bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Exercise or Meditation on Reported Stress and Cortisol in an Undergraduate Population
Authors: Clarke Alicia M , Cohen Brian D 
Published: June 2021

Stress is a daily factor that is directly correlated with negative physiological and psychological effects including stroke, heart attacks and problem drinking. A stressor that is perceived by the body activates the hypothalamic‐pituitary‐adrenal (HPA) axis which causes the synthesis and release of the glucocorticoid hormone cortisol from the adrenal cortex. Studies have shown meditation or exercise programs help decrease stress and cortisol levels but this has not been tested in college‐aged adults. In this study, undergraduate students were assigned to either meditation, exercise or control groups for four weeks to measure the effects of introducing either meditation or increased exercise on reported stress and physiological response to stress in the form of salivary cortisol levels. Participants' stress was measured using the Revised Undergraduate Student Hassles Scale (RUSH‐S) which measures a variety of stressors including academic, social, and personal hassles. Students completed the RUSH‐S 3 times: at baseline and at 2 week intervals. Simultaneously, saliva samples were collected to analyze salivary cortisol levels using an enzyme‐linked immunosorbent assay (ELISA). A one‐way between subjects ANOVA was conducted to compare the effect of interventions on personal, academic and social stressors as measured by the RUSH‐S. Both personal and social stressors were reduced for the meditation and exercise groups compared to the control group (p=0.037 and p=0.052, respectively). No significant reduction of academic stress was observed in either group compared to the control. Cortisol levels tended to correlate with RUSH‐S results. This study suggests that interventions such as meditation or exercise may be beneficial to reducing stress in undergraduate populations.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Immunological Response to Chronic Stress in Obese Mice
Authors: Parsley Matthew , Burrage Emily , Marshall Kent D , Clemons Garrett D , Tice Abigail , Bryner Randy W , Brundage Kathleen , Kelley Eric E , Chantler Paul D 
Published: June 2021

Chronic stress is a major risk factor for cardiovascular disease. We have shown that chronic stress, which acts as a trigger for anxiety and depression, significantly reduces vascular function in obese rats and mice. Such vascular dysfunction is linked to an increase in systemic inflammation. The spleen and adipose tissue are major sources of these peripheral immune cells. We sought to identify the immunological changes in the spleen after chronic unpredictable stress (UCMS).Spleen and gonadal adipose tissue immune cells from male obese mice who underwent either 8 weeks of non‐UCMS (controls, n=6) or UCMS (n=6) for 5 days/week/7Hrs/day to elicit a depressive phenotype were analyzed by flow cytometry.Spleen size was 23% lower (p=0.08) in the UCMS group vs. controls, yet the body weight for the UCMS mice was reduced compared to obese controls (48±0.7 vs. 42±0.8, p<0.01), resulting in no differences in the ratio of spleen/body weight. To evaluate and quantify changes in the cellular immune composition of the spleen with UCMS, we harvested spleens from control and UCMS obese mice. UCMS mice tended to have lower numbers of CD45 compared to controls. Although no differences in CD8, CD4 or the CD4/CD8 ratio, or B‐cells were noted, the number of M2 macrophages were generally lower in the UCMS vs. control group, with no differences in M1 macrophages. In the visceral adipose tissue, CD45+ cells were lower in the UCMS group, which was accompanied by a lower number of CD8+ and CD4+ cells in the UCMS groups.Our data suggests that chronic stress in obese mice alters the immune cell populations in the spleen and visceral fat of obese mice. Given that these tissues play an important role in the release of immune cells into the systemic circulation, the immune changes could play an important role on the vascular dysfunction noted in our mice with exposure to chronic stress.Support or Funding InformationOD016165 (KB)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hepatic Knockdown of RECK Increases NASH Susceptibility
Authors: Cunningham Rory P. , Moore Mary P. , Nguyen Nhu , Dashek Ryan , Boccardi Luigi , Jepkemoi Vivien , Meers Grace M. , Chandrasekar Bysani , Rector R. Scott 
Published: June 2021

IntroductionNonalcoholic steatohepatitis (NASH) is characterized by hepatic steatosis, hepatocellular inflammation and fibrosis. Reversion‐inducing‐cysteine‐rich protein with Kazal motifs (RECK) exerts anti‐fibrotic effects in the heart, although its role in NASH is unknown. We have previously shown that western diet (WD)‐induced NASH and fibrosis were associated with RECK downregulation in the liver. Here, we examined whether RECK knockdown, specifically in liver, increases NASH susceptibility.MethodsHomozygous RECK floxed mice on a C57/BL6J background were injected with either an AAV8‐TBG‐Cre (1×1012) (RECK‐KD) for liver‐specific knockdown of RECK or an AAV8‐TBG‐GFP control (RECK‐CON). Following AAV injections, mice (n = 5–8) were fed either a control diet (CD; 10% fat) or WD (45% fat, 17% sucrose) for 8 weeks. An additional set of mice injected with AAV8‐TBG‐Cre or AAV8‐TBG‐GFP were fed WD for 30 weeks (n = 8).ResultsAfter 8 weeks, WD feeding significantly increased body weight and body fat percentage vs CD (p≤0.05). There were no differences in animal characteristics between RECK‐KD and RECK‐CON in either CD or WD groups. Nonalcoholic fatty liver disease activity score (NAS; combination of steatosis, ballooning, and inflammation) was significantly elevated in WD vs CD fed mice (p<0.05), with further exacerbation with RECK‐KD for NAS and inflammation scores (main effect for genotype, p<0.05). Furthermore, RECK‐KD mice had a ~3‐fold increase in hepatic fibrosis compared to RECK‐CON (main effect for genotype, p≤0.05). Thirty weeks of WD feeding significantly elevated NAS (p<0.01) and fibrosis scores (P<0.01) compared with 8 weeks of WD feeding. In addition, RECK knockdown exacerbated NAS (p<0.05), inflammation score (p=0.001), and fibrosis (p=0.06) compared to RECK‐CON mice following 30 weeks of WD feeding. Further investigations revealed that RECK‐KD (vs. RECK‐CON) expressed significantly higher IKK‐β gene expression (p<0.05), along with trends for increases in hepatic inflammatory markers NF‐κB, TGF‐β, and JUN at 30 weeks. Expression of matrix metalloproteases‐2 and −14 also tended to be elevated in RECK‐KD mice (vs RECK‐CON) at 30 weeks.ConclusionHere we demonstrate for the first time that liver‐specific RECK knockdown exacerbates western diet induced NASH. Further investigation is warranted to determine the role and precise mechanisms by which RECK regulates hepatocellular inflammation and NASH progression.Support or Funding InformationVA Merit Grant I01BX003271‐01 (R.S.R.), VA Merit Grant I01BX004220‐01 (B.C.)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Systemic Exposure of Orally Ingested Fructose is Similar between Fructose‐tolerant and Fructose‐intolerant Functional Gastrointestinal Disorder (FGID) Patients
Authors: Lee Sze Han , Low Jing Yi , Kioh Dorinda Yan Qin , Wilder‐Smith Clive , Chan Eric Chun Yong 
Published: June 2021

BackgroundDietary intolerance to fructose is common (60%) in Functional Gastrointestinal Disorder (FGID) patients, yet poorly characterized and empirically managed. Fructose is postulated to be malabsorbed in fructose‐intolerant FGID patients, resulting in gastrointestinal symptoms when unabsorbed fructose is fermented by gut microbiota to form gases. Malabsorption can be indirectly characterized by gas breath tests (i.e. methane, hydrogen) and measurement of systemically absorbed fructose and its metabolites. However, both methods are typically done independently, and the mechanism leading to fructose intolerance remains poorly understood.ObjectiveWe aim to correlate plasma fructose and its metabolites in FGID patients after fructose ingestion in their relation to fructose intolerance.MethodsThirty‐one FGID patients, as defined by Rome III criteria, were enrolled into a randomised crossover study in Switzerland (1). Blood (plasma) were collected at 0, 0.5, 1 and 2 h post‐ingestion of 35g fructose or water. Plasma fructose and its metabolites (glucose, alanine, lactate, glycerate) were quantified via liquid chromatography tandem mass spectrometry. Symptoms were recorded using standardized questionnaires, while breath concentrations of hydrogen and methane were measured via BreathTracker Analyzer.ResultsIntolerance symptoms correlated positively with hydrogen (r=0.7175) and methane (r=0.6093) breath test over the 2 h period, with fructose‐intolerant patients producing significantly more hydrogen (p = 0.0406) and methane (p=0.0400) than fructose‐tolerant patients. However, intolerance symptoms correlated poorly with systemic exposure (AUC0–2h) of fructose (r=−0.0066). AUC0–2h of fructose and its metabolites (glucose, alanine, lactate, glycerate) were similar between fructose‐tolerant and fructose‐intolerant phenotypes.ConclusionFor the first time, our study demonstrated fructose intolerance and its higher levels of gases are not associated with fructose malabsorption. Our findings alluded to the potential role of modulated gut microbiota activity in characterizing the differential fructose fermentation phenotypes.Support or Funding InformationFunded by Brain‐Gut Research Group, Bern, SwitzerlandThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Obesity and Exercise on Pancreatic Oxidative Stress, Morphology, and Health
Authors: Tice Abigail , Branyan Kayla W , DeVallance Evan R , Marshall Kent L , Kelley Eric , Olfert Mark , Chantler Paul D , Bryner Randy 
Published: June 2021

Obesity is concomitant with hyperglycemic conditions and increased oxidative stress. Under hyperglycemia, thioredoxin interacting protein (TXNIP) causes increased oxidative stress and β‐cell apoptosis within the pancreas.Lean rats (LZR) and obese rats (OZR) were randomly assigned to control (n=12) and exercise (n=12) groups. Exercise LZR (n=6) and OZR (n=6) underwent 8 weeks of multi‐lane motor treadmill running for 60 minutes at 60–70% maximum determined intensity. Pancreas tissue was harvested at approximately 20 weeks and mounted on cork using OTC freezing medium.Pancreas sections of 8μm thickness were cut and collected on slides then stained using DAPI and Alexa‐Fluor 546 targeting primary insulin antibodies. Slides were then imaged using the Zeiss LSM 510 Confocal microscope and Zeiss computer software; islet area and β‐cell number were determined. Nitrate analysis was measured using the Sievers Nitric Oxide Analyzer (NOA 280) using pancreas lysates. The WES system was used for Western analysis of TXNIP protein quantification.Body mass, glucose and insulin were significantly greater in OZR vs LZR (p<0.05). OZR also had higher beta‐cell numbers and islet areas to LZR (Table 1), although not significant. There was an almost 3‐fold increase in TXNIP in OZR compared to LZR (p=0.03). OZR that exercised experienced an approximate 2‐fold decrease in TXNIP expression when compared to the OZR control (p=0.02). No difference was observed between OZR exercised and LZR control (p=0.18).This study showed an increase in the expression of TXNIP in the pancreas of obese compared to lean groups. Eight weeks of treadmill running was associated with decreasing the expression of TXNIP in OZR to almost the same level as the LZR controls, suggesting that exercise may be used as a means to reduce oxidative stress even in a hyperglycemic obese environment.Current studies are being conducted to further assess markers of oxidative stress and nitric oxide associated with these perturbations, as well as pro‐apoptotic markers within the pancreas.Support or Funding InformationNIHGMS 5U54GM104942‐03 (PDC)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Alterations to the Gut Microbiome Prevent Glucocorticoid induced Osteoporosis
Authors: Schepper Jonathan , Rios‐Acre Naiomy , Collins Fraser , Parameswaran Narayanan , McCabe Laura 
Published: June 2021

Glucocorticoids are important anti‐inflammatory drugs that can have significant side effects including glucocorticoid‐induced osteoporosis (GIO). Glucocorticoids directly induce apoptosis of osteoblasts and osteocytes but have also been shown to alter the gut microbiota composition. Previously, our lab and others have shown that the microbiota is involved in the regulation of bone density, however, little is known about the role of the gut in regulating GIO. Therefore, we investigated the role of microbiota alterations in GIO. Male C57BL/6J (16‐weeks‐old) mice received 8‐weeks of glucocorticoid treatment (GC, 2.5 mg/kg/day, slow release pellet subQ) with or without chronic antibiotic treatment (ABX, ampicillin and neomycin) to deplete the microbiota. Strikingly, the ABX‐GC mice did not lose bone, whereas the non‐ABX GC mice lost 40% trabecular bone volume. Based on this previously unknown link between microbiota and GIO, we examined if GIO can be prevented by using probiotics to modify the microbiota of the GC mice. Male mice were GC treated with or without oral Lactobacillus reuteri (LR; 108 cfu/day) supplementation. After 8 weeks, analyses of stool and colon samples revealed that LR treatment significantly alters the microbiota composition compared to GC treated mice. More importantly, LR treatment prevented GIO. Analyses of intestinal permeability established that GC treatment increases intestinal permeability, an outcome that was prevented by treatment with chronic ABX and LR. To determine if intestinal barrier function was mechanistically important for GIO, we treated GC‐mice with a mucus supplement (MDY). Strikingly, enhancement of barrier function prevented both GC‐induced barrier dysfunction and GIO. Together these data highlight the unappreciated role of the gut microbiota in GIO pathogenesis, and identify novel therapeutic targets for preventing GIO.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Consequences on Gametogenesis and Reproduction Performances of a High Carbohydrate Nutrition During the Whole Reproductive Cycle of Male and Female Trout
Authors: Marandel Lucie , Hu Huihua , Liu Jingwei , Mennigen Jan , Bobe Julien , Corraze Geneviève , Burel Christine , Panserat Stéphane 
Published: June 2021

Salmonids and more particularly rainbow trout are carnivorous species, and thus usually consider as glucose‐intolerant (GI) species and poor user of dietary carbohydrates displaying a decrease in growth and a persistent postprandial hyperglycaemia when fish meal is substituted at more than 20% by digestible carbohydrates in the diet. Nevertheless, these findings were mainly deduced from experiments conducted on immature juvenile trout and only scarce data are available in sexually mature males and females. In this regard, we investigated the impact of a high carbohydrate diet (HC diet) on gametogenesis and reproductive performances of 2 year‐old broodstocks fed with such a diet a whole year. Our results showed that both males and females ate and growth well when fed the HC diet even if, at the end of the trial, males, but not females, displayed growth retardation compared to control males. The glycaemia of fish fed the HC diet was higher than fish fed the control diet independently of the sex but these fish were not hyperglycaemic. Surprisingly, both sex displayed a precocious maturation. Whole body and gonads biochemical composition of fish did not differ during the whole year from one treatment to the other whereas liver of fish fed the HC diet retained more glycogen but less proteins compared to the control fish. We also monitored glucose metabolism modifications at the molecular level in both livers and gonads at different gametogenesis time points. Our results demonstrated that glucose metabolism strongly varied in female liver during gametogenesis independently of the diet whereas in male no significant difference where found. By contrast in both ovaries and testis, glucose metabolism related genes were found differentially expressed during gametogenesis but independently again of the diet. At spawning period, we performed cross‐fertilization between groups. For the 4 groups, both fertilization and early developmental rate were equivalent from one group to the other. In overall, our results highlight strong but sex‐dependent effects of a high carbohydrate diet on both oogenesis and spermatogenesis and a variation of glucose metabolism in both liver and gonads. However, these effects do not seem to affect reproductive performances.Support or Funding InformationThis study was supported by the French National Research Agency (ANR‐18‐CE20‐0012‐01 ‘SweetSex’).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Metabolic Consequences of Exposure to Maternal High Fat Diet in Offspring
Authors: Thakali Keshari M , Piccolo Brian D , Sikes James D , Wahl Elizabeth C , Shankar Kartik 
Published: June 2021

The increased risk for obesity in offspring born to obese mothers may be driven by changes in energy expenditure. To examine the effects of maternal high fat diet (HFD)‐induced obesity on offspring energy expenditure, female C57BL6/J mice were fed a control (17% fat, TD95092) or HFD (45% fat, TD8811) ad libitum for 12 weeks prior to and during pregnancy and during lactation. Female mice were bred with lean male mice at 17 wk of age. At weaning, male offspring from control and HFD‐dams were randomized to control (C) or HFD (H), provided ad libitum, generating 4 groups of offspring: CC, CH, HC, and HH, where the first letter corresponds to maternal diet and the second to offspring post‐weaning diet. At 20 weeks of age, energy intake and expenditure (EE) were assessed in male offspring over 48 h using the Promethion Continuous Indirect Calorimetry system (Sable Systems). HFD consumption in offspring was associated with reduced respiratory exchange ratio (RER, CC vs CH: 0.89±0.02 vs 0.82±0.02; p<0.01, n=13–16). There was no effect of maternal HFD on offspring RER (CC vs HC, p= 0.66; CH vs HH, p=0.54). To examine the effect of maternal HFD on offspring energy expenditure, ANCOVA using offspring total body weight (measured at the beginning of the indirect calorimety experiment) as a covariate for the 48 h recording period (both light and dark cycles) was performed. When comparing the effect of maternal HFD in offspring fed either a control diet (CC vs HC) or HFD (HC vs HH) postweaning, the covariate (offspring total body weight) significantly predicted EE for both comparisons (CC vs HC, p<0.05; HC vs HH, p = 0.05), while there was no significant effect of maternal diet on EE. Offspring food intake (in both light and dark cycles) was not altered by maternal HFD (CC vs HC, p=0.22; CH vs HH, p=0.21). In control‐fed offspring, maternal HFD had no effect on body weight at 20 wk of age (CC vs CH, 26.84±0.79g vs 28.91±1.03g, p=0.12), while in HFD‐fed offspring, males exposed to maternal HFD were significantly heavier than males from control‐fed dams (CH vs HH, 33.81±1.46g vs 38.42±1.59g, p=0.04). The observed changes in RER indicate that offspring post‐weaning HFD, but not maternal HFD, is associated with a shift in substrate utilization, specifically with increased fat oxidation in response to post‐weaning HFD. In the context of maternal HFD, the EE data suggest that offspring total body weight, and not maternal obesity may be driving offspring changes in energy expenditure.Support or Funding InformationUSDA ARIS Project 6026‐51000‐010‐05SThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Sex‐dependent protection from high fat diet‐induced metabolic disease in mice lackingDegenerin proteins
Authors: Drummond Heather , Mitchell Zachary , Hildebrandt Emily , Stec David E 
Published: June 2021

Degenerin proteins, such as βENaC and ASIC2, and Transient Receptor Potential Channel 6 (TrpC6) have been implicated in cardiovascular function. However, their roles and potential interaction in metabolic disease has not been studied. To begin to assess this interaction, we evaluated the impact of a high fat diet (HFD) on in mice lacking normal levels of ASIC2, βENaC and TrpC6. Twenty week old male and female mice were placed on a 60% HFD for 12 weeks. Body weight was measured weekly, body composition by non‐invasive ECHO MRI and fasting blood glucose were measured at 0, 4, 8 and 12 weeks. A glucose tolerance test was administered after 12 weeks. Differences between ASIC2/βENaC/TrpC6 and WT groups were compared using independent t‐tests within each sex. Data are presented as mean ± SEM, ASIC2/βENaC/TrpC6 vs. WT. At 20 weeks of age, female ASIC2/βENaC/TrpC6 mice (n=6) weighed less (22.7±1.0 vs 26.3±0.8g, p=0.029) and gained less weight (12.1±1.7 vs. 20.5±1.3g, p=0.004) than WT (n=5). Total body fat (16.2±2.0 vs 23.2±1.1g, p=0.017) and lean body masses (19.2±1.0 vs 24.8±0.7, p=0.0014) were reduced in female ASIC2/βENaC/TrpC6 mice. In contrast, male ASIC2/βENaC/TrpC6 (n=5) mice had similar body weight (34.1±0.8 vs. 36.8±1.8g, p=0.165) at 20 weeks and 12 week HFD weight gain (11.8±1.5 vs. 12.1±0.9g, p=0.881) compared to WT (n=4). Fasting blood glucoses were lower in female (166±6.4 vs.212±5.3 mg/dL, p=0.0004) and male (181±2.8 vs.210±9 mg/dL, p=0.006) ASIC2/βENaC/TrpC6 mice after 12 weeks HFD. The area under the curve for the glucose tolerance test was reduced in female (18263 ± 510 vs 34623±4719 min.mg/dL), but increased in male (26100±1639 vs. 19408±1364 min.mg/dL) ASIC2/βENaC/TrpC6 mice. Liver (0.83±0.05 vs. 1.93±0.34g, p=0.0066) and liver fat (0.011±0.007 vs.0.333±.158, p=0.05) masses, as well as percent liver fat (1.1±0.6 vs. 14.4±4.1%, p=0.006), were reduced in female ASIC2/βENaC/TrpC6 mice after HFD. While liver (1.77±0.13 vs. 2.49±0.15g, p=0.007) and liver fat (0.17±.06 vs. 0.37±.03g, p=0.044) masses were reduced in male ASIC2/βENaC/TrpC6 mice, percent liver fat was not statistically lower (8.8±2.6 vs. 14.7±0.7%, p=0.11). These highly novel findings suggest that ASIC2, βENaC and/or their interaction with TrpC6, protects against HFD induced‐metabolic disease in female, but not male, mice. The mechanisms underlying this response will be examined in future studies.Support or Funding InformationThis work was support by NIH P01HL051971, P20GM104357, P20GM121334 and R01HL136684.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.