effects of Potato Presentation on Vegetable Intake in School-Aged Children: A Cross-Over Study.

Vegetables are an essential component of a healthy dietary pattern in children; however, their consumption is often insufficient due to lack of preference. To address this, the influence of combining vegetables (mixed peas and carrots-MPACs) with potatoes, a generally liked food, on overall vegetable consumption among children aged 7-13 years was explored. The research involved a cross-over study design with 65 participants who completed five lunchtime meal conditions, each with different combinations of MPACs and potatoes versus a control (MPACs with a wheat roll). The meals were provided in a cafeteria setting, and plate waste was used to measure vegetable consumption. Anthropometric data and other variables were also measured. Notably, self-reported hunger did not significantly differ between conditions. Meal condition was a significant predictor of MPACs (F = 5.20; p = 0.0005), with MPAC consumption highest when combined with shaped potato faces in the same bowl (+8.77 g compared to serving MPACs and shaped potato faces in separate bowls) and lowest when combined with diced potatoes in the same bowl (-2.85 g compared to serving MPACs and diced potatoes in separate bowls). The overall model for MPAC consumption was influenced by age, height z-score, body fat percentage z-score, and condition (likelihood ratio = 49.1; p < 0.0001). Age had the strongest correlation with vegetable consumption (r = 0.38), followed by male gender, height z-score (r = 0.30), and body fat z-score (r = -0.15). The results highlight the positive impact of combining potatoes with vegetables in school meals, particularly when using shaped potato faces. These findings emphasize the potential of potatoes as a valuable vegetable option in promoting healthier eating habits among children. Additionally, future research could explore the impact of different potato combinations and investigate other factors influencing meal consumption in school settings.

Influence of almond and coconut flours on Ketogenic, Gluten-Free cupcakes.

Ketogenic, gluten-free cupcakes containing varying amounts of almond and coconut flours were evaluated for textural and sensory attributes. Coconut-flour particle-size influenced cupcake volume and crumb structure, with smaller flour-particle size resulting in increased volume and decreased crumb density. Although almond-flour particle size itself did not directly influence cupcake properties, volume increases were observed in cupcakes with higher percentages of almond flour. Addition of coconut flour increased cell size and decreased cell density. Mechanical testing showed almond flour resulted in a cupcake that was more tender. Adhesion and cohesion values showed no statistical difference after 24 h and minimal change at subsequent evaluation periods. Quantitative descriptive analysis and consumer acceptance evaluation indicated that cupcakes containing almond flour were more moist and tender, and were preferred over cupcakes made with only coconut flour. Almond and coconut flours may be used in gluten-free, ketogenic cupcakes, with almond flour performing better in evaluated parameters.

Mechanical, sensory, and consumer evaluation of ketogenic, gluten-free breads.

Ketogenic, gluten-free breads comprised of almond flour, oat bran fiber, or combinations of both were compared. The textural properties, sensory attributes, and consumer acceptance were analyzed on each bread containing 100% almond flour (AF), 66.7% almond flour with 33.3% oat bran fiber (AOB), 66.7% oat bran fiber with 33.3% almond flour (OBA), and 100% oat bran fiber (OB). AF and AOB breads had a more open crumb structure composed of cells between 1-4 mm2. OBA and OB had a significantly dense crumb pattern made up of more cells less than one millimeter squared. Quantitative-descriptive analysis (QDA) and consumer acceptance testing was conducted 24 hr after baking and mechanical endpoints were evaluated 24, 72, and 120 hr after baking. AF and AOB breads were preferred over OBA and OB breads in QDA evaluation and consumer acceptance scores. Greater percentages of oat bran fiber resulted in a bread that was less moist, firmer in texture, and chewier with trained panelists. In both sensory evaluations, higher amounts of almond flour resulted in higher values in eggy flavor while increased amounts of oat bran fiber correlated with higher values in earthy flavor. Mechanical testing identified higher percentages of almond flour resulted in bread that was less firm and less chewy. Over time, all variations with almond flour became softer and less chewy, while the OB bread increased in firmness. Sensory cohesiveness did not correlate with the mechanical equivalent, identifying a need to re-evaluate the parameters used to calculate this objective endpoint.

Oncogene expression profiles in K6/ODC mouse skin and papillomas following a chronic exposure to monomethylarsonous acid.

We have previously observed that a chronic drinking water exposure to monomethylarsonous acid [MMA(III)], a cellular metabolite of inorganic arsenic, increases tumor frequency in the skin of keratin VI/ornithine decarboxylase (K6/ODC) transgenic mice. To characterize gene expression profiles predictive of MMA(III) exposure and mode of action of carcinogenesis, skin and papilloma RNA was isolated from K6/ODC mice administered 0, 10, 50, and 100 ppm MMA(III) in their drinking water for 26 weeks. Following RNA processing, the resulting cRNA samples were hybridized to Affymetrix Mouse Genome 430A 2.0 GeneChips(R). Micoarray data were normalized using MAS 5.0 software, and statistically significant genes were determined using a regularized t-test. Significant changes in bZIP transcription factors, MAP kinase signaling, chromatin remodeling, and lipid metabolism gene transcripts were observed following MMA(III) exposure as determined using the Database for Annotation, Visualization and Integrated Discovery 2.1 (DAVID) (Dennis et al., Genome Biol 2003;4(5):P3). MMA(III) also caused dose-dependent changes in multiple Rho guanine nucleotide triphosphatase (GTPase) and cell cycle related genes as determined by linear regression analyses. Observed increases in transcript abundance of Fosl1, Myc, and Rac1 oncogenes in mouse skin support previous reports on the inducibility of these oncogenes in response to arsenic and support the relevance of these genomic changes in skin tumor induction in the K6/ODC mouse model.

Folate deficiency enhances arsenic effects on expression of genes involved in epidermal differentiation in transgenic K6/ODC mouse skin.

Chronic arsenic exposure in humans is associated with cancers of the skin, lung, bladder and other tissues. There is evidence that folate deficiency may increase susceptibility to arsenic effects, including skin lesions. K6/ODC mice develop skin tumors when exposed to 10ppm sodium arsenite for 5 months. In the current study, K6/ODC mice maintained on either a folate deficient or folate sufficient diet were exposed to 0, 1, or 10ppm sodium arsenite in the drinking water for 30 days. Total RNA was isolated from skin samples and gene expression analyzed using Affymetrix Mouse 430 2.0 GeneChips. Data from 24 samples, with 4 mice in each of the 6 treatment groups, were RMA normalized and analyzed by two-way ANOVA using GeneSpring. Top gene ontology (GO) categories for genes responding significantly to both arsenic treatment and folate deficiency include nucleotide metabolism and cell organization and biogenesis. For many of these genes, folate deficiency magnifies the response to arsenic treatment. In particular, expression of markers of epidermal differentiation, e.g., loricrin, small proline rich proteins and involucrin, was significantly reduced by arsenic in the folate sufficient animals, and reduced further or at a lower arsenic dose in the folate deficient animals. In addition, expression of a number of epidermal cell growth/proliferation genes and cellular movement genes was altered. These results indicate that arsenic disrupts the normal balance of cell proliferation and differentiation, and that folate deficiency exacerbates these effects, consistent with the view that folate deficiency is a nutritional susceptibility factor for arsenic-induced skin tumorigenesis.

Early alterations in protein and gene expression in rat kidney following bromate exposure.

Bromate, a common disinfectant byproduct of drinking water ozonation, has been linked to human and animal renal toxicity, including renal cell carcinomas in multiple animal species. Here, we evaluate changes in protein and gene expression through two-dimensional difference gel electrophoresis (2D-DIGE) and Affymetrix arrays to identify potential modes of action involved in potassium bromate carcinogenicity. Male rats were exposed to potassium bromate in drinking water at concentrations of 0, 1, 20 and 400 ppm for two weeks. Differential expression of glycolytic proteins including enolase 1 (Eno1), triosephosphate isomerase 1 (Tpi1) and glyceraldehyde-3-phosphate dehydrogenase (Gapdh) suggests that bromate toxicity is associated with changes in energy consumption and utilization in renal cells involving up-regulation of glycolytic processes that may be the result of altered mitochondrial function. Several alterations in glycolysis and mitochondrial gene transcripts were also observed to be consistent with this mode of action. These studies provide insight into early events in renal cell physiology altered by bromate exposure.

Transcriptional changes associated with reduced spontaneous liver tumor incidence in mice chronically exposed to high dose arsenic.

Exposure of male C3H mice in utero (from gestational days 8-18) to 85ppm sodium arsenite via the dams' drinking water has previously been shown to increase liver tumor incidence by 2 years of age. However, in our companion study (Ahlborn et al., 2009), continuous exposure to 85ppm sodium arsenic (from gestational day 8 to postnatal day 365) did not result in increased tumor incidence, but rather in a significant reduction (0% tumor incidence). The purpose of the present study was to examine the gene expression responses that may lead to the apparent protective effect of continuous arsenic exposure. Genes in many functional categories including cellular growth and proliferation, gene expression, cell death, oxidative stress, protein ubiquitination, and mitochondrial dysfunction were altered by continuous arsenic treatment. Many of these genes are known to be involved in liver cancer. One such gene associated with rodent hepatocarcinogenesis, Scd1, encodes stearoyl-CoA desaturase and was down-regulated by continuous arsenic treatment. An overlap between the genes in our study affected by continuous arsenic exposure and those from the literature affected by long-term caloric restriction suggests that reduction in the spontaneous tumor incidence under both conditions may involve similar gene pathways such as fatty acid metabolism, apoptosis, and stress response.

Impact of life stage and duration of exposure on arsenic-induced proliferative lesions and neoplasia in C3H mice.

Epidemiological studies suggest that chronic exposure to inorganic arsenic is associated with cancer of the skin, urinary bladder and lung as well as the kidney and liver. Previous experimental studies have demonstrated increased incidence of liver, lung, ovary, and uterine tumors in mice exposed to 85 ppm (approximately 8 mg/kg) inorganic arsenic during gestation. To further characterize age susceptibility to arsenic carcinogenesis we administered 85 ppm inorganic arsenic in drinking water to C3H mice during gestation, prior to pubescence and post-pubescence to compare proliferative lesion and tumor outcomes over a one-year exposure period. Inorganic arsenic significantly increased the incidence of hyperplasia in urinary bladder (48%) and oviduct (36%) in female mice exposed prior to pubescence (beginning on postnatal day 21 and extending through one year) compared to control mice (19 and 5%, respectively). Arsenic also increased the incidence of hyperplasia in urinary bladder (28%) of female mice continuously exposed to arsenic (beginning on gestation day 8 and extending though one year) compared to gestation only exposed mice (0%). In contrast, inorganic arsenic significantly decreased the incidence of tumors in liver (0%) and adrenal glands (0%) of male mice continuously exposed from gestation through one year, as compared to levels in control (30 and 65%, respectively) and gestation only (33 and 55%, respectively) exposed mice. Together, these results suggest that continuous inorganic arsenic exposure at 85 ppm from gestation through one year increases the incidence and severity of urogenital proliferative lesions in female mice and decreases the incidence of liver and adrenal tumors in male mice. The paradoxical nature of these effects may be related to altered lipid metabolism, the effective dose in each target organ, and/or the shorter one-year observational period.

Dose response evaluation of gene expression profiles in the skin of K6/ODC mice exposed to sodium arsenite.

Chronic drinking water exposure to inorganic arsenic and its metabolites increases tumor frequency in the skin of K6/ODC transgenic mice. To identify potential biomarkers and modes of action for this skin tumorigenicity, we characterized gene expression profiles from analysis of K6/ODC mice administered 0, 0.05, 0.25, 1.0 and 10 ppm sodium arsenite in their drinking water for 4 weeks. Following exposure, total RNA was isolated from mouse skin and processed to biotin-labeled cRNA for microarray analyses. Skin gene expression was analyzed with Affymetrix Mouse Genome 430A 2.0 GeneChips, and pathway analysis was conducted with DAVID (NIH), Ingenuity Systems and MetaCore's GeneGo. Differential expression of several key genes was verified through qPCR. Only the highest dose (10 ppm) resulted in significantly altered KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways, including MAPK, regulation of actin cytoskeleton, Wnt, Jak-Stat, Tight junction, Toll-like, phosphatidylinositol and insulin signaling pathways. Approximately 20 genes exhibited a dose response, including several genes known to be associated with carcinogenesis or tumor progression including cyclin D1, CLIC4, Ephrin A1, STAT3 and DNA methyltransferase 3a. Although transcription changes in all identified genes have not previously been linked to arsenic carcinogenesis, their association with carcinogenesis in other systems suggests that these genes may play a role in the early stages of arsenic-induced skin carcinogenesis and can be considered potential biomarkers.