bluuebunny/crossref_metadata_2025_split huggingface dataset:
Are Foods of Higher Nutritional Quality More Expensive Than Their Less Healthy Counterparts? An Analysis of Canadian Packaged Foods
Authors: Labonté Marie‐Eve , Noorhosseini Sheida , Bernstein Jodi , Ahmed Mavra , L'Abbé Mary 
Published: November 2023

Price‐related differences in the nutritional quality of food products may create unintended disparities in healthy food availability between different socioeconomic segments of the population. This study assessed whether healthier products are more expensive than less healthy products within specific food categories in the Canadian food supply. Data on nutritional composition and price were obtained from the University of Toronto Food Label Information Program (FLIP) 2013 database, which contains information on n=15,401 packaged products from the four largest national retailers by sales. Ready‐to‐eat breakfast cereals (n=250) and yogurts (n=236) were included in the present analyses. The Food Standards Australia New Zealand Nutrient Profiling Scoring Criterion (FSANZ‐NPSC) was used to calculate a summary score of the healthfulness of each product based on its content of nutrients to limit (e.g. sodium) and nutrients to encourage (e.g. fibre). Additionally, food products were classified either as “healthier” or “less healthy” based on the established cutoff score in the FSANZ‐NPSC model. The Student's t‐test was used to compare different price measures (price per 100 g, per serving, and per 100 Kcal) between “healthier” and “less healthy” breakfast cereals and yogurts. “Healthier” breakfast cereals had a higher price per serving than breakfast cereals of lower nutritional quality (geometric mean [95% confidence interval] = CAD $0.53 [0.49–0.57] vs. 0.44 [0.41–0.47], respectively, P=0.0004). Price per 100 g and price per 100 Kcal did not differ according to the degree of healthfulness of breakfast cereals (both P≥0.60). “Healthier” yogurts had a lower price per serving and price per 100 g than yogurts of lower nutritional quality (per serving: CAD $0.82 [0.77–0.87] vs. 1.13 [0.91–1.40], respectively, P=0.006; per 100g: CAD $0.67 [0.64–0.70] vs. 0.81 [0.72–0.92], P=0.03), but a higher price per 100 Kcal (CAD $0.93 [0.88–0.98] vs. 0.61 [0.57–0.65], P<0.0001). These data suggest that healthier food products are not necessarily more expensive than less healthy products. Importantly, the relationship between the healthfulness of foods and their price varies depending on the type of food products evaluated and the selected price measures. These factors must be taken into consideration when communicating research results to a general audience.Support or Funding InformationCanadian Institutes of Health Research (CIHR) Fellowship (MEL); CIHR Open Operating Grant (ML); and Burroughs Wellcome Fund – Innovation in Regulatory Science (ML)
Mapping inflammation and cancer‐modifying regions in broccoli genome
Authors: Bussler Weston , Alley Jessica , Chandler Holli , Thetford Claire , Yousef Gad , Brown Allan , Esposito Debora , Lila Mary Ann , Komarnytsky Slavko 
Published: November 2023

Consuming a healthy diet is one of the controllable factors that influences the development or severity of multiple chronic diseases, including metabolic, inflammatory, and neoplastic disorders. Diets high in cruciferous vegetables consistently show a decreased incidence of colorectal cancer and cardiovascular disease. Understanding the dynamic interrelationships that exist between bioactive food components in broccoli and human disease prevention is recognized as a high priority. A collection of 125 near‐isogenic broccoli lines (Brassica oleracea subsp. italica) previously developed by our group, represents a unique tool for studying effects of multiple dietary bioactive components by utilizing physiologically relevant concentrations of the agents and eliminating experimental noise associated with food matrix effects. By using broccoli near‐isogenic lines, we successfully observed direct nutrient‐nutrient or nutrient‐disease interactions that vary significantly (order of magnitude) in their ability to suppress inflammation in RAW 264.7 macrophages or inhibit proliferation of HT‐29 colorectal cancer cells. When combined with quantitative trait loci (QTL) or genome‐wide association (GWAS) studies, this approach allowed for direct mapping of human health‐modifying regions (HMRs) in the broccoli genome – even if the interacting bioactive metabolites, or their respective biosynthetic and genetic regulatory pathways, were unknown. Our findings suggested that 3 health‐modifying regions (HMRs) on 2 chromosomes were sufficient to explain over 52% of the variation in health‐promoting activity observed among broccoli varieties tested. Within these regions, known gene sequences were assessed for relevance to synthesis or regulation of bioactive metabolites to identify candidate genes and advance breeding programs aimed at targeted improvement of broccoli nutritional value.Support or Funding InformationThis work was supported in part by NCSU faculty start‐up funds (SK); Plant Pathways Elucidation Project; and Cell Culture and Phenotyping Core of the Plants for Human Health Institute, NC State University.
The Metabolic Fate of Isotopically‐Labeled Trimethylamine‐N‐oxide (TMAO) in Humans
Authors: Taesuwan Siraphat , Cho Clara E , Malysheva Olga V , Bender Erica , Yan Jian , Thalacker‐Mercer Anna , Caudill Marie A 
Published: November 2023

Although trimethylamine‐N‐oxide (TMAO) is associated with chronic disease risk, little is known about the metabolic fate of orally consumed TMAO. As part of a randomized, controlled cross‐over study, healthy young men (n=40) consumed 50 mg deuterium‐labeled methyl‐d9‐TMAO (d9‐TMAO) and TMAO metabolites were measured in plasma, urine, stool and muscle. Plasma d9‐TMAO comprised ~75% of total TMAO at 2 h and remained elevated after 6 h. d9‐trimethylamine (d9‐TMA) and d6‐dimethylamine (d6‐DMA) became enriched in plasma with averages of 52% and 3% of total TMA and DMA, respectively, at 6 h. d9‐TMAO was excreted more rapidly during 0–6 h than 6–24 h, comprising 67% and 52%, respectively, of urinary TMAO. No d9‐TMAO was detected in feces. Interestingly, d9‐TMAO and d9‐TMA were detected in skeletal muscle (n=6) at 6 h, and the enrichment ratio of d9‐TMAO:d9‐TMA was influenced by a genetic variant in flavin‐containing monooxygenase (FMO3 G472A). The heterozygous GA genotype had lower muscle d9‐TMAO:d9‐TMA than the homozygous wildtype GG genotype. In conclusion, orally consumed TMAO is rapidly absorbed, is metabolized in part to TMA and DMA, and is taken up by skeletal muscle, where evidence of impaired conversion of TMA to TMAO among carriers of the FMO3 472A variant allele is observed.Support or Funding InformationEgg Nutrition Center, Beef Checkoff through the National Cattlemen's Beef Association, Canadian Institutes of Health Research Postdoctoral Fellowship.
Phenolic recovery and bioaccessibility from milled and finished whole grain oat products
Authors: Li Min , Koecher Katie , Hansen Laura , Ferruzzi Mario G 
Published: November 2023

Whole grain oats and oat products are a rich source of nutrients, fiber and dietary phenolics. While much is known regarding the benefits of oat fiber, limited information is available on the relevance of dietary phenolics from oat products. This study focused on defining the profile and stability of phenolics in native oats during common milling and processing and to determine the bioaccessibility of oat phenolics from common food preparations. Phenolic content from 26 oat cultivars as well as milled oat ingredients and ready to eat (RTE) products (puffed cereals and snack bars) were profiled. Free phenolic content ranged from 17.2~228.1 μg/g DW with avenanthramides accounting for 41~91% of free phenolics. Bound phenolic content ranged from 100.5~680.9 μg/g DW with ferulic acid accounting for 62~94 % of bound phenolics. Selected oat groats were ground to flour and prepared as wet cooked porridges (~20 % oat flour in boiling water) or introduced as RTE products to a three stage in vitro digestion to determine phenolic bioaccessibility. Relative bioaccessibility for wet cooked porridges ranged 0.3~1.6% and 3.4~37.0% for individual phenolic acids and avenanthramides, respectively. Puffed oat cereal had significantly higher bioaccessibility compared to matching wet‐cook porridge made from the same oat flour (e.g. 83.8% versus 19.1% for Ave A; P<0.05). Intestinal uptake of bioaccessible oat phenolics from digesta was confirmed by experiments with Caco‐2 human intestinal cells. Overall intestinal uptake of oat phenolics was low ranging between 0.16 % and 2.7 % across digesta from all oat products tested. In conclusion, these experiments demonstrate that phenolics naturally present in whole grain oats are well recovered through traditional grain processing, milling and food processing. Processing oat cultivars to a RTE cereal may have positive impact on digestive release and bioaccessibility of oat phenolics in the upper GI tract.Support or Funding InformationSupported by General Mills, Inc and the Purdue University Ingestive Behavior Research Center.
Through Metabolic Reprogramming Walnut May Mitigate the Stemness of Colon Cancer Stem Cells
Authors: Choi Sang Woon , Choi Jina , Kim Junil , Friso Simonetta , Kim Yuri 
Published: November 2023

The advent of the cancer stem cell (CSC) theory has accelerated our understanding of cancer. CSCs are defined as a small population of cells within a tumor that can self‐renew and drive tumorigenesis. The major reason for the failure of treatment is ascribed to the presence of CSCs in the tumor mass. Strategies that reduce CSC number or expansion represent a rational approach for colorectal cancer treatment. It is also well known that CSCs have demonstrated impaired mitochondrial functions and cancer cells exhibit altered metabolism to meet energy need, such as the Warburg effect. In our previous study, walnut phenolic extracts (WPEs) decreased the stemness of colon CSCs by suppressing their self‐renewing capacity and enhancing the differentiation ability. To investigate the mechanism behind the effect of walnuts on CSCs, using the Illumina HiSeq2500 we performed RNA‐sequencing on CSCs isolated from the HCT116 colon cancer cell line by the fluorescence‐activated cell sorting method and treated with or without 40ug/ml WPE (n=3). Among the total of 28305 transcripts, 1983 genes were found to be differentially expressed by WPE treatment (1168 genes were up‐regulated and 815 genes were down‐regulated)(fold change >1.5, p<0.05). Differentially expressed genes were categorized into functional clusters using the bioinformatic analysis tools, such as Database for annotation, visualization and integrity discovery (DAVID), Gene regulatory network (GRN) and Ingenuity pathway analysis (IPA). We found a novel phenomenon that WPE alters the expression of CSC genes associated with metabolic pathways, such as oxidative phosphorylation (NDUFSs, CYC1, COX8A, ATP5D), pentose phosphate pathway (TKT, TALDO1, ALDOA), glycolysis (GPI, PFKL, ENO1), TCA cycle (MDH2, IDHs), purine metabolism (APRT, GUK1), and pyrimidine metabolism (TK1, NME1, POLD2). The expression patterns of genes encoded for mitochondrial enzymes, such as NDUFB10, ATP5D, CYC1, and COX8A, as well as genes encoding mitochondrial ribosomal‐structure proteins, such as MRPLs, were also up‐regulated, indicating that WPE may affect the mitochondrial function. It appears that the WPE reduces the stemness of colon CSCs by restoring altered metabolic pathways and mitochondrial function.Support or Funding InformationThis work has been supported by the California Walnut Commission and the Korean Food Research Institute.
The Role of Intra‐abdominal Adipose Tissue in Cancer
Authors: Bernard Jamie , Bullard Blair 
Published: November 2023

The obesity pandemic is causing worldwide morbidity and mortality. Recent research suggests that a high‐fat diet (HFD) and/or obesity (increased adiposity) are key players in the pathogenesis and prognosis of many common cancers. However the molecular changes induced by adipose tissue (AT) that actually enhance cancer development are poorly understood. Our preliminary studies directly implicate secreted factors from parametrial (around the uterus) AT (the largest visceral fat pad in female mice) in promoting tumor formation. We demonstrated an increase in pro‐inflammatory adipocytokines in parametrial AT of mice fed a diet high in saturated animal fats (HFD). Removing the parametrial AT of these HFD‐fed mice by lipectomy surgery reduced the number of UVB‐induced skin cancers by 80% compared to sham‐operated mice. Similarly, in an obesity‐resistant mouse model of mammary tumor growth, we showed that a HFD increased parametrial adiposity and pro‐inflammatory adipocytokines in parametrial AT suggesting that diet‐induced parametrial adiposity and adipocytokine increases are not unique to diet‐induced obesity models. We hypothesize that a diet high in saturated animal fat promotes tumor formation by increasing pro‐inflammatory adipocytokines/growth factors from an enlarged parametrial fat pad. To understand the role that parametrial AT and saturated HFDs play in cancer, we developed a system where molecules released and filtered from AT (fat tissue filtrate) stimulate JB6 P+ cell proliferation and transformation. The mouse BALB/c skin epithelial JB6 P+ cell line is a well‐characterized model for neoplastic transformation that is responsive to tumor promoter‐induced transformation growth in soft agar and is uniquely suited for studying tumor promotion and promotion‐relevant molecular events in vitro. Our data demonstrate that fat tissue filtrate made from the parametrial AT of obese mice fed a HFD had 160% more transforming activity than that from mice fed a LFD and formed malignant mesenchymal tumors in vivo. These differences between parametrial AT from mice fed a saturated HFD and a LFD were associated with their density of crown‐like structures (CLS; surrogate markers for dead adipocytes) and adipocytokine secretomes. Moreover, we have found specific pro‐inflammatory adipocytokines and growth factors that are preferentially induced in the parametrial AT in both obese and obesity‐resistant mice with HFD‐feeding that stimulate the transformation of JB6 P+ cells. These studies provide an in vitro model and the basis for investigations on the mechanisms of parametrial AT‐induced cell transformation and tumor growth. Findings from these studies may lead to the discovery of new therapeutic targets for saturated HFD‐promoted cancer and will have implications for the prevention and reversal of disease.Support or Funding InformationCA177868, ES007148
Novel Role of Glutathione Peroxidase‐1 in Liver and Muscle Protein Metabolism of Mice
Authors: Tao Ling , Zhao Ze Ping , Lei Xin Gen 
Published: November 2023

Our laboratory has revealed novel roles and mechanisms of glutathione peroxidase‐1 (GPX1) in glucose and lipid metabolism, whereas little is known about its function in protein metabolism. This study was conducted to elucidate the physiological impacts of the GPX1 overexpression and knockout on gene expression and activity of key factors related to protein/amino acid synthesis, transport, and catabolism in mice. Three genotypes of Se‐adequate young adult (2‐mo old) mice: wild type (WT), GPX1 knockout (GKO), and GPX1 overexpressing (OE), were used to collect tissue samples (n = 5 to10). Although the GPX1 genotype showed no effects on total protein of liver and muscle, and plasma activities of alanine transaminase and aspartate aminotransferase, the concentrations of plasma urea nitrogen were approximately 33% lower (P < 0.05) in both GKO and OE mice than WT mice. Meanwhile, a number of protein degradation‐related genes including cathepsin K, calpain 2, ubiquitin‐like modifier activating enzyme 1, and ubiquitin protein ligase E3A were down‐regulated (P < 0.05) in the liver of OE (29%–49% of decrease) and GKO (13–38% of decrease) mice. In contrast, amino acid transporter and protein synthesis‐related genes such as solute carrier family 3 member 2, mechanistic target of rapamycin (serine/threonine kinase), ribosomal protein S6 and eukaryotic translation initiation factor 4E binding protein 1 were down‐regulated (P < 0.05) in the liver of only GKO but not OE mice. The muscle mRNA levels of genes involved in protein degradation were decreased (P < 0.05) and elevated (P < 0.05), respectively, by the overexpression and knockout of GPX1, compared with the wild‐type controls. Additionally, the muscle glutamate deamination activities of glutamate dehydrogenase (GDH), an important enzyme involved in oxidative deamination, were elevated (P < 0.05) in the GKO mice. In conclusion, both GPX1 overexpression and knockout exerted effects on the gene expressions and biochemical functions of multiple pathways of protein metabolism in the liver and muscle of mice. The net metabolic outcome and human health implication of those effects warrant future research.Support or Funding InformationSupported in part by a NIH grant DK53018
Removal of Glutathione Peroxidase 4 in Mouse Liver Leads to Early Lethality and Vitamin E Can Compensate for Its Loss
Authors: Carlson Bradley A. , Tobe Ryuta , Yefremova Elena , Tsuji Petra A. , Hoffmann Victoria J. , Schweizer Ulrich , Gladyshev Vadim N. , Hatfield Dolph L. , Conrad Marcus 
Published: November 2023

Glutathione peroxidase 4 (GPx4) is one of several glutathione peroxidases found in mammals and its targeted deletion is early embryonic lethal. The primary functions of GPx4 are to protect cells against membrane lipid peroxidation and to govern a novel form of non‐apoptotic cell death, called ferroptosis, which appears to be relevant in a select set of organs. To study the role of GPx4 in liver tissue, a conditional knockout of Gpx4 in hepatocytes was used, along with thioredoxin reductase 1 (TrxR1) and selenocysteine (Sec) tRNA (Trsp) hepatocyte knockout mice as controls. In contrast to TrxR1‐ and Trsp‐deficient mice, Gpx4 knockout mice died within 48 hours after birth and presented extensive hepatocyte degeneration. We further found that Gpx4 knockout pups born from mothers fed a vitamin E‐enriched diet did not experience early death, demonstrating that vitamin E rescued Gpx4 knockout‐induced cell death. When vitamin E was subsequently removed from the diet, Gpx4‐deficient mice had an average survival time of approximately four weeks. We also crossed Trsp‐deficient and Gpx4‐deficient mice and were unable to obtain combined Trsp/Gpx4‐deficient mice at birth, indicating that the combined deficiency resulted in embryonic death. Combined Trsp/TrxR1‐deficient mice were born but had significantly shorter lifespans than either single knockout, suggesting that TrxR1 plays an important role in longevity of mice lacking Trsp in hepatocytes. This study demonstrates that GPx4 is critical for hepatocyte survival and proper liver function, and that vitamin E can compensate for its loss by protecting cells against lipid peroxidation.Support or Funding InformationThis work was supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research.
A comprehensive nutrition program improved nutritional status among children aged 6 to <24 months in rural Malawi
Authors: Kang Yunhee , Hurley Kristen , Monclus Assumpta Bou , Ruel‐Bergeron Julie , Oemcke Rachel , Wu Lee Shu Fune , Mitra Maithilee , Phuka John , Christian Parul 
Published: November 2023

To evaluate the one‐year impact of a comprehensive nutrition program—provision of daily Lipid‐based Nutrient Supplement (LNS) and a comprehensive infant and young child feeding (IYCF) and water and sanitation, and hygiene (WASH) behavior change communications (BCC) package—on the nutritional status of children in Malawi. The study design was quasi‐experimental with one program district and one comparison district. The program impact was evaluated using cross‐sectional baseline (January–March, 2014; n=2,404) and midline (January–March, 2015; n=2,378) survey data for children aged 6 to <24 months, who were measured for their length, weight, mid‐upper arm circumference (MUAC), and head circumference (HC) at each survey. Estimates of impact over one year were generated using Kernel Propensity Score Matching Difference‐in‐Differences (PSM‐DID) analyses using both baseline and midline data in the program and comparison districts. The burden of undernutrition was high at both baseline and midline with approximately half of children stunted (length‐for‐age z score, LAZ<‐2) in both districts. There was no significant difference in LAZ or in the prevalence of stunting between two districts using the PSM‐DID analysis. However, the changes in nutritional status between midline and baseline in child weight, MUAC, weight‐for‐age z score (WAZ), and weight‐for‐length z score (WLZ) favored the program district over the comparison district by 0.22kg, 0.29cm, 0.23 z‐score and 0.30 z‐score, respectively (all P<0.05). In the same way, the prevalence of children wasted, underweight, severely wasted, or experiencing moderate acute malnutrition (MAM, ‐3<WLZ<‐2) reduced by 3.9%, 6.4%, 1.1%, and 2.8%, respectively (all P<0.05). However, prevalence of overweight/obese was not increased significantly (1.3%; P=0.39). No significant differences were seen in HC. The impact evaluation showed that the LNS and IYCFWASH‐ BCC program was successful in reducing wasting, MAM, and underweight after only a year of implementation. Subsequent analysis will be key to evaluate the impact of sustained exposure (for 3.5 years) to the program on linear growth and the prevalence of stunting in Malawi.Support or Funding InformationThis study was funded by Children's Investment Fund Foundation, UK