bluuebunny/crossref_metadata_2025_split huggingface dataset:
Saturated or Monounsaturated Fatty Acids Have Different Effect on Body Weight and Feed Intake
Authors: Tamer Funda , Nergiz‐Unal Reyhan 
Published: November 2023

INTRODUCTIONVarious epidemiologic studies showed that high intake fat, with a rapid and extensive growth of the processed food industry in the last three decades, is considered to be the major risk factors for weight control and obesity. Currently, not only consumption of high quantities of fat but also type of fatty acids is recognized as a vital factor in the development of obesity. Therefore, the aim of this study was to investigate the variations in body weight and food intake of male C57Bl/6 mice after high fat diet either with different fatty acid contents.METHODSMale C57Bl/6 mice (8 weeks of age) were individually housed and fed ad libitum with a control chow diet (CD, 3.5 kcal/g diet, 10% calories from fat), high monounsaturated fatty acid consisting diet (MUFA, 5 kcal/g diet, 40% calories from fat), or high saturated fatty acid consisting diet (SFA, 5 kcal/g diet, 40% calories from fat) for 15 weeks after a two‐weeks of wash out period. Food intake was measured daily and body weight were measured at least two times in a week. Body weight change was calculated from the terminal and initial body weights. Analysis were carried out by Kruskal‐Wallis test using SPSS software version 23.RESULTSThe mean feed intake was highest in MUFA diet group (4.2±0.21g) significantly compared to the control CD (3.9±0.14g) and SFA (3.6±0.13g) groups (p<0.05). Despite the food intake, the mean body weight change was different between dietary groups (CD: 5.5±0.49g; SFA: 9.5±0.66g; MUFA: 8.4±0.62g) (p<0.05) after 15 weeks with the highest change in high saturated fat diet (p<0.05).CONCLUSIONIn conclusion, a high monounsaturated fatty acid diet might stimulate the food intake but high saturated fatty acid diet adversely affected the body weight. Although feed consumption was higher in MUFA intake compared to the SFA intake, the body weight change was higher with SFA intake revealing a lipogenic potential of the saturated fatty acids.
Eicosapentaenoic acid (EPA) promotes differentiation of human brown precursor cells into metabolically active classical brown adipocytes via Gq/11 signaling
Authors: Fan Rong , Kim Jiyoung , Giraud David , Chung Soonkyu 
Published: November 2023

Eicosapentaenoic acid (EPA) supplementation exerts a plethora of health benefits. Previously, we demonstrated that EPA promotes brown adipogenesis by mediating G‐coupled protein receptor 120 (GPR120) activation in rodent brown precursor cells. The aim of this study is to establish the role of EPA in regulating brown adipogenesis in human classical brown precursor cells. The immortalized human brown precursor cells were employed to induce differentiation in the presence of oleic acid, palmitic acid, and EPA. EPA treatment significantly increased brown‐specific gene expressions including Ucp1, Prdm16, Cidea, DiO2, UCP1 protein expressions and oxygen consumption rate. To further investigate the role of GPR120, a receptor family involved in Gq/11 subtype, human brown precursor cells were treated with either GPR120‐specific agonist cdpA or a potent Gq/11 inhibitor (YM‐254890) during differentiation. GPR120 agonism significantly promoted EPA‐mediated brown adipogenesis, while inhibition of Gq/11 signaling completely abrogated brown adipogenesis. Consistently, the genetic deletion of GRR120 by CRISPR/Cas9 abrogated EPA‐mediated brown adipogenic effects. Collectively, these results demonstrate that EPA supplementation mediates Gq/11 signaling of GPR120 leading to augmentation of brown adipogenesis in human brown precursor cells.Support or Funding InformationNIH 1P20GM104320
Roles of Vascular Endothelial Growth Factor in Skeletal Development, Postnatal Homeostasis and Disease
Authors: Olsen Bjorn R , Berendsen Agnes D , Duan Xuchen , Hu Kai , Nagao Masashi 
Published: November 2023

Vascular endothelial growth factor (VEGF), critical for cardiovascular development, is essential for skeletal development, growth and homeostasis. It couples angiogenesis with bone formation, and it stimulates differentiation of chondrocytes, osteoblasts and osteoclasts during development of synovial joints and membranous as well as endochondral bones. Loss of VEGF expression in chondrocytes during development results in increased apoptotic cell death. Loss of trabecular bone with an increase in marrow fat is the consequence of reduced VEGF expression in bone marrow‐derived osteoblastic progenitors in long bones.In endochondral bone development, VEGF has a major role in establishing primary ossification centers within cartilage models of future bones. High expression of VEGF by hypertrophic chondrocytes establishes a VEGF gradient that induces migration of osteoclasts, endothelial cells, preosteoblasts and hematopoietic stem cells from the perichondrium into the center of ossifying cartilage. As the primary ossification center expands, hypertrophic chondrocytes continue to express high levels of VEGF and as osteoclasts, endothelial cells and preosteoblasts continue to invade the VEGF‐rich environment, metaphyseal growth plates are established.VEGF produced by osteoblastic progenitor cells in periosteum and perichondrium of developing membranous and endochondral bones, stimulates angiogenesis and induces differentiation of progenitor cells to preosteoblasts and bone‐forming osteoblasts. The stimulatory effect on angiogenesis in turn results in endothelial‐derived osteogenic factors that may induce periosteal/perichondrial bone formation. In addition, osteoblast lineage cell‐derived VEGF may also induce osteoblast differentiation based on autocrine/intracrine mechanisms involving cytoplasmic and/or nuclear VEGF.Intracellular VEGF functions are made possible by a gene that contains two transcriptional start sites. Transcripts from the downstream site are translated into proteins with a signal peptide, allowing direct entry into the secretory pathway. In contrast, transcripts from the upstream site are translated into proteins that are about twice the size of secreted VEGF. This “long” VEGF is processed in the cytoplasm to forms that can enter the secretory pathway, or high molecular weight forms that are entering the nuclear compartment.VEGF expression by chondrocytes is required for synovial joint development and the timely differentiation of articular chondrocytes. However, in aging joints the growth factor shows its dark side in that increasing expression levels of VEGF in cells of synovial joints stimulate both articular cartilage degeneration and increased joint pain in osteoarthritis.Support or Funding InformationNIH‐NIAMS
Excessive Free Fatty Acid Oxidation in Non‐obese Healthy Asian Men with Insulin Resistance is Associated with Impaired Branched‐chain Amino Acid Oxidation
Authors: Tan Hong Chang , Hsu Jean W. , Sidney Yu , Khoo Chin Meng , Tai E Shyong , Jahoor Farook 
Published: November 2023

BackgroundBranched‐chain Amino Acids (BCAA) are elevated in insulin resistant (IR) states and may be involved in the pathogenesis of IR in non‐obese individuals. It remains unclear whether this could be secondary to impairment in clearance from oxidation or increased rate of appearance (Ra) because of IR.ObjectivesOur study compared leucine and palmitate kinetics between 14 insulin sensitive (IS) and 12 IR non‐obese healthy Asian men. We hypothesized that greater free fatty acid (FFA) availability for oxidation in IR impairs BCAA oxidation leading to higher blood BCAA concentration.MethodsSubjects underwent oral glucose tolerance testing for measurement of their whole body insulin sensitivity index (WBISI) and body composition measured using the 2H2O method. [U‐13C16] palmitate and [U‐13C6] leucine were infused at least 1‐week apart for quantification of their rates of oxidation and Ra. Kinetic data are expressed as μmol/kgFFM/h.ResultsCompared to IS subjects, IR subject had significantly lower WBISI (3.30 ± 0.26 vs. 8.03 ± 0.92), higher body mass index (24.4 ± 0.6 vs. 23.0 ± 0.3 kg/m2), body fat % (29.8 ± 2.4 vs. 23.7 ± 1.3) and total blood BCAA (438.1 ± 21.7 vs. 385.0 ± 14.5 umol/L, p = 0.048). Palmitate Ra was much higher in IR subjects (189.0 ± 13.5 vs. 151.8 ± 8.5, p = 0.027) indicating greater exposure of skeletal tissue to circulatory FFA. This was accompanied by greater palmitate oxidation (60.6 ± 4.3 vs. 46.2 ± 3.5, p = 0.016) such that plasma concentration was not significantly different between the comparator groups (124.7 ± 5.7 vs. 108.9 ± 13.1, p = 0.295). Leucine Ra (152.8 ± 5.5 vs. 144.6 ± 3.2, p = 0.067) and oxidation (19.2 ± 0.4 vs. 16.3 ± 0.7, p = 0.028) were also higher in IR but leucine oxidative capacity, defined as percentage leucine flux oxidized, was significantly lower (11.9 ± 0.4 vs. 10.6 ± 0.4, p = 0.028).ConclusionsElevated blood BCAA in healthy non‐obese but IR men is a consequence of both greater Ra and impaired BCAA oxidative capacity and this is associated with excessive FFA oxidation.Support or Funding InformationSupported by SingHealth Medicine Academic Clinical Program (03/FY2014/P1/06‐A16)
Effects of an encapsulated fruit and vegetable juice concentrate on obesity‐induced systemic inflammation
Authors: Wood Lisa G , Williams Evan J , Berthon Bronwyn S , Baines Katherine A 
Published: November 2023

Study ObjectivesPhytochemicals from fruits and vegetables have been shown to reduce systemic inflammation. This study examined the effects of an encapsulated fruit and vegetable juice concentrate on risk factors for chronic disease in overweight and obese adults.MethodsA double‐blinded, parallel, randomised placebo‐controlled trial was conducted in 56 adults aged ≥40 years, with BMI ≥28 kg/m2. Before and after 8 weeks daily treatment with 6 capsules of fruit and vegetable juice concentrate or placebo, peripheral blood gene expression (microarray and qPCR), plasma TNFα (ELISA), plasma carotenoids (HPLC), body composition (DEXA), HbA1c, cholesterol and triglycerides were assessed.ResultsTotal carotenoids (0.73mg/L (week 0) versus 0.85mg/L (week 8), p=0.017) and β‐carotene (0.11mg/L versus 0.16mg/L, p<0.0001) were significantly increased in plasma following consumption of the juice concentrate. Correspondingly, total cholesterol (5.70mmol/L versus 5.50mmol/L, p=0.015), LDL cholesterol (3.63mmol/L versus 3.50mmol/L, p=0.032), plasma TNF‐α (1.04pg/mL versus 1.02pg/mL, p=0.037) and systolic blood pressure (131.7mmHg versus 125.9mmHg, p=0.005) were decreased and total lean mass (49.3kg versus 50.0kg, p=0.018) was increased following supplementation with the juice concentrate. Between group differences were observed for plasma total carotenoids, lycopene and β‐carotene. Gene expression of various signalling pathways was altered, including 3 genes involved in lipogenesis, 10 NF‐kB associated genes and 2 AMPK associated genes.ConclusionsSystemic inflammation, blood lipids and body composition were improved in obese individuals following an 8 week intervention with an encapsulated fruit and vegetable juice concentrate. Hence, this supplement may provide a useful strategy for reducing the risk of obesity‐induced chronic disease.Support or Funding InformationFinancially supported by research grant from NSA, LLC (Collierville, TN).
Dietary Blueberries Attenuate Vascular Inflammation and Dysfunction in Diabetic db/db Mice
Authors: Bharat Divya , Petersen Chrissa , Gholami Samira , Denetso Christopher , Cutler Brett , Kim Ji‐Seok , Symons J David , Velayutham Anandh Babu Pon 
Published: November 2023

BackgroundPatients with diabetes are 2–4 fold more susceptible to cardiovascular complications. High glucose‐induced vascular inflammation and the subsequent vascular dysfunction play a major role in the development of atherosclerosis in the context of diabetes. In preliminary studies we showed that relative to vehicle (BSA) treated arteries, dysfunction was less severe in segments that incubated 18–24 h with palmitate + blueberry metabolites vs. palmitate alone. Based on these data from arterial segments treated ex vivo with blueberry metabolites, we tested the hypothesis that blueberry supplementation attenuates vascular complications in diabetic db/db mice.MethodsSeven week old male diabetic db/db mice that consumed standard chow (db/db) or chow supplemented with 3.8% freeze‐dried blueberries (db/db+BB) for 10 weeks were compared to non‐diabetic control mice (db/+). Based on normalization to body surface area, this dose in mice is equivalent to ~1.5 servings of BB (~240 g) in humans. At ~17 weeks the following in vivo analyses were completed: (i) body weight and food intake; (ii) glucose (GTT) and insulin (ITT) tolerance; and (iii) systemic arterial blood pressure (tail cuff). Ex vivo analyses included the assessment of vascular inflammation (fluorescent labeled monocyte binding to aortic endothelium), and determination of mesenteric arterial reactivity (isometric tension procedures).ResultsCompared to db/+ animals, both diabetic groups displayed similar increases (p<0.05) in weight gain and impairments (p<0.05) in glucose and insulin tolerance. Arterial pressure (systolic, diastolic, and mean) was higher (p<0.05) in db/db vs. db/+ mice, but the severity of hypertension was attenuated (p<0.05) in db/db+BB mice. After precontraction with ~ 10−6 M phenylephrine, acetylcholine (ACh; 10−8–10−6 M) evoked vasorelaxation was impaired (p<0.05) in db/db vs. db/+ animals, but no differences existed between db/db+BB vs. db/+ mice. Vasorelaxation to sodium nitroprusside (10−9–10−4 M) was complete and similar among groups. Fluorescent‐labeled mouse monocyte WEHI 78/24 cells exhibited higher (p<0.05) binding to aortic endothelium from db/db vs. db/+ mice, but this response was reduced (p<0.05) in aortic endothelium from db/db+BB mice. Ongoing studies are focused on identifying the effect of blueberries on inflammatory molecules in the vasculature, and exploring the molecular signaling mechanisms responsible for the protective effects of blueberries.ConclusionBlueberry consumption may be a potential adjunct therapy to prevent, delay, and/or limit the severity of vascular complications in diabetes.Support or Funding InformationSupported by University of Utah Seed Grant and College of Health Research Pilot Grant.
Anti‐inflammatory Activity of Aronia Berry Polyphenols in Jurkat T Cells
Authors: Martin Derek , Bolling Bradley 
Published: November 2023

INTRODUCTIONInflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract resulting from an aberrant immune response to the microbiota. T cells and their cytokines influence contribute to the ongoing inflammation in IBD. Diets rich in fruits and vegetables have been shown to decrease the risk of developing IBD. Dietary polyphenols are considered to be responsible for many of the benefits of fruit and vegetable consumption. Aronia berries are a concentrated source of polyphenols including anthocyanins, proanthocyanidins, and phenolic acids. Polyphenols, in general, have limited intestinal absorption and are extensively metabolized by the gut microbiota. Microbial catabolism may contribute to the health benefits associated with polyphenol consumption.OBJECTIVEThe objective of this study was to determine the anti‐inflammatory activities of an aronia berry extract, aronia polyphenol fractions, and microbial polyphenol metabolites in Jurkat T cells.METHODSAronia anthocyanin and neutral phenols fractions were obtained from an ethanolic aronia extract by elution from a C18 solid phase extraction column. Aronia proanthocyanidin rich fraction was obtained from whole aronia berries extracted with acetone/water/acetic acid (70/29.5/0.5 v/v) followed by elution from a Sephadex LH‐20 column. Polyphenols in the extract and fractions were determined by HPLC. Jurkat T cells were stimulated with 50 ng/mL phorbol myristate acetate and 1 μg/mL ionomycin for 4 h in the presence of a commercial aronia berry extract, aronia berry polyphenol fractions, or known microbial polyphenol metabolites. Tumor necrosis factor (TNF)α in supernatant was determined by immunoassay. Statistical significance was determined by one‐way ANOVA.RESULTSAt 250 μg/mL, the aronia extract significantly inhibited TNFα production by 33.6% (p<0.01) without reducing cell viability. At 50 to 100 μg extract/mL, there was no inhibition of TNFα. The anthocyanin and proanthocyanidin rich fractions did not affect TNFα production, but the neutral phenols fraction exhibited dose‐dependent inhibition. 3,4‐Dihydroxyphenylpropionic acid inhibited TNFα production at 100 and 0.1 μM, by 14.1 and 15.1% (p<0.05 and p<0.01, respectively) and 3,4‐dihydroxyphenylacetic acid inhibited TNFα production by 20.6% at 0.1 μM (p<0.0001). 3,4‐Dihydroxybenzoic acid (protocatechuic acid) and ferulic acid did not inhibit TNFα production at any tested concentration.CONCLUSIONThe aronia extract, neutral phenols fraction, and select microbial metabolites inhibited T cell TNFα without apparent loss of cell viability. The anti‐inflammatory capacity of aronia berry polyphenols may help to prevent and minimize intestinal inflammation associated with IBD by inhibiting T cell TNFα.Support or Funding InformationUSDA Hatch WIS01836
Effect of Bonded Arginine Silicate on Inflammatory Markers and Arthritis
Authors: Ojalvo Sara Perez , Sahin Kazim , Komorowski James 
Published: November 2023

BackgroundThe purpose of this preclinical study was to examine the effects of inositol‐stabilized arginine silicate supplementation (ASI; Nitrosigine®) on inflammatory markers and joint health in an arthritis‐joint health model. ASI is a sports nutrition ingredient that has been clinically shown to provide efficacious levels of arginine and silicon, reduce markers of muscle damage, and increase nitric oxide levels among other sports nutrition endpoints. This preclinical study was designed to evaluate the potential of ASI to reduce inflammatory markers and promote joint health, important endpoints to athletes, fitness enthusiasts and people with joint pain due to inflammation. The study recorded arthritis score, inflammation score, inflammatory markers, and serum and joint arginine and silicon levels upon administration of ASI in rats with collagen‐induced arthritis.MethodsFemale Wistar rats were reared at 22 ± 2°C in a 12/12 hour light/dark cycle and randomized into four groups (n=7 in each group; 8 weeks‐old):

Control group
Arthritic control group
Arthritic group supplemented with a simple mixture of arginine HCl + silicon + inositol (A+S+I) at doses equivalent to those in ASI
Arthritic group supplemented with ASI at a dose of 1.81 g/kg/day (corresponding to a human dose of 1500mg/day)
Rats were dosed for 30 days. On day 14 and day 29, rats were analyzed for arthritis score, inflammation score, and 10 inflammatory markers in the blood and tissue: TNF‐α, IL‐17, IL‐6, ghrelin, obestatin, sclerostin, DKK‐1, Cox‐2, NF‐κB, and B‐catenin.ResultsDay 29 arthritis scores and inflammation scores were both significantly lower in the ASI group (IV) compared to the arthritic control group (II) and the A+S+I group (III). Seven inflammatory markers tested in the blood — TNF‐α, IL‐17, IL‐6, ghrelin, obestatin, sclerostin, and DKK‐1 — were significantly lower in the ASI group (IV) compared to the arthritic control group (II). Four of five inflammatory markers tested in the tissue — Cox‐2, TNF‐α, IL‐6, NF‐κB, and B‐catenin — were significantly lower in the ASI group (IV) compared to the arthritic control group (II).ConclusionsASI supplementation significantly improved markers of inflammation and overall arthritis and inflammation score over the arthritic control group and the A+S+I group. These results demonstrate that ASI may be effective in reducing inflammation and that the ASI complex is more effective than a combination of the individual ingredients. ASI may also be of physiological benefit to athletes and fitness enthusiasts concerned with joint health and inflammation and to those experiencing joint pain due to inflammation.Support or Funding InformationFunding for this study was provided by Nutrition 21, LLC (Purchase, NY, USA) through a restricted grant.
Comparison of the Predictive Ability of an Empirical and a Literature‐derived Index of Dietary Inflammation Potential
Authors: Tabung Fred K. , Smith‐Warner Stephanie A. , Chavarro Jorge E. , Fung Teresa T. , Hu Frank B. , Willett Walter C. , Giovannucci Edward L. 
Published: November 2023

BackgroundInflammation plays an important role in the development of many chronic diseases and dietary factors can modulate inflammation. An empirical dietary inflammatory pattern (EDIP) comprised of food groups as reported on a food frequency questionnaire (FFQ) and a literature‐derived dietary inflammatory index (DII) comprised mainly of nutrients, exist to describe dietary inflammation potential.ObjectiveTo compare the ability of the EDIP and DII in predicting levels of inflammation markers in two cohorts.DesignBoth EDIP and DII scores were calculated from FFQ data reported by 5826 women in the Nurses' Health Study‐II and 5227 men in the Health Professionals Follow‐up Study. We used multivariable‐adjusted linear regression analyses to calculate relative concentrations of four plasma inflammation markers: C‐reactive protein (CRP), interleukin‐6 (IL6), tumor necrosis factor alpha receptor 2 (TNFαR2) and adiponectin across quintiles of the dietary indices.ResultsCorrelations between the EDIP and DII scores were modest (Spearman r=0.28, women; 0.23, men; all P<0.0001). In both women and men, higher index scores were associated with higher (lower for adiponectin) concentrations of inflammation markers, except for no association between DII and adiponectin in men. EDIP scores explained a higher proportion of variance in biomarker concentrations and with associations of higher magnitudes compared to DII scores except for IL6 in men; e.g., in EDIP quintile 5, the percent change in relative concentrations of biomarkers was: CRP, +23.2%; IL6, +2.4%; TNFαR2, +0.1%; and adiponectin, +13.9% higher compared to DII quintile 5 in women; and CRP, +5.8%; IL6, −9.7%; TNFαR2, +1.9%; and adiponectin, +9.1% higher in men.ConclusionDespite design differences, the EDIP and DII both assess dietary inflammation potential, with the EDIP showing a higher ability to predict concentrations of plasma inflammation markers in these cohorts. Both indices may be useful in predicting inflammation‐mediated diet‐disease associations.Support or Funding InformationDrs. Fred K. Tabung, Jorge E. Chavarro and Frank B. Hu were supported by National Institutes of Health (NIH) grants K99 CA207736, P30 DK046200 and U54 CA155426 respectively. The HPFS and NHS‐II cohorts are supported by NIH grants: UM1 CA167552 and UM1 CA176726, respectively