bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of dietary intake and red blood cell membrane fatty acid profile on the incidence of metabolic syndrome in Hispanic children from 2 to 10 years of age
Authors: Dysart Anna , Clark William Andrew , Marrs Jo‐Ann Summitt , Peterson Jonathan M. , Johnson Michelle Eileen , Alamian Arsham 
Published: November 2023

Metabolic syndrome (MetS) is a grouping of criteria including hypertension, glucose intolerance, truncal obesity/high BMI, insulin resistance, increased VLDL, high triglycerides (TAG), and low HDL. MetS is a problem in Hispanic children due to increasing obesity rates and a predisposition for insulin resistance.MethodsHispanic children aged 2 to 10 years of age were evaluated during a well child visit and data including demographic information, food frequency questionnaire, anthropometric measures, and blood samples were collected. Children were considered “at risk” for this study if they exhibited 3 or more risk factors for developing MetS. Risk factors included abdominal obesity, elevated blood pressure, elevated triglycerides, low HDL and/or elevated plasma glucose concentrations. A total of 112 children were included in this analysis with 33 (~29%) in the “at risk” category. Statistical analysis was via SPSS 22 multivariate General Linear Model evaluating differences between “normal” and “at risk” children.Results“At risk” children had higher serum levels for total cholesterol (159.4 vs 146.5 mg/dL, p=0.010), VLDL (32.4 vs 20.5 mg/dL, p=0.0001), LDL (82.9 vs 74.9 mg/dL, p=0.074), Cholesterol/HDL ratio (3.73 vs 2.98, p=0.0001), Triglycerides (161.4 vs 103.0 mg/dL, p=0.0001), and had lower levels for HDL (44.2 vs 51.0 mg/dL, p=0.002). Ferric Reducing Ability of Plasma (FRAP) was higher for “at risk” children (0.416 vs 0.349, p=0.017) but results may have been influenced by plasma uric acid. FFQ results (Block Kids Screener) indicated that dietary saturated fat (p=0.070), meat, poultry, fish, (p=0.146), protein (p=0.067), total fat (p=0.058), carbohydrates (p=0.032), fiber (p=0.003), kcal (p=0.042) and glycemic load (p=0.049) were lower for “at risk” children; they also tended to consume less food. Red blood cell membrane fatty acid profile revealed no significant differences for membrane saturated, MUFA, PUFA, n‐3 or n‐6 fatty acids.ConclusionIndicators of fat metabolism show that children with higher levels of lipid serum markers are at risk for developing metabolic syndrome. The relationship between red blood cell membrane fatty acid profile and dietary intake do not completely explain why certain Hispanic children are “at risk” for developing MetS.Support or Funding InformationResearch supported by Tennessee Board of Regents Diversity Grant and several Small Research Development Committee Grants from East Tennessee State University's Office of Research and Sponsored Programs.
Reduced risk factors of metabolic syndrome in immigrant compared to resident South Asian Indian young men
Authors: Nguyen Dan Q , Sukumar Deeptha , Kanjana K , Victor Ann Quang , Pop Claudia , Shapses Sue 
Published: November 2023

South Asian Indians are at higher risk for developing metabolic syndrome (MetS) than the general USA population, and at risk of developing diabetes and cardiovascular disease. We hypothesized that USA (immigrant) SA men develop MetS in their early adulthood to a greater extent than men living in India (resident), and this is due to a combination of dietary changes and stress. We examined 73 men (ages of 19–29 y; BMI >23 kg/m2) in the USA and in India. Because a heavier group was recruited in India than in the USA, we used ANCOVA in all analysis, to control for BMI. In contrast to our hypothesis, immigrant compared to resident Indians had lower total cholesterol (165±37 vs 183±31 mg/dl), low density lipoprotein (LDL) (95 ± 33 vs. 122 ± 27 mg/dl) and higher high density lipoprotein (HDL) (49 ±10 vs. 41±6 mg/dl) (p < 0.05). Glucose was 89±6 in immigrants and 93±7 mg/dl in resident Indians (p≤0.06). Systolic blood pressure was lower in immigrant (113±13) than resident Indians (130±11) (p < 0.001), and USA men also had a lower perceived stress score (p<0.05). This was consistent with fewer risk factors for MetS in immigrant than resident Indians (i.e., 10% vs 26% had at least 2 components of MetS). We also found that men in the USA were taller (p <0.001) and that the percent protein intake was greater in immigrant (20 ± 9%) than resident men (12 ±6%; p < 0.001), whereas the lower %fat intake (22±11% vs. 37±9%) did not differ significantly between the groups. Interestingly, men living in the USA > 10 years (vs shorter duration) had higher serum HDL levels (p <0.05), suggesting a possible effect of acculturation. Immigrant Indian young men living in the USA are at lower risk for MetS, possibly due to lower stress compared to their resident Indian counterparts.Support or Funding InformationCenter for Global Advancement and International Affairs (Rutgers GAIA)
Hyperlipidic diet induced glomerular morphometric alterations and renal damage in hypertensive rats
Authors: Pereira Renata Oliveira , de Souza Marina Soares , Araujo Iara , Fiorino Patricia , Fonteles Manassés , Farah Vera 
Published: November 2023

The aim of this study was to evaluate the renal function in hypertensive hyperlipidic‐fed animals submitted to an acute NaCl overload. Weaned male spontaneously hypertensive rats (SHR) with 21 days old (40–50g) followed by 8 weeks, were divided into 4 groups (n=6/group): SHR Control (SC); SHR Salt (SS, NaCl 1% in drinking water for the 10 last days); SHR Hyperlipidic (SHL, hyperlipidic diet, 30% lipids) and SHR Hyperlipidic Salt (SHLS, hyperlipidic diet and NaCl). All the procedures followed the rules of the Committee of Research and Ethics of the Mackenzie University (CEUA Nº 127/08/2015). Metabolic evaluations consisted of glucose tolerance test, triglycerides, and total cholesterol measurements. Urine samples were collected during 24h using metabolic cages. At the end of the protocol, the animals were euthanized by anesthesia overload, serum was collected and the left kidney and the visceral fat pad were removed and weighted. Kidney slices were stained with picrosirius red to evaluate the area of the Bowman's capsule (AB) and space (BS), and glomerular tuft diameter (TD). Creatinine concentration (serum and urine) was determined by colorimetric methods and sodium concentration of the urine was measured using electrolyte analyzer. Hyperlipidic diet promoted glucose intolerance, increased triglycerides and visceral fat pad in SHL and SHLS groups. NaCl consumption determined an increase in urinary volume and sodium concentration in SS and SHLS groups. Hyperlipidic diet induced a reduction in TD (SHL: 82±0,6; SHLS: 83±0,5 vs. SC: 88±1,5 μm) and an increase of BS in SHL group (29,5%) and in SHLS group (43,4%), with no changes in AB, compared with SC. These results are associated with a reduction in glomerular filtration rate (creatinine clearance) (SHL: 0,7±0,1; SHLS: 0,8±0,2 vs. SC: 1,4±0,1 mL/min). In conclusion, our data suggests that hyperlipidic diet in hypertensive animals changed the renal morphometry with damage in renal function. However, when stimulated by NaCl consumption, there was no further impairment in renal function in hyperlipidic‐fed animals.Support or Funding InformationCAPES/Mackpesquisa
“Catalytic” Doses of Fructose and its Epimers on Glycemic Control: A Systematic Review and Meta‐Analysis of Controlled Feeding Trials
Authors: Noronha Jarvis C , Braunstein Catherine , Mejia Sonia Blanco , Cozma Adrian I , Khan Tauseef , Glenn Andrea , Noseworthy Rebecca , Kendall Cyril W.C. , Wolever Thomas M , Leiter Lawrence A , Sievenpiper John L 
Published: November 2023

ObjectiveContrary to the concerns that fructose may have adverse metabolic effects, an emerging literature has shown that small, ‘catalytic’ doses (≤ 50‐g/day) of fructose and its epimers (allulose, tagatose and sorbose) decrease the glycemic response to high glycemic index meals in humans. This effect appears to be mediated by upregulation of glucokinase, leading to increased hepatic glycogen synthesis. Whether this acute ‘catalytic’ mechanism of fructose and its epimers will manifest as an improvement in long term glycemic control is unclear. To address this question, we synthesized evidence from controlled feeding trials assessing the effect of small, ‘catalytic’ doses of fructose and its epimers on HbA1c.MethodsWe searched MEDLINE, EMBASE, and Cochrane Library through Feb 12, 2016. We included controlled feeding trials of ≥ 2 weeks investigating the effect of small, ‘catalytic’ doses (≤ 50‐g/day) of fructose and its epimers in comparison to control diets. Two independent reviewers extracted relevant data. Risk of bias was assessed using the Cochrane Risk of Bias Tool. Data were pooled using the generic inverse variance method and expressed as mean differences (MD) with 95% confidence intervals (CIs). Heterogeneity was assessed using the Cochran Q statistic and quantified using the I2 statistic. The overall quality of the evidence was assessed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach.Results7 trials (n = 467) over a median follow‐up of 3 months met the eligibility criteria. ‘Catalytic’ doses of fructose significantly reduced HbA1c (MD = −0.40% [95% CI −0.72 to − 0.08]), but not allulose and tagatose for which there was only one trial comparison for each of the sugars. The overall quality of the evidence was graded as “moderate” quality for a decreasing effect of fructose on HbA1c due to a downgrade for serious imprecision. The evidence for allulose and tagatose was not graded.ConclusionPooled analyses indicated that small, ‘catalytic’ doses of fructose improve glycemic control over the shorter term. The evidence for allulose and tagatose remains inconclusive due to the limited number of trials. There is a need for large high quality, long‐term randomized trials for all 3 sugars to improve our confidence in the effect estimates.Protocol registration: clinicaltrials.gov identifier, NCT02776722Support or Funding Information Funding: The Tate and Lyle Nutritional Research Fund at the University of Toronto, Canadian Diabetes Association (CDA), Banting & Best Diabetes Centre, and PSI foundation.
Race/Ethnicity evaluation of postprandial glycemic and triglyceride response
Authors: Zhu Lanjun , Xiao Di , Huang Yancui , Edirisinghe Indika , Burton‐Freeman Britt 
Published: November 2023

Health disparity is well documented, revealing certain race/ethnic groups at higher risk than others for metabolic diseases. The reason for these differences is uncertain and requires further investigation. Identifying early indicators of dysmetabolism is critical for starting disease risk interventions and preventing transition into disease. Personalizing approaches depends on a number of factors, including understanding patterns of dysmetabolism as well as when they become evident. This study was undertaken to characterize and test for potential postprandial metabolic response differences among an ethnically diverse population.The study utilizes metabolic data from previous randomized clinical trials conducted in our lab utilizing a fixed meal, 6‐hour postprandial multiple blood sampling paradigm. Fasting and postprandial insulin, glucose and triglyceride (TG) concentrations were obtained from 208 relatively adults representing African American (AA, n=81), Caucasian (n=67), Hispanic (n=25) and Asian (n=36) populations. One‐way ANOVA was used for preliminary analysis to compare the 6 h total Area under the curve (AUC) of postprandial glycemic and TG response. Analysis within the study groups demonstrated that AUC for insulin was significantly higher in the AA study groups, compared to Caucasian (P=0.03). However, AUC for TG was relatively lower in AA than in Caucasian and Hispanic groups (P<0.01). Subgrouping by sex indicated Asian males had higher insulin AUC values compared to Caucasian males (P<0.05) and not different between all other subgroups. TG responses were significantly higher in Caucasian females than AA females (p<0.001). No differences were observed on postprandial glycemia between race/ethnic groups in this simple model analysis. Subsequent more complex analyses will unveil the influence of time, age, BMI and other factors to better understand their influence and inter‐relationship impacting dysmetabolism.
Improvement of Exercise on Diabetes‐Reduced LHR Sensitivity via Increasing Expression of StAR Protein.
Authors: Chou Shih‐Yun , Tsai Shiow‐Chwen , Lu Chien‐Chen , Chen Chiao‐Nan , Chen Chih‐Chieh 
Published: November 2023

IntroductionDiabetes mellitus is a highly prevalent chronic disease worldwide. Diabetes patient has suffered from testicular dysfunction including testosterone deficiency. Acute swimming test has been demonstrated the beneficial effect on gonadotropin‐stimulating testosterone via activate cAMP pathway in rats.PurposeThe purpose is to assess the effect of streptozotocin (STZ)‐induced diabetes on testosterone production and investigate the mechanisms of endurance training improved on diabetes‐induced testosterone dysregulation.MethodsThe study used 8 weeks old male Sprague Dawley rats, were divided into four groups, including control, exercise (Ex), diabetes (DM), diabetes combined with exercise (DM+Ex). The rats were intraperitoneally injected with STZ (50 mg/ml, dissolved in citric acid buffer, pH 4.5) to induce diabetes. While the control group were injected with citric buffer. After successfully induced diabetes, endurance running for Ex and Ex+DM rats was carried out on the treadmill for four weeks, and then the animals were sacrificed. The blood were centrifuged, and plasma testosterone (T) and luteinizing hormone (LH) were measured by radioimmunoassays. The Leydig cells were extracted to analyzed expression of LH receptor (LHR) and steroidogenic acute regulatory protein (StAR) by Western blot. All data were presented as mean ± standard error mean. One way analysis of variances (ANOVA) was used to compare the differences for mean of each group. The alpha level was set at 0.05 (p<0.05) for accepting statistical difference for all comparisons.ResultsThe results showed that both groups of STZ‐induced diabetes and exercise training significantly reduced plasma testosterone secretion (p<0.05). Plasma LH were significantly increased in DM group when compared with control group (p<0.01), exercise did not alter plasma LH release, but partially attenuated diabetes‐stimulated LH release (p<0.05). Expression of LHR, extracted from Leydig cells was significantly higher in DM and Ex group than that of control (P <0.05). Compared with control group, expression of StAR protein were also significantly inhibited (P <0.01) in DM group. Ex did not altered the expression of StAR but significantly reversed DM‐inhibited StAR expression (p<0.01).ConclusionsThe study concluded that diabetes mellitus resulted a lower level of plasma testosterone through decreased the sensitivity of LHR and then decrease the expression of StAR protein and production of testosterone secretion. Exercise is benefit to improve diabetes reduced‐LHR sensitivity via increasing expression of StAR protein.Support or Funding InformationMOST I102‐2410‐H‐845‐014‐MY3
Increased Physical Activity Ameliorates High Fat Diet‐Induced Bone Resorption in Mice
Authors: Chen Jin‐Ran , Lazarenko Oxana P. , Blackburn Michael L. , Carvalho Eugenia , Shankar Kartik , Børsheim Elisabet 
Published: November 2023

It has been recognized that mechanical stresses associated with physical activity (PA) have beneficial effects on increasing bone mineral density (BMD) and improving bone quality. On the other hand, high fat diet (HFD) and obesity increase bone marrow adiposity leading to increased excretion of pro‐inflammatory cytokines to activate RANKL‐induced bone resorption. In the current study, we investigated whether increased PA via access to voluntary wheel running protects against HFD‐induced bone resorption. One‐month‐old male C57BL6/J mice were provided ad libitum access to either control (17% fat) or HFD [20% protein (casein), 35% carbohydrate (dextrose and maltodextrin), and 45% fat (corn oil)] for 8 wk. Mice in each diet group were further divided into subgroups with or without PA by providing access to voluntary running wheels for 8 wk (8 to 9 km running per day). Using peripheral quantitative CT scan (pQCT) on tibias ex vivo, we found that bone mass especially trabecular BMD was significantly increased with PA in control diet animals compared to sedentary animals without access to wheels (102.8±3.5 vs. 91.5±4.2 mg/cm3, n=6, p<0.05). PA ameliorated HFD‐induced trabecular bone loss (PA+HFD, 93.6±5.2 vs. HFD, 81.3±4.7 mg/cm3, n=6, p<0.05). Femur bone marrow cells were aspirated and cultured, and non‐adherent hematopoietic cells collected the following day were used for RANKL‐induced osteoclastogenesis assay. We found that PA significantly blunted increases of HFD‐induced osteoclastogenesis. In accordance with these data, signal transduction real‐time PCR analysis showed that PA significantly inhibited HFD‐induced Ezh2 and NFATc1 gene expression, but IRF8 expression was decreased in non‐adherent hematopoietic cells from HFD mice. In conclusion, increased PA is capable of altering the HFD‐induced bone marrow hematopoietic cell differentiation program to protect against increased bone resorption.Supported in part by USDA‐ARS Project 6026‐51000‐010‐05S.Support or Funding InformationUSDA‐ARS Project 6026‐51000‐010‐05S
ZIP14 (SLC39A14) protects against muscle atrophy and attenuates inflammatory responses in murine skeletal muscle
Authors: Kim Jinhee , Aydemir Tolunay Beker , Kim Min‐Hyun , Cousins Robert J. 
Published: November 2023

Inflammation increases the risks of metabolic diseases and conditions such as atrophy of skeletal muscle. Thus, the prevention of inflammation is critical. Zinc is an essential trace mineral and has important roles in growth, development, and immune function. It has been demonstrated that zinc deficiency can result in increased cytokine expression and secretion. Skeletal muscle secretes cytokines such as interleukin‐6 (IL‐6) during exercise. This process is increased during inflammation. Using a mouse model, we identified that Zip14 (slc39a14) exhibited greater upregulation in skeletal muscle of wild type (WT) mice treated by LPS (endotoxin) to mimic acute inflammation. However, the role(s) of ZIP14 in skeletal muscle in response to inflammation needs to be defined. The aim of this study was to determine muscle ZIP14 expression and cytokine expression during both acute inflammation induced by LPS injection and chronic inflammation induced by a high‐fat diet (HFD) in muscle of WT and Zip14−/− (KO) mice. Our results demonstrated that Zip14 KO mice exhibited growth abnormalities with smaller body size. Furthermore, reduced hind leg length and greater atrophic muscle fibers were also shown in Zip14 KO mice based on morphology and physiological measurements. Following LPS stimulation, ZIP14 was upregulated and an increase in zinc concentrations were observed in muscle of WT mice. However, this increase was not observed in Zip14 KO mice, suggesting impaired zinc uptake in this genotype. More importantly, Zip14 KO mice showed greater IL‐6 production in muscle than WT mice after LPS administration, which was coincident with greater NF‐κB activation. This suggests that ZIP14‐mediated zinc uptake in muscle may reduce inflammatory signaling activation. Consistent with the LPS model, ZIP14 expression also increased in muscle of WT mice during chronic inflammation induced by the HFD treatment for 16 weeks. Strikingly, we found that Zip14 KO mice fed the HFD began to die at week 14 of the study. These observations suggest that ablation of Zip14 may accentuate systemic inflammatory responses. In order to examine ZIP14 involvement on muscle secretions, we investigated IL‐6 expression and production by using an ex vivo explant culture model from muscles of WT and Zip14 KO mice. In agreement with in vivo data, we confirmed that IL‐6 expression in Zip14 KO muscle greatly increased after LPS treatment. In conclusion, muscle ZIP14‐mediated cellular zinc uptake reduces IL‐6 production most likely by mediating the NF‐κB or other signaling pathways during inflammation. This may partially explain the protective effects of muscle zinc in chronic inflammatory diseases of muscle.Support or Funding InformationSupported by grant DK94244 from the National Institutes of Health
Selenoprotein K functions to promote melanoma progression and metastasis
Authors: Hoffmann Peter , Marciel Michael , Kilicasian Pascal , Pham Andrew , Hoffmann FuKun 
Published: November 2023

We have found that selenoprotein K (Selenok) is crucial for calcium flux in immune cells, but had not investigated its role in cancer cells. A recent study showed that calcium flux was important for melanoma cells to proliferate and migrate. Thus, we set out to determine if Selenok plays an important role in melanoma using in vitro and in vivo models. Analyses of four different NCI‐60 human melanoma cell lines found that Selenok levels varied in these cells and one cell line in particular, SK‐Mel28, was subjected to CRISPR/Cas9 genome editing to mutate Selenok. Mutating wild‐type (WT Selenok) to a truncated version (Trunc Selenok) led to reduced calcium flux, migration using a scratch assay, and lower colony formation. These functions were rescued with a plasmid expressing GFP‐Selenok but not with GFP alone. An established transgenic mouse strain, Grm1‐Tg, develops spontaneous melanoma that metastasizes to lymph nodes at 4 months of age and was crossed with Selenok KO mice to generate the following: GRM1‐Tg/Selenok−/−, GRM1‐Tg/Selenok−/+, GRM1‐Tg/Selenok+/+. These littermates allowed us to determine how loss of one or both or none of Selenok alleles on the Grm1‐Tg background affected progression and metastasis of melanoma in vivo. We used both male and female mice and results showed that lack of Selenok expression in GRM1‐Tg/Selenok−/− mice led to lower primary tumors on tails and ears and less melanoma cells in draining lymph nodes. The presence of one or two Selenok alleles were similar and showed significantly higher levels of melanoma and metastasis. Overall, these results suggest that melanoma cells require Selenok expression for primary tumor growth and metastasis to other tissues.Support or Funding InformationWe sincerely thank Ann Hashimoto for her hard work in maintaining mouse colonies for this study. This research was supported by NIH grant R01AI089999, and core facilities supported by P30GM114737, P30GM103341, G12RR003061, G12MD007601.