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Funding | There was no funding for this work. | PMC10523642 | ||
Availability of data and materials | The trial has been registered at ClinicalTrials.gov (identifier NCT03590509). Deidentified individual participant data will not be made available. | PMC10523642 | ||
Declarations | PMC10523642 | |||
Ethics approval and consent to participate | Ethics approval was obtained from all participants, as described in Mosquera et al. | PMC10523642 | ||
Consent for publication | All the authors have consented to the publication. | PMC10523642 | ||
Competing interests | The authors declare that they have no competing interests. | PMC10523642 | ||
References | PMC10523642 | |||
2. Materials and Methods | PMC10000597 | |||
2.2. Mouse Splenocyte Stimulation and Enzyme-Linked Immunosorbent Assay–Based Detection of Cytokines | LYSIS, FRANKLIN | The mouse spleen was excised, passed through a 45 µm cell strainer (BD Biosciences, Franklin Lakes, NJ, USA) for conversion into a single-cell suspension, then subjected to red blood cell lysis by using RBC lysis buffer (eBiosciences Inc., San Diego, CA, USA). Isolated splenocytes were seeded into a 96-well-plate at a cell density of 4 × 10 | PMC10000597 | |
2.3. Antimicrobial Susceptibility Profiling | SEPARATION, FRANKLIN, MRS | Antimicrobial susceptibility was determined by using the broth microdilution method and lymphocyte separation medium (LSM, including 90% IST medium [Cat. No. CM0473; Oxoid, Basingstoke, Hampshire, UK] and 10% MRS medium (Cat. No. 288130; Difco Laboratories Inc., Franklin Lakes, NJ, USA) in accordance with the guidelines of the Quality and Standards Authority of Ethiopia (ES ISO10932:2012). Twofold dilutions of clinically relevant antibiotics (clindamycin, chloramphenicol, erythromycin, gentamicin, kanamycin, streptomycin, tetracycline, and ampicillin, all from Sigma-Aldrich, Saint Louis, MO, USA) were prepared in LSM. Approximately 50 μL of 6 × 10 | PMC10000597 | |
2.4. DNA Extraction, Whole-Genome Sequencing, and Hybrid Genome Assembly | We established a whole-genome sequencing (WGS) assembly pipeline in accordance with a previously reported procedure [ | PMC10000597 | ||
2.5. Annotation of Protein-Coding Genes, Virulence Factors, and Antibiotic Resistance | The protein-coding genes in the GM-080 genome were annotated by using Prokka [ | PMC10000597 | ||
2.6. OVA-Induced AHR Mouse Model | Allergic airway inflammation | Seven-week-old female BALB/c mice were purchased from The Experimental Animal Facility of the College of Medicine, National Taiwan University (Taipei, Taiwan). Allergic airway inflammation was induced with an intraperitoneal injection of 50 µg of OVA (purchased from Sigma-Aldrich) mixed with the Th2-adjuvant aluminum hydroxide on day 0 and was followed by the administration of 25 µg of OVA on days 14, 28, 42, and 56 to sensitize the mice and then by intranasal challenge with OVA (100 µg) on days 67 and 68. Sera were collected from the retro-orbital sinus on the day before the first OVA sensitization; on post sensitization days 35, 49, and 63; and on the day of sacrifice. | PMC10000597 | |
2.7. ELISA Determination of OVA-Specific Immunoglobulins | A 96-well plate was coated with OVA at 1 µg/well and then incubated with blocking solution (1% bovine serum albumin in PBS buffer) at room temperature. The wells were added with mouse serum followed by antibodies diluted with the blocking solution (1:50, 1:1000, and 1:10,000 dilutions for IgE, IgG2a, and IgG1, respectively) and incubated at 4 °C overnight. Biotin-conjugated antibodies against mouse IgE, IgG1, or IgG2a (BD Biosciences) were added after the wells were washed with 0.05% Tween-20/PBS buffer. Then, the plate was incubated at room temperature for 2 h. Next, streptavidin-conjugated horseradish peroxidase was added to the wells. 3,3′,5,5′-Tetramethylbenzidine substrate was used for color development. After the termination of the reaction by using 2 N H | PMC10000597 | ||
2.8. AHR Determination | In mice, the development of AHR was determined on a Buxco system (Biosystem XA; Buxco Electronics, Sharon, CT, USA). The enhanced pause (Penh) values were calculated with the following formula: ( | PMC10000597 | ||
2.9. BALF Collection and White Blood Cell Count | BALF was collected through lung flushing with HBSS buffer containing 2% bovine serum albumin three times by using a trachea cannula (Angiocath, BD Biosciences). BALF cells were then collected through centrifugation at 300× | PMC10000597 | ||
2.10. Patient Recruitment | PAR was diagnosed in accordance with the definition of Saleh and Durham, i.e., symptoms lasting more than 4 days per week and illness duration lasting more than 4 weeks [ | PMC10000597 | ||
2.11. Randomized, Double-Blind, Placebo-Controlled Trial Design | ALLERGY | The randomized, double-blind, placebo-controlled trial on PAR was designed in accordance with the guidance for developing drug products for AR treatment published by the Division of Pulmonary, Allergy, and Rheumatology Products in the Center for Drug Evaluation and Research at the Food and Drug Administration (April 2000 version). All patients who met the eligibility criteria were randomized to either the probiotic-treated or control group. In total, 137 patients were double-blinded and randomized to four groups, namely, one placebo group and three groups that received live GM-080 at different dosages: group A (2 × 10 | PMC10000597 | |
2.12. Skin Prick Tests and Serum Biomarkers | SKIN | Skin prick tests were performed with commercial allergen extracts of egg, milk, crab, mite, cockroach, and animal dander (ALK-Abell & Oacute, Round Rock, TX, USA). Skin reactivity to allergen sensitization was classified into four grades as previously described [ | PMC10000597 | |
2.13. Statistical Analysis | inflammation | INFLAMMATION | The data from in vitro and OVA-induced airway inflammation mouse model experiments were presented as means ± standard deviations and were analyzed for differences between groups by using one-way analysis of variance (ANOVA), followed by Tukey’s Honestly Significant Difference test. The chi-square test was conducted to compare clinical symptoms. Intragroup comparisons for TNSSs and blood biomarkers at baseline and 3 months after treatment commencement were carried out by using paired | PMC10000597 |
3. Results | PMC10000597 | |||
3.1. GM-080 Induces Th1 Cytokine Production in Mouse Splenocytes | The Th1 cytokines of IFN-γ or IL-12 have been demonstrated to suppress AHR in response to allergens [ | PMC10000597 | ||
3.2. WGS Analysis Revealed That GM-080 Is a Safe L. paracasei Strain | We performed WGS analysis on GM-080 by using next-generation sequencing. The genetic organization of GM-080 was illustrated in a genome atlas created by using Circos ( | PMC10000597 | ||
3.3. GM-080 Genome Contains Immunosuppressive Motifs and CpG-Containing Oligonucleotides That Induce Th1 Cytokines in Mouse Splenocytes | We compared the genomes of GM-080 and BCRC 16100 to identify the potential functional genes in GM-080. As indicated by the phylogenetic tree ( | PMC10000597 | ||
3.4. Orally Gavage GM-080 Alleviates OVA-Induced Allergic Airway Inflammation in Mice | We established an OVA-induced AHR mouse model by using the protocol shown in | PMC10000597 | ||
3.5. GM-080 Alleviates PAR in Children | Finally, we conducted a double-blind, randomized, placebo-controlled trial to investigate the beneficial effects of GM-080 in children with PAR. The study design was summarized in We next examined the effects of GM-080 on patients’ quality of life by using TNSSs. TNSSs are a convenient tool for symptom description and the assessment of functional problems (physical, emotional, social, and occupational) associated with AR. We noted a nonsignificant decrease in TNSSs over time in groups A, B, and C (Additional well-designed clinical trials are warranted to identify the most effective dosage of GM-080. | PMC10000597 | ||
Supplementary Materials | The following supporting information can be downloaded at: Click here for additional data file. | PMC10000597 | ||
Author Contributions | W.-H.T. designed the in vitro and animal studies. C.-H.C. performed the in vitro and animal studies. J.-H.J. performed the WGS analysis. W.-H.T. and I.-J.W. analyzed the data. E.-K.L., W.-W.C., W.-H.T. and I.-J.W. wrote the article. All authors have read and agreed to the published version of the manuscript. | PMC10000597 | ||
Institutional Review Board Statement | The study was conducted in accordance with the Declaration of Helsinki, and approved by the Institutional Review Board of Taipei Veterans General Hospital (Taipei City, Taiwan) with a reference number of 05-016-A at the date of 13 November 2006, and it was registered on ISRCTN registry (ISRCTN14829274, | PMC10000597 | ||
Informed Consent Statement | Informed consent was obtained from all subjects involved in the study. Written informed consent has been obtained from the patient(s) to publish this paper. | PMC10000597 | ||
Data Availability Statement | The whole genome sequencing data of BCRC 16100 were available in GenBank | PMC10000597 | ||
Conflicts of Interest | Taipei Hospital, Ministry of Health and Welfare Authority has a contract with GenMont Biotech, which provided funds for probiotics. W.H.T. and C.H.C. are the employee in GenMont Biotech. | PMC10000597 | ||
Abstract | Acute exercise suppresses appetite and alters food‐cue reactivity, but the extent exercise‐induced changes in cerebral blood flow (CBF) influences the blood‐oxygen‐level‐dependent (BOLD) signal during appetite‐related paradigms is not known. This study examined the impact of acute running on visual food‐cue reactivity and explored whether such responses are influenced by CBF variability. In a randomised crossover design, 23 men (mean ± SD: 24 ± 4 years, 22.9 ± 2.1 kg/mWe investigated the impact of a single running bout on cerebral blood flow (CBF) and food cue reactivity using functional magnetic resonance imaging (fMRI) in healthy men. Running did not alter the time‐course of grey matter or regional CBF up to 30 min after exercise cessation but increased food cue reactivity in brain regions implicated in attention, reward and episodic memory retrieval. Exercise‐related BOLD signal changes were detected in the presence of underlying CBF.
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INTRODUCTION | SECONDARY | The interaction of exercise with appetite control and food intake attracts widespread interest due to the ability of exercise to influence weight management (Blundell et al., Appetite‐related brain responses can be explored using blood‐oxygen‐level‐dependent (BOLD) functional magnetic resonance imaging (fMRI), which is often performed during visual food cue reactivity tasks (Dagher, Exploring immediate exercise‐induced effects on food cue reactivity could be influenced by the dynamic cardio‐pulmonary changes that alter cerebrovascular function in response to an exercise bout. The elevated brain neural activity and metabolic demands of exercise are met by a concomitant increase in cerebral blood flow (CBF) up to intensities of ~60% of maximum oxygen uptake beyond which CBF typically declines towards baseline values (Ogoh & Ainslie, Investigations of the time‐course of exercise‐induced changes in regional CBF have demonstrated both increased (Steventon et al., The primary aims of this study were to (i) track the temporal pattern of CBF in the immediate post‐exercise period to identify the optimum time to conduct fMRI acquisitions using a food cue paradigm and (ii) determine the importance of accounting for CBF effects that may influence the BOLD signal during a food cue reactivity task. As a secondary aim, we sought to characterize the effect of acute exercise on neural responses to food cues varying in energy density. It was hypothesized that exercise would increase grey matter and regional CBF compared to a resting control trial, but the changes would show a time‐dependent effect, returning to baseline within 30 min of exercise cessation. | PMC10203797 | |
METHODS | PMC10203797 | |||
Ethical approval and participant eligibility | RECRUITMENT | The study received approval from Loughborough University's Research Ethics Sub‐Committee. Twenty‐three healthy men provided written informed consent to participate in the study. Recruitment was restricted to men as previous work has identified sex‐based differences in neural responses to visual food cues particularly under fasted conditions (Chao et al., Participant characteristics.
Abbreviation: MET, metabolic equivalent. | PMC10203797 | |
Preliminary measures | Participants were screened to determine eligibility for the study and completed questionnaires assessing general health status, MRI safety, habitual physical activity levels (short form International Physical Activity Questionnaire; Craig et al., | PMC10203797 | ||
Experimental design | SE, HED | Using a within‐measures, crossover design, participants completed two experimental trials in a random order separated by at least 1 week: (1) exercise and (2) control. The study design is presented in Figure Schematic of the study protocol. (a) Timeline of the trial procedures and functional magnetic resonance imaging (fMRI) scan protocol. Scans were conducted before and after 60 min of running and rest and involved iterations of the following sequences: (1) 3D sagittal T1‐weighted fast spoiled gradient echo (FSPGR) anatomical; (2) pseudo‐continuous arterial spin labelling (pCASL); (3) task‐based blood‐oxygen‐level‐dependent (BOLD) fMRI; and (4) spin‐echo echo‐planar imaging (SE EPI). Ratings of perceived appetite were measured using visual analogue scales (VAS). (b) Block design of the task‐based BOLD fMRI scan. Participants viewed eight blocks containing visually matched images of high‐ and very high‐energy density foods (HED) (total | PMC10203797 | |
Main trials | HEART, STAGGERED | Participants were instructed to consume 250 mL of plain water before arrival at the laboratory between 08:00 and 08:30 having fasted overnight for at least 12 h. Body mass and body fat percentage were measured at the start of each trial using bioelectrical impedance analysis (Seca Ltd, Hamburg Germany). After 20 min of seated rest, participants underwent a baseline fMRI scan for the assessment of CBF and food cue reactivity. Baseline fMRI scans were staggered to start at either 08:45 or 09:30 and participants were scanned in identical time slots for both trials. After the baseline fMRI scan, participants rested in a semi‐supine position for 60 min in the control trial or ran for 60 min at ~70% of their peak oxygen uptake during the exercise trial. Heart rate was monitored continuously during exercise, and breath‐by‐breath exhaled gas samples were measured in both trials to calculate the net energy expenditure and substrate oxidation during exercise (Frayn, | PMC10203797 | |
Ratings of perceived appetite | fullness | Subjective ratings of hunger, fullness, satisfaction and prospective food consumption were recorded using 100 mm visual analogue scales (Flint et al., | PMC10203797 | |
Food cue paradigm | HED | During the food cue reactivity task, four categories of colour images were presented in a single run using a block design: (1) very low‐ and low‐energy density foods (LED; Stimuli were presented in eight blocks each containing five images from the LED, HED and non‐food object categories, which were interspersed with 16 blocks each comprised of five scrambled images (Figure Participants viewed the stimulus via a mirror attached to the head coil on a MR‐compatible monitor at the head of the scanner. Visual stimulus presentation and synchronization to fMRI acquisition was controlled using the software package Presentation® version 21.1 (Neurobehavioral Systems, Inc., California, USA). Images were marginally offset from the centre of the screen and participants used a hand‐held button box connected to a Lumina LSC‐400 controller (Cedrus Corporation, California, USA) to indicate left or right position to ensure they were attentive during the task. At the end of the study, food images were rated for familiarity, consumption and liking, and object images were rated for familiarity, using an online survey (supplementary results, Section | PMC10203797 | |
Structural and functional MRI was performed on a GE 3.0 T Discovery MR750w scanner (General Electric, Boston, USA) using a 32‐channel head coil. A timeline of the scan protocol is shown in Figure | PMC10203797 | |||
Analysis of functional data (pCASL and task based) was conducted in the FMRIB Software Library (FSL) version 6.0.4 (Jenkinson et al., | PMC10203797 | |||
Pre‐processing stages and regions of interest | Detailed information on pre‐processing of functional data is presented in the supplementary methods (Section | PMC10203797 | ||
Main analysis | PMC10203797 | |||
Pseudo‐continuous arterial spin labelling | Using a non‐parametric permutation approach in FSL's Randomise (Winkler et al., a the Separate models were run for each grey matter and ROI mask using threshold‐free cluster enhancement (TFCE) and a family‐wise corrected | PMC10203797 | ||
Task‐based fMRI | HED | In whole‐brain analysis at the first level, explanatory variables were entered into a general linear model in FSL's fMRI Expert Analysis Tool (FEAT) for the three image categories (LED, HED and non‐food cues) with a separate model run for each scan session per participant. Three contrasts were defined to examine responses to food cues minus non‐food objects ([i] food [HED + LED] > non‐food cues; [ii] HED > non‐food cues; and [iii] LED > non‐food cues) and a further two contrasts were defined to compare responses between high‐ and low‐value foods ([iv] HED > LED; and [v] LED > HED). The first three volumes (5.4 s) of the functional data were discarded to account for saturation effects. Clusters of activation were identified after thresholding the z‐statistic images at z > 3.1 using a corrected cluster significance threshold of The contrasts of parameter estimates generated at the first level were used to conduct higher‐level group analysis on the five contrasts in four stages:a a the a Analysis was performed both with and without adjustment for CBF by adding the appropriate CBF map as a voxelwise (confound) explanatory variable in the higher‐level FEAT model. Information on the peak value of activated clusters was obtained using the atlasquery tool in FSL (and the associated autoaq script), specifying the Harvard–Oxford cortical and subcortical atlases. The FSL tool FEATquery was used to extract the percentage change in BOLD signal for the peak of each activated cluster. | PMC10203797 | |
Regions of interest analysis | For the primary analysis, pre‐to‐post difference images for the exercise and control trials were created from the first level contrasts of parameter estimates to generate the input images. Paired In all functional analysis (pCASL and task‐based fMRI), only clusters comprising ≥10 continuous voxels are reported. In sensitivity models, all functional data were re‐analysed excluding participants who were left hand dominant ( | PMC10203797 | ||
Statistical analyses | The model residuals of the appetite perceptions were shown to follow a Gaussian distribution after inspection using histograms and are presented as mean ± SD unless indicated otherwise. Time‐averaged (per hour) area under the curve (AUC) values for each rating of perceived appetite were computed using the trapezium rule for the pre‐intervention (0–70 min) and intervention (70–190 min) periods. Between‐trial differences in time‐averaged intervention AUC for appetite perceptions were analysed with a linear mixed‐effects model using the In exploratory analyses, Pearson's product moment correlation coefficients or Spearman's rank correlation coefficients were calculated to explore associations of between‐trial changes in CBF (pCASL) or BOLD signal (task‐based fMRI) with the exercise net energy expenditure and between‐trial differences in appetite perceptions. Time‐averaged (per hour) total AUC (0–190 min) for appetite perceptions was used in the correlational analysis to incorporate responses during the entire study period (baseline, pre fMRI scan, intervention period and post‐fMRI scan). Correlations for pCASL were performed after calculating a session average for CBF in the exercise and control trials, and correlations for task‐based fMRI were conducted using the BOLD signal change in the peak voxel for activated clusters in the CBF‐adjusted primary analysis (whole brain only). | PMC10203797 | ||
RESULTS | PMC10203797 | |||
Exercise responses | Treadmill running was performed at an average speed of 11.6 ± 1.4 km/h which elicited a mean heart rate of 169 ± 14 beats/min and a mean oxygen consumption of 3.08 ± 0.39 L/min equivalent to 68% ± 3% of peak oxygen uptake. The non‐protein respiratory exchange ratio was 0.93 ± 0.03, which corresponded to a proportional energy contribution of 80% ± 10% carbohydrate and 20% ± 10% fat (assuming zero contribution from protein). The estimated net oxidation of carbohydrate and fat were 174 ± 35 g and 19 ± 9 g, respectively, with an estimated net energy expenditure of 3.62 ± 0.53 MJ. | PMC10203797 | ||
Ratings of perceived appetite | Time‐averaged intervention AUC for appetite perceptions (Figure Ratings of perceived (a) hunger, (b) fullness, (c) satisfaction and (d) prospective food consumption (PFC) in the control and exercise trials ( | PMC10203797 | ||
Grey matter and regional | PMC10203797 | |||
Baseline analysis | Grey matter and regional CBF was not statistically different between the exercise and control trial at baseline (all | PMC10203797 | ||
Primary analysis | CORTEX | Main effects of trial identified voxel clusters with greater CBF in the exercise than control trial in grey matter, bilaterally in the region of the amygdala/hippocampus and in the right posterior insula (all Differences in regional cerebral blood flow (CBF) measured using pseudo‐continuous arterial spin labelling (pCASL) in the (a) amygdala, (b) hippocampus and (c) insula between the exercise and control trial (Differences in regional cerebral blood flow (CBF) measured using pseudo‐continuous arterial spin labelling (pCASL) in the (a) orbitofrontal cortex (OFC) and (b) striatum between the exercise and control trial ( | PMC10203797 | |
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Whole‐brain analysis | HED | CORTEX | Activation in the left frontal pole and right central opercular cortex was lower at baseline in the exercise than control trial in response to food (HED + LED) versus non‐food cues and LED versus non‐food cues (Table CBF‐adjusted whole‐brain analysis results of voxel clusters activated in the baseline difference between the exercise and control trials in each contrast (
Abbreviations: BOLD, blood‐oxygen‐level‐dependent; Con, control trial; Ex, exercise trial; HED, high‐ and very high‐energy density foods; LED, very low‐ and low‐energy density foods; MNI, Montreal Neurological Institute. | PMC10203797 |
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Whole‐brain analysis | HED | Whole‐brain group analysis revealed exercise increased the neural response to food (HED + LED) versus non‐food cues and LED versus non‐food cues in the left paracingulate gyrus compared to control (Figure Voxel clusters showing greater blood‐oxygen‐level‐dependent (BOLD) activity in the pre‐to‐post change between the exercise versus control trial during a food cue reactivity task for the contrasts (a) food (HED + LED) versus non‐food cues and (b) HED versus non‐food cues (CBF‐adjusted whole‐brain analysis results of voxel clusters activated in the pre‐to‐post change between the exercise and control trials in each contrast (
Abbreviations: BOLD, blood‐oxygen‐level‐dependent; Con, control trial; Ex, exercise trial; HED, high‐ and very high‐energy density foods; LED, very low‐ and low‐energy density foods; MNI, Montreal Neurological Institute; post, fMRI scan performed after the exercise/rest period; pre, fMRI scan performed at baseline before the exercise/rest period. | PMC10203797 | |
Regions of interest analysis | HED | Greater pre‐to‐post reactivity to food (HED + LED) versus non‐food cues was identified in the left hippocampus in the exercise compared to control trial ( | PMC10203797 | |
Unadjusted | Analysis of food cue reactivity at baseline and in response to exercise without adjustment for CBF yielded broadly comparable findings to the CBF‐adjusted models and is presented in the supplementary results (Sections | PMC10203797 | ||
Exploratory correlations | fullness | REGRESSION | The exercise‐induced change in time‐averaged total AUC for fullness was positively correlated with the between‐trial difference in hippocampus (Correlation between the exercise‐induced change in (a) hippocampus and (b) striatum cerebral blood flow (CBF) measured using pseudo‐continuous arterial spin labelling (pCASL) and the exercise‐induced change in fullness time‐averaged total area under the curve (AUC) in 23 healthy men. Grey shaded area represents the 95% confidence interval of the regression line (black solid line). | PMC10203797 |
DISCUSSION | HED, adiposity, emotions and external stimulus‐orientated | RECRUITMENT, ADIPOSITY, CORTEX | The main findings from this study are that overall between‐trial differences in grey matter and regional CBF were apparent but the time‐course of CBF was not influenced directly by exercise in healthy young men. A single bout of running suppressed subjective appetite ratings and increased food cue reactivity in brain regions linked to attention, anticipation and encoding of reward, and episodic memory retrieval. However, the sensitivity of the exercise‐induced BOLD signal changes during a food cue reactivity task was not altered substantially after accounting for the underlying CBF.The main effect of trial analysis revealed that CBF was higher in grey matter, the posterior insula and in the region of the amygdala/hippocampus, and lower in the medial OFC and dorsal striatum in the exercise versus control trial. This extends previous findings demonstrating pre‐to‐post exercise alterations in ASL derived CBF quantified globally and in regions linked to cognitive processing (MacIntosh et al., Despite identifying overall between‐trial differences in CBF, we did not detect any temporal patterns in grey matter or regional CBF when tracked ~8–28 min after exercise/rest supported by the absence of any trial‐by‐time interactions. This appears to contrast previous findings that have reported pre‐to‐post exercise changes in CBF when assessed at multiple time‐points after exercise. Specifically, greater hippocampus CBF has been reported 15‐, 40‐ and 60‐min after a moderate‐intensity exercise bout (Steventon et al., Analysis of the BOLD data identified greater exercise‐induced food cue reactivity in the medial frontal pole, whereas reactivity to HED versus non‐food cues was lower in the middle frontal gyrus after exercise. Although knowledge of the precise function of these frontal cortical regions in human behaviour is still evolving, the medial frontal pole appears to hold distinct functions in self‐monitoring of emotions and external stimulus‐orientated thought (Bludau et al., The CBF‐adjusted primary model identified greater food cue reactivity in the paracingulate gyrus and posterior cingulate gyrus, located on the superior aspect and in the caudal region of the cingulate cortex, respectively, in addition to the precuneous cortex located adjacent to the posterior cingulate gyrus. Previous work has reported lower food cue reactivity in the posterior cingulate and cingulate gyrus after exercise (Crabtree et al., Alongside the elevated hippocampus CBF in the exercise trial, exercise evoked greater food cue responsiveness in this region of the temporal lobe which persisted after adjustment for CBF. This supports previous findings in children (Masterson et al., Our BOLD analysis also revealed lower reactivity to HED versus LED and greater reactivity to LED versus HED food images in response to exercise in the precentral gyrus. This region is primarily involved in motor responses but appears sensitive to food cue exposure (Huerta et al., Previous literature has demonstrated consistent but transient suppressions of appetite during and immediately after acute exercise bouts (Dorling et al., Key strengths of this study include the acquisition of adjacent pCASL and BOLD data and the food cue stimuli comprised distinct low and high hedonic value categories of known energy density which were confirmed to activate reward‐related brain regions. Furthermore, the pre‐intervention fMRI scan and the rest control trial allowed variability at baseline and without an exercise stimulus, respectively, to be captured appropriately in the analysis. A notable limitation is the recruitment of a small sample of healthy, lean young men and, therefore, future extension of this work to larger, more diverse and clinical populations is encouraged including women and in individuals with excess adiposity who typically display heightened food cue reactivity (Meng et al., | PMC10203797 |
CONCLUSION | Despite identification of overall between‐trial differences in CBF, acute vigorous‐intensity running did not directly influence the time‐course of CBF suggesting food‐cue related BOLD acquisitions immediately after exercise may not be time sensitive at least in relation to any residual influence of CBF. Acute running transiently suppressed appetite and increased food cue reactivity in brain regions implicated in attention, anticipation and encoding of reward, and episodic memory retrieval independent of CBF. These data provide insights into the immediate effects of exercise on central appetite responses and highlight important methodological considerations for future work exploring the interaction of exercise with brain food‐cue responsiveness. | PMC10203797 | ||
AUTHOR CONTRIBUTIONS | PMC10203797 | |||
CONFLICT OF INTEREST STATEMENT | The authors declare no conflicts of interest. | PMC10203797 | ||
Supporting information |
Click here for additional data file. | PMC10203797 | ||
ACKNOWLEDGEMENTS | This research was funded by King Saud bin Abdulaziz University for Health Sciences (Saudi Arabia), Jeddah University (Saudi Arabia), and the National Institute for Health and Care Research (NIHR) Leicester Biomedical Research Centre (United Kingdom). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health. The SMS EPI sequence was provided by GE Healthcare under a research agreement with Loughborough University and supported by Dr Gavin Houston from GE Healthcare. | PMC10203797 | ||
DATA AVAILABILITY STATEMENT | The de‐identified neuroimaging, physiological and behavioural data generated in this study are available from the corresponding author upon reasonable request. | PMC10203797 | ||
REFERENCES | PMC10203797 | |||
Background | inflammation, Periodontitis | INFLAMMATION, CHRONIC INFLAMMATORY DISEASE, CHRONIC PERIODONTITIS, PERIODONTITIS | Periodontitis is one of the most common chronic inflammatory diseases in the world, which affects oral health. Resveratrol is a polyphenol with therapeutic effects on the inflammation caused by periodontal pathogens. This study aimed to evaluate the impact of resveratrol supplementation on clinical parameters and inflammatory markers in patients with chronic periodontitis. | PMC10045616 |
Methods | PD, bleeding | BLEEDING, CHRONIC PERIODONTITIS, PLAQUE | In this randomized, double-blind study, 40 chronic periodontitis patients underwent non-surgical therapy and were randomly assigned to two intervention and control groups, receiving either resveratrol supplements or a placebo for four weeks. Salivary levels of interleukin-8 (IL-8), interleukin-1β (IL-1β), and clinical parameters, including pocket depth (PD), clinical attachment level (CAL), plaque index (PI), and bleeding index (BI), were measured before and after the intervention. | PMC10045616 |
Results | PD, bleeding | BLEEDING, PLAQUE | The results showed that in both the case and control groups, after four weeks of using resveratrol, only plaque index (PI) was significantly different compared to the control group (P = 0.0001). However, there were no significant differences in the mean pocket depth (PD), clinical attachment loss (CAL), bleeding index (BI), and salivary levels of IL-8 and IL-1β between the two groups after the intervention. | PMC10045616 |
Conclusion | CHRONIC PERIODONTITIS | Resveratrol complement was helpful as an anti-inflammatory food supplement, along with other non-surgical periodontal treatments in chronic periodontitis patients. | PMC10045616 | |
Supplementary Information | The online version contains supplementary material available at 10.1186/s12903-023-02877-4. | PMC10045616 | ||
Keywords | PMC10045616 | |||
Introduction | tooth loss, Periodontitis | PERIODONTITIS, PERIODONTAL DISEASES, INFLAMMATORY DISEASE, PERIODONTITIS | Periodontitis is an inflammatory disease that leads to the destruction of dental supporting tissues and tooth loss [Given the complex processes created by different pro-inflammatory and anti-inflammatory mediators, studies have investigated different strategies for regulating immune-inflammatory responses to periodontal diseases. Previous studies have shown that both non-steroid anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors regulate the host immune-inflammatory activities [Antibiotics have been widely used for treating periodontal diseases; however, using them frequently contributes to antibiotic resistance [To date, different surgical and non-surgical treatments have been used for periodontitis; however, few drugs are available for the treatment of periodontitis. Herbal medicines have been used adjunctive to treat inflammatory diseases and recently to treat and prevent periodontitis, too [ | PMC10045616 |
Methods | PMC10045616 | |||
Subjects and study design | renal and hepatic diseases, periodontitis, allergy | OVARIAN CANCER, PERIODONTITIS, DISEASE, ALLERGY, PEMPHIGUS, LEUKOPLAKIA | In this randomized, double-blind clinical trial, 40 periodontitis patients referring to the Periodontics Department of Dental School, Shahid Sadoughi University of Medical Sciences, Yazd, were selected. According to the principles of the Helsinki declaration, after examination and diagnosis of periodontal symptoms and considering inclusion and exclusion criteria, the necessary information was provided, and written consent was obtained. Then, the subjects were randomly assigned to two groups: case (n = 20) and control (n = 20). The patients were free to leave the study at any time they wished.The inclusion criteria consisted of an age range of 30–60 years and moderate to severe periodontitis. The exclusion criteria consisted of pregnancy, lactation, traveling for > 2 weeks, smoking, taking immunosuppressive medications, taking non-steroidal anti-inflammatory drugs, antihypertensive agents, antibiotics drugs, anti-coagulant drugs like warfarin, taking insulin, and patients treated for uterine, breast, and ovarian cancer, patients with advanced renal and hepatic diseases, those with an allergy to grapes, blackberry, or blueberry, history of periodontitis treatment in the past six months and patients with active oral disease like pemphigus, leukoplakia.This clinical trial was approved by the Ethics Committee of Shahid Sadoughi University of Medical Sciences under the code IR.SSU.REC.1396.206, and the IRCT Registration code was IRCT20171015036782N6. | PMC10045616 |
Periodontal examination | periodontitis, teeth and disease, tooth loss, PD | PERIODONTITIS, PLAQUE, PERIODONTITIS | Periodontitis patient with stage II (moderate periodontitis) to stage IV (advanced periodontitis with extensive tooth loss) based on clinical attachment loss (CAL) of ≥ 3 mm around the teeth and disease severity according to 2017 international periodontology workshop were selected. As all patients in our study didn’t have full mouth periapical radiography and no risk factor that may affect systemic health according to eligible patients, the grade of periodontitis was estimated with moderate progression rate (grade B).For all the patients, the probing depth (PD) was measured by the Williams probe, which is a distinctive and calibrated device, at six points of each tooth: mesiobuccal, mid-buccal, distobuccal, mesiolingual, mid-lingual, and distolingual. These areas were coded, and 10 points were randomly selected from at least three quadrants for the post-intervention clinical measurements [Clinical attachment loss (CAL) was also recorded in these areas by measuring the distance between the CEJ (cementoenamel junction) and the pocket depth. In addition, the O’Leary plaque index [ | PMC10045616 |
Biochemical measurement | STERILE, CAVITY | Salivary samples of all the patients were collected at baseline and four weeks after the intervention to assess IL-8 and IL-1β levels. All the salivary samples were collected between 9 a.m. and 12 p.m. The patients were asked to refrain from brushing 12 h before sampling and refrain from eating, drinking, and chewing gum two hours before the sampling. To investigate the inflammatory interleukin levels, the unstimulated saliva of the patients was collected before any action. The patients were asked to avoid swallowing their saliva for five minutes, and then the accumulated saliva in the oral cavity floor was passively drooled into sterile disposable test tubes [ | PMC10045616 | |
Intervention | For all the patients (both case and control groups), scaling and root planning by an ultrasonic scaler (ultrasonic piezo scaler Uds-K, Woodpecker, China) was performed. Patients in the case group received 480 mg (2 capsules) of resveratrol (HERBAFIT Co.) daily for four weeks, while patients in the control group received 480 mg (2 capsules) of placebo containing starch [ | PMC10045616 | ||
Outcome (primary and secondary) | PD | SECONDARY, PLAQUE | The primary outcome of this study was to determine the CAL and PD before and after the intervention. The secondary outcome of this study was to evaluate the O’Leary plaque index, BI and the mean salivary levels of IL-8 and IL-1β before and after intervention between two groups. | PMC10045616 |
Sample size calculation | Considering a 5% significance level, 80% test power, and according to the results of a previous study [ | PMC10045616 | ||
Statistical analysis | SPSS 23.0 was used to compare the results and determine the differences in different experiments. A Kolmogorov-Smirnov test was to assess distribution normality. Also, the chi-squared test, independent-samples t-test, and paired-samples statistics were used to compare the changes between the two groups. Statistical significance was set at P < 0.05. | PMC10045616 | ||
Discussion | PD, bleeding, periodontitis, periodontium | SYSTEMIC DISEASE, BLEEDING, PERIODONTITIS, CHRONIC PERIODONTITIS, PLAQUE, TYPE 2 DIABETES | The present research is one of the first studies to investigate the effect of resveratrol supplementation on periodontitis. In this double-blind study with a placebo control, the effectiveness of resveratrol as a supplementary treatment for clinical indicators (PD, CAL, PI, and BI) and salivary inflammatory indicators (IL-8 and IL-1β) was investigated in chronic periodontitis patients without any systemic disease.According to the results, there were no significant differences between the control and experimental groups in gender and age; in this regard, the two groups were homogenous. According to the comparisons between the two groups, after four weeks of resveratrol supplementation in the experimental group, the only clinical indicator with a significant decrease compared to the control group was plaque index (PI) (P = 0.0001). However, there were no significant differences between the two groups in pocket depth (PD), clinical attachment level (CAL), bleeding index (BI), and IL-8 and IL-1β levels in salivary samples (Table In this research, the changes in PD levels were not significantly different between the experimental and control groups, which is different from the results of a study by Zare et al. (2017), who investigated the effect of resveratrol on 43 patients with type 2 diabetes and chronic periodontitis over four weeks [Several studies have investigated the effect of non-surgical periodontal treatments, such as oral hygiene instructions, scaling, and root planning, as the key treatments for these patients [In the four weeks of the study, CAL decreased by 1.23 mm in the experimental group and 1.8 mm in the control group; these changes are statistically significant (Table The O’Leary plaque index significantly decreased in both the experimental and control groups compared to the baseline (P = 0.0001), and it also significantly decreased in the experimental group compared to the control group (P = 0.0001) (Table In this study, the bleeding index (BI) significantly decreased in both groups after four weeks (P = 0.0001). However, there was no significant difference between the two groups (P = 0.2), which might be due to the significant effect of non-surgical periodontal treatment, frequent oral hygiene instructions, and the Hawthorne effect in both groups that can diminish the effectiveness of resveratrol.The salivary IL-1β levels decreased significantly in both the experimental and control groups compared to the baseline; however, there was no significant difference between the two groups after the intervention (P˃0.05). Casati et al. (2013) treated 10-week-old rats with 10 mg/kg of daily resveratrol and measured IL-1β, IL-7, and IL-4 levels. They did not observe any significant difference between the two groups in IL-1β and IL-4 levels, but IL-7 levels decreased in the resveratrol treatment group compared to the control group (receiving placebo) [Several studies have reported an increase in the salivary or gingival crevicular fluid IL-8 levels in inflamed areas compared to healthy areas. In contrast, some other studies have suggested decreased IL-8 levels in inflamed areas. Therefore, the results are contradictory [Although the mentioned evidence suggests the treatment potential of resveratrol in the host inflammatory modulation, the primary mechanism causing this effect is still unknown. Oral treatment with resveratrol has limited bioavailability, and it is quickly affected by metabolism. Its local treatment or injection might have a higher anti-inflammatory effect on the periodontium. Therefore, although the immunologic findings of this study do not suggest the modulation of immune-inflammatory responses by resveratrol, its molecular mechanism should be studied further. The limitations of the present study included the small number of sample size and short follow-up period. Further studies with larger sample size and longer follow up periods needed to explore the impact of resveratrol supplementation on clinical parameters and inflammatory markers in periodontitis patients. | PMC10045616 |
Conclusion | periodontitis | PERIODONTITIS, PLAQUE | In view of the above findings and within the limits of present study the results indicated that supplementation with resveratrol in combination with non-surgical periodontal treatment has significant effect on reduction of plaque index (PI) during 4 weeks. Collectively, it seems that using resveratrol along with nonsurgical periodontal treatment may be beneficial in improvement the clinical parameters and inflammatory condition in periodontitis patients. | PMC10045616 |
Acknowledgements | We would like to thank the Vice-Chancellor for Technology Research of Shahid Sadoughi University of Medical Sciences in Yazd for approving and fnancially supporting the project with the code no: 5824. | PMC10045616 | ||
Authors’ contributions | Shabnam Nikniaz | All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Farzane Vaziri, Reza Mansouri and Shabnam Nikniaz. The first draft of the manuscript was written by Shabnam Nikniaz and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript. | PMC10045616 | |
Funding | The Vice Chancellor for Research and Technology of Yazd Shahid Sadoughi University of Medical Sciences. (Grant no: 5824). | PMC10045616 | ||
Data availability | The data generated and analyzed during the current study are available from the corresponding author on reasonable request. | PMC10045616 | ||
Declarations | PMC10045616 | |||
Ethics approval and consent to participate | The study was approved in the Ethics Committee of Shahid Sadoughi University of Medical Sciences under the code IR.SSU.REC.1396.206, and the IRCT Registration code was IRCT20171015036782N6. After examination and diagnosis of periodontal symptoms, the necessary information was provided and written informed consent was obtained from all patients. | PMC10045616 | ||
Consent for publication | Not applicable. | PMC10045616 | ||
Competing interests | The author declare there is no competing interest. | PMC10045616 | ||
Abbreviations | Interleukin 8Interleukin 1 betaPocket depthClinical attachment lossPlaque index (oral hygiene)Bleeding index | PMC10045616 | ||
References | PMC10045616 | |||
Key Points | PMC10277935 | |||
Question | aneurysmal subarachnoid hemorrhage | Does prophylactic lumbar cerebrospinal fluid drainage improve clinical outcomes measured by the modified Rankin Scale score among patients with aneurysmal subarachnoid hemorrhage? | PMC10277935 |
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