bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of Eggs on Dietary Nutrient Adequacy and Cardiovascular Risk in U.S. Adults
Authors: Melough Melissa Moser , Chung Sang‐Jin , Fernandez Maria Luz , Chun Ock K 
Published: November 2023

It is well known that eggs are rich sources of micronutrients including choline, selenium, vitamin B12, and carotenoids. It has not been well assessed, however, how egg consumption contributes to overall nutrient adequacy in the American diet, and how consumption of eggs may affect cardiovascular disease (CVD) risk factors. Therefore, the aim of this study was to determine how egg consumption contributes to nutrient intake and affects blood biomarkers of CVD risk in U. S. adults ≥ 19 years (n=4,297) using a nationally representative sample from the National Health and Nutrition Examination Survey (NHANES) 2011–2012.Consumers and non‐consumers of whole egg products were identified from two days of 24‐hour dietary recalls in the NHANES data, and egg consumers were separated into tertiles of intake level. Approximately 63% were classified as egg consumers with mean intake of 52 g/d. In an adjusted model, men were more likely than women to be high consumers of eggs. Those aged 40–59 years were more likely to be egg consumers than those in other age groups. Differences in egg consumption patterns also existed among ethnicities, with African Americans consuming eggs more frequently than any other group. Egg consumption was associated with greater intakes of protein, saturated fat, mono‐ and poly‐unsaturated fats, magnesium, calcium, selenium, riboflavin, and choline. The odds of meeting the RDA for choline in the highest tertile of egg consumption were 14.8 times that of the non‐consumers. Similarly, the odds of achieving the recommended intakes for riboflavin, vitamin A, and vitamin K were 2.0, 1.8, and 1.4 times that of non‐consumers, respectively.Egg intake was positively associated with dietary cholesterol, but not with serum total cholesterol (TC) when adjusted for energy intake, age, gender, ethnicity, BMI category, and multiple lifestyle factors. Triglyceride/HDL‐cholesterol ratio was significantly decreased with egg consumption. Egg consumption did not significantly alter triglycerides, apoliporotein B, LDL‐cholesterol, TC/HDL‐cholesterol ratio, LDL‐cholesterol/HDL‐cholesterol ratio, fasting glucose, or insulin.Eggs are important dietary contributors of many essential nutrients, including mono‐ and poly‐unsaturated fats, choline, and several vitamins and minerals. Egg consumption improves triglyceride/HDL‐cholesterol ratio and does not alter other important CVD risk biomarkers including TC, LDL‐cholesterol, and triglycerides.Support or Funding InformationThis study was supported by the Allen Foundation Research Grant (PI: Ock K. Chun).
Effects of Dietary Inflammatory Index and History of Gestational Diabetes Mellitus on Insulin Resistance
Authors: Shin Dayeon , Lee Kyung Won , Tande Desiree L. , Hur Junguk , Shivappa Nitin , Wirth Michael D. , Hébert James R. 
Published: November 2023

ObjectiveThe combined impact of previously diagnosed gestational diabetes mellitus (GDM) and dietary sources of inflammation on insulin resistance have yet to be fully examined. The objective of this study was to explore the effect modification of history of GDM on the association between the Dietary Inflammatory Index (DII)TM and beta‐cell function and insulin resistance, using homeostatic model assessment for insulin resistance (HOMA‐IR).Research Design and MethodsData from the National Health and Nutrition Examination Survey for 2007 through 2012 were used. A total of 2,674 women (mean age=52 y) including patients with type 2 diabetes who completed one‐day 24‐hour dietary recall with information on history of GDM and HOMA‐IR were included. The DII was calculated to examine inflammatory potential of diet. Insulin resistance was estimated using the HOMA‐IR. Multivariable logistic regressions models were examined to estimate the association between history of GDM, current DII scores and insulin resistance after adjusting for age, body mass index, race/ethnicity, education, family poverty income ratio, and marital status.ResultsA history of GDM was reported by 7% (n=176) of women. The difference in HOMA‐IR levels (mean ± standard error) between women with a history of GDM and women without a history of GDM was of borderline significance (4.3 ± 0.4 vs. 3.5 ± 0.1, P=0.06). Among the women without a history of GDM, women who were in the highest (most pro‐inflammatory) tertile of DII scores had increased risk for insulin resistance compared to the lowest (most anti‐inflammatory) tertile of the DII (adjusted odds ratios=1.56; 95% CI=1.07–2.27). However, no such association was observed among the women with a previous GDM diagnosis.ConclusionsWithin a nationally representative sample, the DII was associated with insulin resistance only in women without a history of GDM. Reducing inflammatory properties of diet may be a strategy for reducing the risk of insulin resistance and eventually type 2 diabetes mellitus among women without a history of GDM.
Lithocholic Acid Induces Apoptosis Of Breast Cancer Cells MCF‐7 And Inhibits Lipogenesis
Authors: Bard Jean‐Marie , Luu Trang Huyen , Carbonnelle Delphine , Chailloux Chloé , Huvelin Jean‐Michel , Bobin‐Dubigeon Christine , Nazih Hassan 
Published: November 2023

ObjectivesBile acids are products of cholesterol metabolism and their principal function is the solubilization of fats and liposoluble vitamins in the intestine.After their secretion into the intestine, primary bile acids are converted into secondary bile acids by intestinal bacteria. Two major secondary bile acids lithocholic acid (LCA) and deoxycholic acid (DCA) are produced from cholic acid and chenodeoxycholic acid, respectively.It has been reported that bile acids, particularly LCA have anti‐carcinogenic properties in several cancer cell models such as colon cancer, neuroblastoma cells, and prostate cancer.On the other hand, it is now recognized that the levels of the FASN enzyme (Fatty Acid Synthase) and lipogenesis are increased in the cancer cells.The aim of our study was to assess the effect of LCA on MCF‐7 breast cancer cells proliferation and apoptosis and to evaluate its influence on lipogenic enzymes and transcription factors related to lipogenesis.Material and MethodsAnti‐proliferative properties of LCA were studied using the cell viability MTT assay and analysis of phospho‐Akt protein by FACS method. Apoptosis of MCF‐7 cells was examined by flow cytometer using Annexin‐FITC. QPCR and western blotting were used to study the expressions of genes and proteins involved in apoptosis (P53, Bcl‐2 and Bax) and in lipogenesis (LXR, SREBP‐1, FASN, ACC (Acetyl‐CoA Carboxylase) and SCD‐1 (Stearoyl‐coenzyme A desaturase‐1). Staining lipids by Oil Red O was used to study the lipid storage.ResultsLCA decreased the cell viability of MCF‐7 cells in a dose (25 to 200 microM)‐ and time (24 and 48h)‐ dependent manner. LCA also reduced Akt phosphorylation in a dose dependent manner (50% reduction at 100 microM, 24h).We also observed a decrease in the anti‐apoptotic protein Bcl‐2 and an increase in pro‐apoptotic protein p53, compared to untreated cells.Analyses by qPCR and Western blotting showed that LCA decreased at least by half the expression of LXR, SREBP‐1, FASN and ACC compared to untreated cells by LCA. Staining lipids by Oil Red O showed that MCF‐7 control cells contained abundant lipid droplets in comparison to LCA‐treated cells.ConclusionThese data show that LCA has anti‐proliferative and pro‐apoptotic properties in MCF‐7 cells. Our study also suggests the potential capacity of LCA to induce apoptosis cancer cells by inhibiting the storage of lipids.Support or Funding InformationSupported by Ligue contre le Cancer
Inhibitory Effects of DHA and its peroxidation product 4‐HHE on proliferation of breast cancer cells.
Authors: Chen Ging , Tang Feng Yao 
Published: November 2023

BackgroundFish oil and its constituent, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have learned to inhibit inflammation and have chemopreventive effects on many kinds of cancer. Epidemiological studies suggest that consumption of fish oil is correlated with reduced risk of breast cancer. In this study we examined effects of DHA and its peroxidation product 4‐hydroxyhexenal (4‐HHE) on breast cancer cells. Lipid peroxidation products may regulate tumourigenesis process and we aimed to compare DHA and 4‐HHE effects on breast cancer cells and investigate if DHA's anticancer effect is due to 4‐HHE.Materials/MethodsBreast cancer cells (MDAMB‐231 and MDAMB‐468) were treated with DHA and 4‐HHE (at concentrations of 0, 1, 5, 10, 25 and 50 μM) for 24 and 48 hours by MTT, cell cycle and western blotting assay. For detection of cell signaling pathway, cancer cells were treated with DHA and 4‐HHE for 1 hour with the concentrations mentioned above.ResultsTreatment of DHA and 4‐HHE decreased cell viability in breast cancer cells in dose and time dependent manners. Both DHA and 4‐HHE treatments induced S phase arrest in MDAMB‐231 breast cancer cells at 24‐hour time point and G2/M phase arrest at 48‐hour time point. G2/M phase arrest was seen in MDAMB‐468 breast cancer cells at 48‐hour time point. Cell cycle regulatory protein expression were also modulated in breast cancer cells. P‐STAT3 protein expression was reduced with DHA and 4‐HHE treatments does dependently in breast cancer cells.ConclusionDHA and 4‐HHE inhibited cell cycle progression and cell viability through suppression of p‐STAT3 pathway in human breast cancer cells. 4‐HHE seemed to be a more effective agent on the inhibition of cell survival in breast cancer cells, especially in MDAMB‐231 cells.Support or Funding InformationDepartment of Nutrition, China Medical University, Taichung, Tiawan.
Quercetin reverses sorafenib‐resistant SK‐Hep‐1 cells to sorafenib by up‐regulation of p53 pathway
Authors: Huang Chin‐Shiu , Huang Shih‐Chien , Jhan Fu‐Wei 
Published: November 2023

Multidrug resistance (MDR) in the human cancer is a major obstacle in sorafenib (SF) therapy. Although the main molecular mechanisms underlying the resistance to SF are largely unknown, it is becoming clear that activation of p53 pathway is one of the strategies for the inhibition of drug resistance. In this study, we invastigated the anti‐cancer effects and anti‐drug resistance of SF in combination with quercetin in human heptocarcinoma SK‐Hep‐1 cells (wild‐type p53). We showed that long‐term treatment of SF (0–10 μM) reduced anti‐proliferative effects of SF and up‐regulated the MDR protein expression, caused drug resistance. Combination with quercetin (30 μM) for 24 h enhanced the SF sensitivity of SF‐resistant SK‐Hep1 (SK‐Hep‐1/SF) cells. Expression of SF‐induced MDR was also down‐regulated after quercetin treatment in SK‐Hep‐1/SF cells. However, p53 protein expression was down‐regulated by SF treatment, whereas it was increased by quercetin treatment. Pifithrin‐α, a p53 inhibitor, was appreciably abolished the inhibition effect of guercetin on SF‐induced MDR. Taken together, these results suggest that quercetin could be used to reduce SF‐induced drug resistance in human hepatoma cells through the regulation of p53 pathway.Support or Funding InformationThis study was supported by a grant (MOST‐103‐2320‐B‐468‐004‐MY3) from the Ministry of Education, Republic of China (Taiwan).
Apoptotic Proteins Expression in Experimental Colon Cancer Model
Authors: Padmanabhan Smitha , Taranikanti Varna , Waly Mostafa 
Published: November 2023

BackgroundColon and rectum cancers are the third commonly diagnosed cancers worldwide. Modifiable risk factors associated with these cancers are B‐vitamins (folate and B12) deficiencies, oxidative stress, and Hyperhomocysteinemia. It is relatively unknown how B viatmins affect oxidative stress and hyperhomocysteinemia‐mediated carcinogenesis in colon tissue.ObjectiveTo study the expression of antiapoptotic and proapoptotic proteins (Bcl2, Bax) on azoxymethane induced colon cancer using B vitamins and also to see any ultrastructural changes using Electron Microscopy.MethodsAzoxymethane (AOM)‐induced colon cancer model was used in Sprague‐Dawley male rats were randomly divided into groups. The control group fed a basal diet with no AOM injection; the AOM‐treated group fed a basal diet with AOM intraperitoneal injections, whereas the other experimental groups received daily doses of folate or vitamin B12 supplementation in the presence or absence of AOM injection. Another 6 groups of rats were tested for the potential synergistic effects of both folate and vitamin B12 supplementation. All animals continuously fed ad‐libitum until 16 weeks, then all rats were sacrificed and the colon tissues were examined for the immunohistochemical and ultrastructural changes. Briefly, 2–3mm of colon tissue sections were stored in glutaraldehyde and from these semithin and ultrathin sections were cut and viewed to delineate the cellular organelles architecture in a transmission electron microscope (TEM). Paraffin blocks were cut and the expression of Bcl2 and Bax was observed under a light microscope using Immunohistochemistry(IHC) technique. Rabbit polyclonal and mouse monoclonal antibodies were procured from ABCAM and Dako respectively.ResultsThere was over expression of Bcl2 and Bax proteins in colon cancer tissues treated with B vitamins however their expression was dose dependent. There were also ultra structural changes in the cell organelles with dilation of endoplasmic reticulum and increase in the number of mitochondria. This is consistent with our earlier finding that early exposure to AOM causes morphological changes in the coloni mucosa of the assayed groups.ConclusionVitamin B12 and folate play a protective role against oxidative stress at both the cellular and protein levels and might ameliorate the metabolic stress on colon cells caused by cancer.Support or Funding InformationAcknowledging Sultan Qaboos University Scholarship for my PhD Studies.
Obesity deteriorates DMBA‐induced tumorigenesis in vitro and in vivo
Authors: Hsieh Chia‐Chien , Peng Shih‐Han , Chou Mei‐Jia 
Published: November 2023

Obesity and overweight are associated to several chronic diseases. Growing body of evidence showed extra adiposity influences multiple cancers progression, such as breast cancer. During the adiposity, macrophages infiltrate into the adipose tissue and accompany inflammatory mediators secretion fertilized a microenvironment that is favorable for neoplastic cells. The aim of this study is to investigate whether obesity correlate to mammary tumor development in vitro and in vivo. In vitro study, the obese‐related mediators, such as leptin and 3T3‐L1 adipocyte conditioned medium, enhanced cancerous foci formation inducted by environmental chemical carcinogen, 7,12‐Dimethylbenz [a] anthracene (DMBA) in fibroblast NIH/3T3 cells. In vivo study, C57BL/6J female mice fed low fat (LF), and high fat (HF) experimental diets, and some of them were oral gavage DMBA to induce breast cancer, as LF+DMBA (LFD), and HF+DMBA (HFD). The results indicated that breast cancer incidence was about 20% in HFD group with 169 mg tumor weight and 14% in LFD group with 77 mg tumor weight, and HFD mice have significantly lower body weight compared to the HF mice. The section of mammary tumor from HFD mice accompanied stromal invasion, morphological aggressiveness and multiple cells infiltration, and showed apparently proliferative marker Ki67, endothelial marker CD31 and macrophage marker F4/80 expressions compared to that in LFD group. The section of epididymal adipose tissue from the DMBA groups showed more macrophage infiltration and these cells polarized to M1 with higher CD11c expression compared to the mice fed the same diet. In addition, the adipose sections from HF groups have lower M2 macrophages accumulation. In summary, obese mediators enhanced cancerous foci formation by DMBA challenge in vitro, and high fat diet caused neoplastic aggravation in mammary tumor, particularly, decreased suppressive M2 macrophages infiltration into adipose tissues in vivo.Support or Funding InformationMinistry of Science and Technology, Taiwan (MOST 103‐2320‐B‐003‐003‐MY3).
Integrating Multi‐Omic Data from Proteome, Phospholipidome, and Oxylipid Profiles Explains a Sizable Proportion of Variance Associated with the Presence of Colon Polyps
Authors: Pickens Charles Austin , Vazquez Ana I. , Sordillo Lorraine M. , Jones A. Daniel , Fenton Jenifer I. 
Published: November 2023

Changes in the proteome and lipidome are associated with increased inflammation, inflammation‐induced colon carcinomas, and colon tumor survival. Our lab has previously reported levels of specific serum proteins and plasma fatty acids are associated with colon polyps. The objective of this study was to determine associations with colon polyps and the proportion of variance explained by integrating entire proteomic and lipidomic profiles. A total of 122 Caucasian males (48–65 years) were categorized by colon polyp type, either: no polyps, 1 or more hyperplastic polyps, or 1 or more adenomas. ELISA was used to quantify 70 serum proteins. The plasma phospholipidome (>2000 lipids) was profiled using UPLC‐untargeted high‐resolution mass spectrometry. Plasma non‐esterified fatty acids and >60 oxylipids were fractionated using solid phase extraction and quantified using HPLC‐MS/MS. All ‐omic data sets were centered and scaled in the same manner. Bayesian generalized additive models were used to integrate the high‐dimensional multi‐omic profiles. Single marker regressions were employed to assess each lipid with polyp type. All models were adjusted for age and smoking, and p‐values were adjusted for false discovery. The serum proteome explained approximately 14% of the variation in polyp type. Of the >2000 lipids in the plasma phospholipidome, none were individually associated with polyp type after false discovery correction. However, the entire plasma phospholipidome accounted for over 20% of the variation in polyp type, which indicates a general change of the lipid profile in different polyp types, rather than a specific change in levels of a specific lipid. In plasma oxylipid single marker regressions, arachidonic acid‐derived oxylipids were significantly elevated in those with polyps. Entire oxylipid profiles only accounted for a marginal (< 9%) amount of variation associated with polyps. When integrating the multi‐omic profiles, there was similar variation explained by the plasma phospholipidome whether adding the serum proteome or plasma oxylipids to the model. Integrating the three ‐omic data sets revealed a decreased amount of variation that each ‐omic profile could explain for polyp type, compared to integrating only 2 of ‐omic data sets. This suggests that changes in biological markers across ‐omics may be correlated. In conclusion, the entire plasma phospholipidome accounted for the largest proportion of variation associated with polyp type, compared to our serum protein and plasma oxylipid profiles. Future studies should investigate the predictive ability of the phospholipidome in larger more diverse populations, and determine if integrating the lipidome with other ‐omic data (i.e., genome, methylome, or gene expression) improves the variation explained with polyp type.Support or Funding InformationUSDA NIFA 201‐67011‐25205
Sex and Race/Ethnic Disparities in Food Security and Chronic Diseases in U.S. Older Adults
Authors: Huffman Fatma G. , Vaccaro Joan A. , Zarini Gustavo G. 
Published: November 2023

BackgroundFood insecurity is rising in older adults in the United States (U.S.) and disproportionately among Blacks and Hispanics. Food quality is diminished for persons with food insecurity and this may compromise health and be associated with chronic disease, particularly in vulnerable populations such as older adults.ObjectiveTo determine the relationships among sex, race/ethnicity and food security with the likelihood of cancer, diabetes, cardiovascular disease and lung disease for a U.S. representative sample of older adults.MethodsThis study extracted data and appended 2 cycles from the National Health and Nutrition Examination Survey, 2011–2012 and 2013–2014 that are available for public use. The sample for this study consisted of N = 3871, adults ages ≥ 55 years from five racial/ethnic groups with measures for waist circumference from the Mobile Examination Center (MEC). Specifically, the racial/ethnic categories had 373 Mexican Americans (MA), 398 Other Hispanics (OH), 958 non‐Hispanic Blacks (NHB), 423 non‐Hispanic Asians (NHA), and 1719 non‐Hispanic Whites (NHW). Cross‐tabulations for percent, 95% CI were performed for food security level by race/ethnicity using SPSS version 23 with the complex sample module, applying the MEC sample weight.ResultsFood security differed by race/ethnicity (p<.001) with approximately 25% of MA and OH having low‐food security as compared to 17% NHB, 7% NHA, and 6% NHW. Low‐food security was associated with lower self‐rated health, less education, and fewer persons with health insurance. Persons with food security had the highest percent of cancer, 22.1 (20.0, 24.3) as compared to those with the lowest food security, 10.4 (7.2, 14.7). A higher percent of persons with low‐food security, 25.2 (20.0, 30.9) had diabetes as compared to those who were food‐secure, 16.8 (15.0, 18.6). Compared to adults who were food‐secure, adults with lower food security was associated with a higher percent of cardiovascular disease [23.7 (18.9, 29.2) vs. 14.6 (13.1, 16.3)], lung disease, [28.9 (23.3, 35.3) vs. 19.2 (16.6, 22.2)], high blood pressure [67.2 (61.7, 72.3) vs 54.0 (51.0, 57.1)] and several obesity indicators.ConclusionThe results of this study have numerous implications for gerontologists since food insecurity was high in older adults and particularly Hispanics. In conclusion, the results of this study have demonstrated the exacerbation of chronic diseases with low‐food insecurity.