bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of circannual variation in relative weight among children in Wisconsin using electronic health records
Authors: Bhutani Surabhi , Schoeller Dale , Kloke John , Hanrahan Lawrence 
Published: November 2023

ObjectiveSummer weight gain (June through August inclusive) has been repeatedly reported in children. This has recently led to the development and implementation of multiple interventions to address the child's summer environment. Most reports on summer weight gain are mainly based on measures of BMI at the beginning (Sept./Oct.) and end of the school season (May/June), and are the only time points used to demonstrate the success of school based obesity prevention interventions. Basing the relative weight outcome on just two measures may be risky and therefore data on the time course of this weight gain in children is necessary. Thus, the objective of this study was to investigate circannual pattern in childhood weight status.MethodWe analyzed cross‐sectional height and weight data from de‐identified electronic medical records of 225,607 children (5–17yr) collected between 2007–2012 from South Central Wisconsin. The average monthly BMI and BMI z‐score were calculated and categorized by age, sex, and minority status.ResultsAveraged across ages, the BMI z‐scores increased during the school year (Sept. – May) by 0.03±0.4 z‐score (P<0.05), but decreased from May to June by 0.08±0.4 z‐score (p<0.01) and then increased from Aug. to Sept. by 0.06±0.4 units (p<0.01). The BMI z‐scores for males were slightly higher than for females and both displayed similar and distinctive differences between May and June and averages being greater beginning in July or Aug. When categorized by race/ethnicity, the BMI z‐scores during July were lowest than those of Sept‐May for Non‐Hispanic White population. Non‐Hispanic Blacks had the lowest BMI z‐score at the beginning of the school year (Sept.) while Hispanics had the lowest BMI z‐score at the end of summer (Aug.).ConclusionOur analysis is consistent with summer weight gain findings from other studies showing a slightly lower BMI z‐score during the school year (Sept. to beginning of June) and higher BMI z‐score during the summer (beginning of Jun to Sept). This pattern would probably be interpreted as a successful intervention by the school followed by regression during the summer, even if there is no effect of the intervention per se. But this also raises issues about adequacy of 2 measures of z‐scores for school evaluations due to lower BMI z‐scores in summer period. We suggest taking additional measures at least in Dec. and March so that a time trend analysis can be performed. An alternate approach might be to move the assessment months to Oct and April. Moreover, a longitudinal study is required to confirm the circannual pattern we observed using cross‐sectional data.
Television food advertisement exposure and FTO genotype in relation to excess consumption in children
Authors: Gilbert‐Diamond Diane , Emond Jennifer , Lansigan Reina Kato , Rapuano Kristina , Kelley William , Heatherton Todd , Sargent James 
Published: November 2023

IMPORTANCEExposure to food advertisements may cue overeating among children, especially those genetically predisposed to eat more in response to food cues.OBJECTIVETo assess how television food advertisements affect eating in the absence of hunger among children in a randomized trial. We hypothesized that the effect of food advertisements would be modified by the Fat Mass and Obesity Associated Gene (FTO) rs9939609 single nucleotide polymorphism.DESIGN, SETTING, AND PARTICIPANTSIn this randomized experiment, 172 children aged 9–10 years old were served a standardized lunch to self‐reported satiety and then shown a children's television show embedded with either food or toy advertisements. Children were provided one food that was advertised during the show (gummy candy) and three that were not advertised (chocolate candy, cookies, chips) to consume ad libitum while watching the show. Children were genotyped for rs9939609. Additional characteristics of the child were collected via questionnaires.EXPOSURESAssignment to view either food or toy advertisements (7.7 minutes) embedded in a child's television show (34 minutes).MAIN OUTCOME MEASURESTotal caloric intake during the experimental exposure (overall and by advertised vs. non‐advertised foods). Analyses assessed the outcome overall and stratified by FTO genotype.RESULTSChildren consumed on average 440 (SD=185) kCals during lunch and 482 (SD=274) kCals during the experimental exposure. There was no main effect of experimental exposure on total snack food consumed while viewing the television show (P = 0.27); however, children who viewed food advertisements consumed an average of 48 kCals (95% CI: 10, 85; P=0.01) more of a recently advertised food than those who viewed toy advertisements. Further, there was a statistically significant interaction between genotype and food advertisement condition (P=0.02), where the difference in consumption of the recently advertised food related to food vs. toy advertisement exposure increased linearly with each additional FTO risk‐allele: −3, 59, and 125 kCals for the TT, AT, and AA genotypes, respectively.CONCLUSIONS AND RELEVANCEFood advertisement exposure was associated with greater caloric consumption of a recently advertised food, and this effect was modified by FTO genotype. Future research is needed to understand the neurological mechanism underlying these associations.Support or Funding InformationThis study was supported by grant R21HD076097 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NIH) (Dr. Gilbert‐Diamond); by grant R01DA022582 from the National Institute of Drug Addiction (NIH) (Heatherton); by grant R01CA077026 from the National Cancer Institute (NIH) (Sargent); by grant R01AA021347 from the National Institute of Alcohol Abuse and Alcoholism (NIH) (Sargent).
Systematic review of anthocyanins and markers of cardiovascular disease
Authors: Wallace Taylor C , Slavin Margaret , Frankenfeld Cara L 
Published: November 2023

Anthocyanins are dietary flavonoids commonly consumed in the diet. Evidence from epidemiological studies suggests cardiovascular disease (CVD) preventative and therapeutic effects of anthocyanins. We systematically reviewed randomized controlled trials (RCT) testing the effects of purified anthocyanins and anthocyanin‐rich extracts on the following markers of CVD: triglycerides, total cholesterol, LDL cholesterol, HDL cholesterol, and blood pressure in both healthy and diseased populations. Eligible studies included RCT of the adult population published in English. We searched PubMed, Web of Science Core Collection, and BIOSIS Previews for relevant articles from inception until July 1, 2014. Twelve RCT representing 10 studies were included in the review. Trials ranged in size (31–152 individuals enrolled), duration (3–24 wk), and anthocyanin dose (7–640 mg/d). Supplementation with anthocyanins did not affect CVD biomarkers among healthy individuals. Triglycerides, total cholesterol, HDL cholesterol, and blood pressure were not changed among diseased individuals after anthocyanin treatment. Anthocyanin treatment did consistently decrease LDL cholesterol in diseased individuals and/or those with elevated biomarkers of CVD. No adverse effects were reported across studies at levels up to 640 mg/d. Major limitations of trials included in the qualitative analyses include short trial durations and large variability in the dose administered within the trials, among others. LDL cholesterol is an established biomarker of CVD risk, and these trials suggest that anthocyanin supplementation may decrease LDL cholesterol among individuals with elevated biomarkers, with little to no safety concerns. Longer‐duration trials assessing dose response are needed to adequately determine whether an effect of supplementation exists.Support or Funding InformationNo funding was accepted for this abstract and manuscript.
Effect of 3 Probiotic Strains on Bile Acids and Glucose Metabolism in Healthy Adults: a Randomized, Double‐Blind Placebo‐Controlled Crossover Study
Authors: Culpepper Tyler , Rowe Cassie C , Nieves Carmelo , Girard Stéphanie‐Anne , Christman Mary , Chung Soonkyu , Thompkins Thomas A , Langkamp‐Henken Bobbi 
Published: November 2023

BackgroundProbiotics have been shown to transiently modify the intestinal microbiota by favoring the growth of endogenous bacteria possessing bile salt hydrolase (BSH) activity. The BSH activity promotes deconjugation and excretion of bile acids and shifts metabolism from cholesterol synthesis to bile formation, thereby attenuating systemic cholesterol levels and decreasing risk of cardiovascular diseases.ObjectiveThe aim of this study was to determine the effect of 3 different probiotic strains on bile acid and glucose metabolism.MethodsIn a randomized, double‐blind crossover study, healthy middle‐aged adults (52.6 ± 7.7 years old) with a larger waist circumference (>102 cm and >88 cm for males and females, respectively) received 1 capsule/day of Bacillus subtilis R0179 (2.5 × 109 CFU/capsule) (n=39), Lactobacillus plantarum HA 119 (5 × 109 CFU/capsule) (n=38), Bifidobacterium animalis subsp. lactis B94 (5 × 109 CFU/capsule) (n=37) or placebo for 6 wks. Following a 4‐wk washout period, participants were crossed to the other treatment (i.e. probiotic to placebo or placebo to probiotic). Stool frequency and consistency were recorded on a daily basis. Blood and stool samples were collected at the beginning and end of each intervention to measure bile acids. Serum lipids and markers of glucose metabolism were measured in the blood. Weekly measures included gastrointestinal symptoms (Gastrointestinal Symptom Rating Scale (GSRS)) and physical activity levels (Internal Physical Activity Questionnaire (IPAQ)).ResultsThe change in deconjugated plasma bile acids was greater with consumption of B. subtilis R0179 (691±378nmol/L, p=0.01) and B. animalis subsp. lactis B94 (380±165nmol/L, p=0.04) than with combined placebo data (98±176nmol/L). This change was only observed in obese participants (Body Mass Index ≥ 30). Additionally, there was a trend towards an increase in HDL plasma levels during the L. plantarum HA 119 intervention (3.0±1.3mg/dL, p=0.0774) versus the placebo (−0.3±0.8mg/dL). No significant differences were observed for any probiotics for stool bile acids, other serum lipids, gastrointestinal symptoms and function, blood glucose and insulin, and physical activity levels.ConclusionsThese data suggest that B. subtilis R0179 and B. animalis subsp. lactis B94 had no effect on glucose metabolism or serum cholesterol but significantly increased deconjugated plasma bile acids. It is possible that de novo bile acid synthesis was inhibited by these probiotics through the Farnesoid X Receptor (FXR) in the ileum. Additional clinical studies should be conducted to confirm these findings and explore the mechanism by which probiotics may simultaneously modulate cholesterol absorption and catabolism to bile acid.Support or Funding InformationLallemand Health Solutions
Plasma Trans Palmitoleic Acid and Cardiometabolic Risk factors in Youth with Type 1 Diabetes: SEARCH Nutrition Ancillary Study
Authors: The Natalie S. , King Irena B. , Crandell Jamie L. , Couch Sarah , Tzeel Benjamin , Liese Angela D. , Dabelea Dana , Mayer‐Davis Elizabeth 
Published: November 2023

The identification of modifiable risk factors associated with cardiometabolic traits is critical for improving health outcomes in persons with type 1 diabetes (T1D). The adverse effects of trans fatty acids from industrial hydrogenation of oils on health outcomes are well‐documented, but less is known about the health effects of trans fatty acids produced from biohydrogenation by bacteria in ruminant gut, such as trans palmitoleic acid (TPA; 16:1n‐7t). We examined the association between plasma TPA and cardiometabolic outcomes using data from the SEARCH for Diabetes in Youth Study, an ongoing multi‐center observational cohort study of youth with diabetes diagnosed at < 20 years of age. Participants included those with physician‐diagnosed T1D and positive diabetes autoantibody (glutamic acid decarboxylase‐65 or insulinoma‐associated‐2 autoantibodies) at enrollment (n=826; diabetes duration mean=10.0 mo). Cross‐sectional, linear regression models adjusted for confounders (gender, age, diabetes duration, human leukocyte antigen risk, insulin regimen, insulin dose, race and ethnicity, study site, and maximum parental education) identified a positive association of plasma TPA with low‐density lipoprotein cholesterol (β=2.1; p=0.02), total cholesterol (β=3.1; p=0.003), and diastolic blood pressure (β=0.9; p=0.003), as well as a positive association with high‐density lipoprotein (HDL) cholesterol (β=0.8; p=0.002). No association was observed between TPA with HbA1C, insulin sensitivity, triglycerides, body mass index z‐score, systolic blood pressure, and waist circumference. An adjusted repeated measures model using a smaller sample of participants who had data at baseline and at a follow‐up visit (either 12‐ or 24‐months after baseline visit; n=379) yielded identical results. Findings suggest a differential and complex relationship of TPA on various cardiometabolic traits in youth with T1D. Additional research is needed to determine long‐term effects of plasma TPA on cardiometabolic health in youth with T1D and identify the mechanisms by which TPA may impact these traits.Support or Funding Information2R01DK077949‐05
High‐Fat Diet‐Induced Obesity Suppresses Adaptive Thermogenesis via Toll‐Like Receptor (TLR) 4‐Mediated Endoplasmic Reticulum Stress
Authors: Okla Meshail , Wang Wei , Chung Soonkyu 
Published: November 2023

Adaptive thermogenesis is a cellular process that dissipates energy as heat, thus defending against obesity, in response to various activators such as cold. Obese subjects are less responsive to thermogenic signaling cues compared to lean subjects. Elevated levels of metabolic endotoxemia and circulating free fatty acids associated with obesity induce innate immune system and TLR4 activation, leading to the development of metabolic disorders. However, whether TLR4 activation plays a role in the adaptive thermogenesis impairment observed in obesity has not been investigated. In this study, we hypothesized that TLR4 activation in a high‐fat (HF) diet‐induced obesity model impairs adaptive thermogenesis. To test this hypothesis, C57BL/6 mice were fed either a low‐fat (LF) or HF diet for 12 weeks, followed by cold acclimation. HF diet‐mediated TLR4 activation concurred with a significant decrease in adaptive thermogenesis, brown‐specific markers, and mitochondrial‐specific markers in subcutaneous white adipose tissue (WAT). To verify the role of TLR4 in WAT browning, chronic low‐dose LPS was administrated to wild type and TLR4 knockout mice. LPS‐injected wild type mice were immune to both cold‐induced WAT browning and β3‐adrenergic receptor agonist (CL‐316,243)‐induced WAT browning, whereas TLR4 knockout mice were able to arouse thermogenesis. Chronic TLR4 activation in our mice resulted in ROS production and ER stress elevation. To understand the molecular link between TLR4 and ER stress in thermogenesis attenuation, ER stress was inactivated by either genetic deletion of CHOP or intraperitoneal injection of a chemical chaperone (PBA). Blunting ER stress protected the mice from TLR4‐induced mitochondrial degradation and rescued WAT browning. Taken together, our results indicate that TLR4 is a pivotal player in thermogenesis impairment observed in obesity. It mediates ROS production and ER stress activation, leading to mitochondrial degradation and WAT browning inhibition. In this study, we identified a novel TLR4/ER stress signaling axis associated with antagonizing WAT browning. Targeting this TLR4/ER stress axis might be efficacious in preventing defective thermogenesis observed in obesity.Support or Funding InformationNIH 1P20GM104320
High Phosphorus Diet Mitigates Impairments in Lipid and Glucose Metabolism Associated with Diet‐Induced Obesity in Male Sprague Dawley Rats
Authors: Bassil Maya , Zeeni Nadine , Farran Natalie , Obeid Omar 
Published: November 2023

Phosphorus (P) nutrition status was found to be inversely related to obesity and metabolic syndrome in observational studies and this is thought to be mediated through an effect of P on liver metabolism (Obeid, 2013). This study thus aims at investigating whether P diet supplementation prevents the metabolic abnormalities associated with diet induced obesity in a controlled animal study. Thirty Sprague‐Dawley adult male rats (mean weight = 201±3g) were allocated into 3 equal groups receiving either a balanced diet (control), high fat diet with regular P concentration of 0.3% (HF) or high fat, high P (0.9%) diet (HFHP). Study lasted for 12 weeks, during which body weight and food intake were measured biweekly and intraperitoneal glucose tolerance test (IPGTT) was performed at the beginning (week2) and end (week 11) of the study. Rats were then sacrificed after 10‐hour fast, abdominal fat and liver were collected and weighed and serum samples were isolated from venous blood drawn from the inferior vena cava. Serum insulin, cholesterol, triglycerides as well as liver enzymes (ALP and ALT) were measured. High fat diet resulted in a significantly higher body weight gain, food intake and liver weight compared with control, irrespective of P supplementation. HF group had higher abdominal fat (0.44±0.12g) compared to control (0.21±0.06g) but this was not observed in HFHP group (0.29±0.10g). IPGTT results at week11 showed similar baseline glucose among groups but significantly (p=0.05) higher glucose at 2 hours post glucose injection in HF group (127±4.2mg/dl) vs. control (113±5.2 mg/dl) indicating glucose intolerance. P supplementation normalized glycemia at 2 hours in HFHP group (113±5.4 mg/dl). Fasting insulin increased significantly (p=0.008) in HF (2.8±0.4ng/ml) vs. control (1.2±0.4ng/ml) but was not different in HFHP group (2.2±0.5ng/ml). High fat induced obesity significantly (p<0.05) increased serum cholesterol, triglycerides and ALP in HF group (46.1±3.9mg/dl, 38.8±4.4mg/dl and 192.8±55.9U/l, respectively) compared to control (19.8±2.7mg/dl, 26.0.1±3.7mg/dl and 76.6±7.3U/l, respectively) but P supplementation in HFHP prevented this increase. In conclusion, high P diet appears to protect against lipid and glucose abnormalities and liver toxicity associated with diet induced obesity in rats. We suggest that P increases hepatic ATP, which drives the shift from lipid synthesis to glycogen and protein synthesis. Further analysis on the liver tissues will help in identifying the exact mechanisms.Support or Funding InformationThe study was funded by the Lebanese American University
Incorporation of Almonds in a Cholesterol‐lowering Diet Improves non‐ABCA1‐mediated Cholesterol Efflux in Normal Weight Adults
Authors: Berryman Claire E. , Fleming Jennifer A. , Kris‐Etherton Penny M. 
Published: November 2023

We previously showed that a cholesterol‐lowering diet with almonds, substituted for an isocaloric high‐CHO snack, maintains greater HDL‐C concentrations. However, recent evidence suggests that the cardioprotective effects of HDL may be more dependent on function than absolute HDL‐C levels. Therefore, a randomized, 2‐period (6 wk/period), crossover, controlled‐feeding study was designed to investigate the effects of 1.5 oz./d almonds vs. a calorie‐matched, high CHO snack, within the context of a cholesterol‐loweringdiet, on measures of global and transporter‐specific [ATP‐binding cassette (ABC)sub‐family A1 and non‐ABCA1 (global minus ABCA1 transporter)] cholesterol efflux. Differences in nutrient profiles of the control (CON: 58% CHO, 15%PRO, 26% FAT, no almonds/d) and almond (ALD: 51% CHO, 16% PRO, 32% FAT, 1.5 oz. of almonds/d) diets were due to nutrients inherent to each snack and did not differ in saturated fat or cholesterol. Participants (n=48) were generally healthy adults (mean ± SD, BMI: 26 ± 3 kg/m2; HDL‐C: 55 ± 16 mg/dL) with elevated LDL‐C (149 ± 20 mg/dL). There were no significant treatment effects of ALD vs. CON on global (10.2 ± 1.8 vs. 10.0 ± 1.7%, respectively) or transporter‐specific (ABCA1: 2.8 ± 1.2vs. 2.7 ± 1.2% and non‐ABCA1: 7.4 ± 1.3 vs. 7.3 ± 1.1%, respectively) cholesterol efflux (P >0.05). However, subgroup analyses revealed that responses to diet were dependent on body mass [diet treatment × baseline BMI category (BMI <25 vs. ≥ 25 kg/m2), P=0.02] and, in normal weight participants (n=14), the almond diet preservednon‐ABCA1 efflux (8.3 ± 1.7 vs. 7.8 ± 1.0%; P=0.01) compared to the control diet; this effect did not persist in overweight and obese (n=34) participants (ALD:7.0 ± 0.2 vs. CON: 7.1 ± 0.2%; P=0.93). Body mass appears to influence responsiveness to dietary manipulations; specifically, when almonds (1.5 oz./d) are incorporated in a cholesterol‐lowering diet, individuals with a normal BMI, but not those who are overweight or obese, show improved non‐ABCA1‐mediatedcholesterol efflux, an important step in the anti‐atherogenic reverse cholesterol transport pathway.Support or Funding InformationSupported by the Almond Board of California.
Ldlr−/− Mice Lacking PEMT Have Elevated Plasma Trimethylamine‐oxide Levels But Are Protected From High Fat Diet‐Induced Atherosclerosis.
Authors: Jacobs Rene , Zia Yumna , Rajabi Ala , Mi Si , Leonard Kelly‐Ann , Zhao Yuan‐Yuan , Field Catherine , Curtis Jonathan , van der Veen Jelske 
Published: November 2023

BackgroundPhosphatidylethanolamine N‐methyltransferase (PEMT) is a hepatic enzyme that converts phosphatidylethanolamine into phosphatidylcholine (PC) via three methylation reactions. The PEMT pathway makes 30% of the PC required in the liver and is the only de novo source of choline. PEMT deficient mice are protected against atherosclerosis when bred with either the Ldlr−/− and Apoe−/− mice. PEMT deficiency causes decreased VLDL secretion, plasma LDL levels and homocysteine, which are risk factors for atherosclerosis. Recently, choline supplementation was shown to enhance atherosclerosis in ApoE−/− mice and was dependent on the conversion of choline to trimethylamine (TMA) by the microbial flora in the gut, which was oxidized to trimethylamine N‐oxide (TMAO) by hepatic enzymes. In addition, plasma choline and TMAO have been associated with increased risk of CVD in multiple cohort studies. The purpose of this study was to examine the effects of dietary choline supplementation on plasma TMAO levels, and investigate whether choline supplementation eliminates the atheroprotective effect of PEMT deficiency in LDLR−/− miceMethodsWe performed two sets of experiments: In first experiment, 10–12 week old Pemt+/+/Ldlr−/− and Pemt−/−/Ldlr−/− mice were fed a chow diet for 12 weeks. In the second experiment, Pemt+/+/Ldlr−/− and Pemt−/−/Ldlr−/− mice were fed a 40% high‐fat/0.5% cholesterol diet (HFD) supplemented with either 3 or 10 g/kg choline for 12 weeks.ResultsPEMT+/+/Ldlr−/− and PEMT−/−/Ldlr−/− mice do not develop atherosclerosis on chow diet and there was no difference in plasma cholesterol between genotypes. When fed a HFD, PEMT−/−/Ldlr−/− mice are protected against atherosclerosis as compared to PEMT+/+/Ldlr−/− mice. Interestingly, choline supplementation did not increase atherosclerosis in the PEMT−/−/Ldlr−/− mice. Plasma cholesterol levels were reduced in PEMT−/−/Ldlr−/−, which did not increase on choline supplementation. Surprisingly, PEMT−/−/Ldlr−/− mice have elevated TMAO levels, which was reduced to control levels by choline supplementation. Furthermore, liver histology showed that PEMT−/−/Ldlr−/− mice developed fatty liver that was improved by choline supplementation.ConclusionCholine supplementation does not reverse the protection of PEMT−/−/Ldlr−/− mice against atherosclerosis. PEMT−/−/Ldlr−/− mice have high TMAO levels and fatty liver on HFD. Surprisingly, choline supplementation normalized TMAO levels and reduced the fatty liver. Therefore, plasma TMAO levels are not associated with atherosclerosis but may be associated with fatty liver disease.Support or Funding InformationFunding: ALMA, NSERC and CIHR