Post-Effort Changes in Autophagy- and Inflammation-Related Gene Expression in White Blood Cells of Healthy Young Men.
Ontology highlight
ABSTRACT:
SUBMITTER: Kostrzewa-Nowak D
PROVIDER: S-EPMC8229752 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:ObjectiveAssociation between white blood cell (WBC) count and diabetes risk has been recently suggested. We assessed whether WBC count is an independent risk factor for diabetes incidence among young healthy adults.Research design and methodsWBC count was measured in 24,897 young (mean age 30.8 ± 5.36 years), normoglycemic men with WBC range of 3,000 to 12,000 cells/mm(3). Participants were periodically screened for diabetes during a mean follow-up of 7.5 years.ResultsDuring 185,354 person-years of follow-up, diabetes was diagnosed in 447 subjects. A multivariate model adjusted for age, BMI, family history of diabetes, physical activity, and fasting glucose and triglyceride levels revealed a 7.6% increase in incident diabetes for every increment of 1,000 cells/mm(3) (P = 0.046). When grouped in quintiles, a baseline WBC count above 6,900 cells/mm(3) had an independent 52% increase in diabetes risk (hazard ratio 1.52 [95% CI 1.06-2.18]) compared with the lowest quintile (WBC <5,400 cells/mm(3)). Men at the lowest WBC quintile were protected from diabetes incidence even in the presence of overweight, family history of diabetes, or elevated triglyceride levels. After simultaneous control for risk factors, BMI was the primary contributor of the variation in multivariate models (P < 0.001), followed by age and WBC count (P < 0.001), and family history of diabetes and triglyceride levels (P = 0.12).ConclusionsWBC count, a commonly used and widely available test, is an independent risk factor for diabetes in young men at values well within the normal range.
| S-EPMC3554323 | biostudies-literature
Project description:AimIn the present study the response of optic nerve head blood flow to an increase in ocular perfusion pressure during isometric exercise was studied. Based on our previous studies we hypothesized that subjects with an abnormal blood flow response, defined as a decrease in blood flow of more than 10% during or after isometric exercise, could be identified.MethodsA total of 40 healthy subjects were included in this study. Three periods of isometric exercise were scheduled, each consisting of 2 minutes of handgripping. Optic nerve head blood flow was measured continuously before, during and after handgripping using laser Doppler flowmetry. Blood pressure was measured non-invasively in one-minute intervals. Intraocular pressure was measured at the beginning and the end of the measurements and ocular perfusion pressure was calculated as 2/3*mean arterial pressure -intraocular pressure.ResultsIsometric exercise was associated with an increase in ocular perfusion pressure during all handgripping periods (p < 0.001). By contrast no change in optic nerve head blood flow was seen. However, in a subgroup of three subjects blood flow showed a consistent decrease of more than 10% during isometric exercise although their blood pressure values increased. In addition, three other subjects showed a consistent decline of blood flow of more than 10% during the recovery periods.ConclusionOur data confirm previous results indicating that optic nerve head blood flow is autoregulated during an increase in perfusion pressure. In addition, we observed a subgroup of 6 subjects (15%) that showed an abnormal response, which is in keeping with our previous data. The mechanisms underlying this abnormal response remain to be shown.
| S-EPMC3855769 | biostudies-literature
Project description:Testosterone is a hormone that plays a key role in carbohydrate, fat, and protein metabolism. Testosterone deficiency is associated with multiple comorbidities, e.g., metabolic syndrome and type 2 diabetes. Despite its importance in many metabolic pathways, the mechanisms by which it controls metabolism are not fully understood. The present study investigated the short-term metabolic changes of pharmacologically induced castration and, subsequently, testosterone supplementation in healthy young males. Thirty subjects were submitted to testosterone depletion (TD) followed by testosterone supplementation (TS). Plasma samples were collected three times corresponding to basal, low, and restored testosterone levels. An untargeted metabolomics study was performed by liquid chromatography-high resolution mass spectrometry (UHPLC-HRMS) to monitor the metabolic changes induced by the altered hormone levels. Our results demonstrated that TD was associated with major metabolic changes partially restored by TS. Carnitine and amino acid metabolism were the metabolic pathways most impacted by variations in testosterone. Furthermore, our results also indicated that LH and FSH might strongly alter the plasma levels of indoles and lipids, especially glycerophospholipids and sphingolipids. Our results demonstrated major metabolic changes induced by low testosterone that may be important for understanding the mechanisms behind the association of testosterone deficiency and its comorbidities.
| S-EPMC9508133 | biostudies-literature
Project description:The effects of genetic polymorphisms on muscle structure and function remain elusive. The present study tested for possible associations of 16 polymorphisms (across ten candidate genes) with fittness and skeletal muscle phenotypes in 17- to 37-year-old healthy Caucasian male endurance (n = 86), power/strength (n = 75) and team athletes (n = 60), and non-athletes (n = 218). Skeletal muscle function was measured with eight performance tests covering multiple aspects of muscular fitness. Along with body mass and height, the upper arm and limb girths, and maximal oxygen uptake were measured. Genotyping was conducted on DNA extracted from blood. Of the 16 polymorphisms studied, nine (spanning seven candidate genes and four gene families/signalling pathways) were independently associated with at least one skeletal muscle fitness measure (size or function, or both) measure and explained up to 4.1% of its variation. Five of the studied polymorphisms (activin- and adreno-receptors, as well as myosine light chain kinase 1) in a group of one to three combined with body height, age and/or group explained up to 20.4% of the variation of muscle function. ACVR1B (rs2854464) contributed 2.0-3.6% to explain up to 14.6% of limb proximal girths. The G allele (genotypes AG and GG) of the ACVR1B (rs2854464) polymorphism was significantly overrepresented among team (60.4%) and power (62.0%) athletes compared to controls (52.3%) and endurance athletes (39.2%), and G allele was also most consistently/frequently associated with muscle size and power. Overall, the investigated polymorphisms determined up to 4.1% of the variability of muscular fitness in healthy young humans.
| S-EPMC9514622 | biostudies-literature
Project description:BACKGROUND: The glucocorticoid (GC) hormone cortisol is the end product of the hypothalamic-pituitary-adrenal axis (HPA axis). Acute psychological stress increases HPA activity and GC release. In humans, chronic disturbances in HPA activity have been observed in affective disorders and in addictive behaviour. Recent research indicates that acute effects of GCs may be anxiolytic and increase reward sensitivity. Furthermore, cortisol acutely influences early cognitive processing of emotional stimuli. METHODS: In order to extend such findings to more complex emotional-cognitive behaviour, the present study tested acute effects of 40 mg cortisol on motivated decision making in 30 healthy young men. RESULTS: Results showed that cortisol indeed increased risky decision making, as predicted. This effect occurred for decisions where making a risky choice could potentially yield a big reward. These results are discussed with respect to currently proposed mechanisms for cortisol's potential anxiolytic effect and GCs' involvement in reward systems.
| S-EPMC2797621 | biostudies-other
Project description:Mutations in the chloride channel 7 gene (CLCN7) cause osteopetrosis, and polymorphisms of CLCN7 in the non-disease allele are associated with penetrance of the autosomal dominant osteopetrosis (ADO) phenotype. Studies have also shown an association between CLCN7 polymorphisms and bone mineral density (BMD) in women. However, there is no study to date that has examined whether CLCN7 polymorphisms underlie normal variation of peak BMD in healthy premenopausal white women and in white men.Six single nucleotide polymorphisms (SNPs) and one variable number tandem repeat (VNTR) polymorphism in the CLCN7 gene were genotyped. Association was tested between CLCN7 gene polymorphisms and both lumbar spine and femoral neck BMD. Healthy premenopausal white sisters (age 33.1+/-7.2, n=1692) and healthy white brothers (age 33.6+/-10.9, n=715) were studied.No significant association between CLCN7 gene polymorphisms and BMD at the lumbar spine or femoral neck was found in white women or white men.Genetic variation in the CLCN7 gene is not a major contributor to the variability in peak BMD at the femoral neck and lumber spine in healthy premenopausal white women and in white men.
| S-EPMC2657035 | biostudies-literature
Project description:The metabolic health benefits of fermented milks have already been investigated using clinical biomarkers but the development of transcriptomic analytics in blood offers an alternative approach that may help to sensitively characterise such effects. We aimed to assess the effects of probiotic yoghurt intake, compared to non-fermented, acidified milk intake, on clinical biomarkers and gene expression in peripheral blood. To this end, a randomised, crossover study was conducted in fourteen healthy, young men to test the two dairy products. For a subset of seven subjects, RNA sequencing was used to measure gene expression in blood collected during postprandial tests and after two weeks daily intake. We found that the postprandial response in insulin was different for probiotic yoghurt as compared to that of acidified milk. Moreover changes in several clinical biomarkers were associated with changes in the expression of genes representing six metabolic genesets. Assessment of the postprandial effects of each dairy product on gene expression by geneset enrichment analysis revealed significant, similar modulation of inflammatory and glycolytic genes after both probiotic yoghurt and acidified milk intake, although distinct kinetic characteristics of the modulation differentiated the dairy products. The aryl hydrocarbon receptor was a major contributor to the down-regulation of the inflammatory genesets and was also positively associated with changes in circulating insulin at 2h after yoghurt intake (p = 0.05). Daily intake of the dairy products showed little effect on the fasting blood transcriptome. Probiotic yoghurt and acidified milk appear to affect similar gene pathways during the postprandial phase but differences in the timing and the extent of this modulation may lead to different physiological consequences. The functional relevance of these differences in gene expression is supported by their associations with circulating biomarkers.
| S-EPMC5831037 | biostudies-literature
Project description:Aims/hypothesisIndividuals with type 2 diabetes have an altered bacterial composition of their gut microbiota compared with non-diabetic individuals. However, these alterations may be confounded by medication, notably the blood-glucose-lowering biguanide, metformin. We undertook a clinical trial in healthy and previously drug-free men with the primary aim of investigating metformin-induced compositional changes in the non-diabetic state. A secondary aim was to examine whether the pre-treatment gut microbiota was related to gastrointestinal adverse effects during metformin treatment.MethodsTwenty-seven healthy young Danish men were included in an 18-week one-armed crossover trial consisting of a pre-intervention period, an intervention period and a post-intervention period, each period lasting 6 weeks. Inclusion criteria were men of age 18-35 years, BMI between 18.5 kg/m2 and 27.5 kg/m2, HbA1c < 39 mmol/mol (5.7%) and plasma creatinine within the normal range. No prescribed medication, including antibiotics, for 2 months prior to recruitment were allowed and no previous gastrointestinal surgery, discounting appendectomy or chronic illness requiring medical treatment. During the intervention the participants were given metformin up to 1 g twice daily. Participants were examined five times in the fasting state with blood sampling and recording of gastrointestinal symptoms. Examinations took place at Frederiksberg Hospital, Denmark before and after the pre-intervention period, halfway through and immediately after the end of intervention and after the wash-out period. Faecal samples were collected at nine evenly distributed time points, and bacterial DNA was extracted and subjected to 16S rRNA gene amplicon sequencing in order to evaluate gut microbiota composition. Subjective gastrointestinal symptoms were reported at each visit.ResultsData from participants who completed visit 1 (n=23) are included in analyses. For the primary outcome the relative abundance of 11 bacterial genera significantly changed during the intervention but returned to baseline levels after treatment cessation. In line with previous reports, we observed a reduced abundance of Intestinibacter spp. and Clostridium spp., as well as an increased abundance of Escherichia/Shigella spp. and Bilophila wadsworthia. The relative abundance at baseline of 12 bacterial genera predicted self-reported gastrointestinal adverse effects.Conclusions/interpretationIntake of metformin changes the gut microbiota composition in normoglycaemic young men. The microbiota changes induced by metformin extend and validate previous reports in individuals with type 2 diabetes. Secondary analyses suggest that pre-treatment gut microbiota composition may be a determinant for development of gastrointestinal adverse effects following metformin intake. These results require further investigation and replication in larger prospective studies.Trial registrationClinicaltrialsregister.eu 2015-000199-86 and ClinicalTrials.gov NCT02546050 FUNDING: This project was funded by Danish Diabetes Association and The Novo Nordisk Foundation.
| S-EPMC6509092 | biostudies-literature
Project description:Study objectivesRecent evidence suggests that certain antidepressants are associated with an increase of periodic leg movements (PLMS) that may disturb sleep. So far, this has been shown in patients clinically treated for depression and in cross-sectional studies for various substances, but not mirtazapine. It is unclear whether antidepressants induce the new onset of PLMS or only increase preexisting PLMS, and whether this is a general property of the antidepressant or only seen in depressed patients. We report here the effect of mirtazapine on PLMS in young healthy men.DesignOpen-labeled clinical trial (NCT00878540) including a 3-week preparatory phase with standardized food, physical activity, and sleep-wake behavior, and a 10-day experimental inpatient phase with an adaptation day, 2 baseline days, and 7 days with mirtazapine.SettingResearch institute.ParticipantsTwelve healthy young (20-25 years) men.InterventionsSeven days of nightly intake (22:00) of 30 mg mirtazapine.Measurements and resultsSleep was recorded on 2 drug-free baseline nights, the first 2 drug nights, and the last 2 drug nights. Eight of the 12 subjects showed increased PLMS after the first dose of mirtazapine. Frequency of PLMS was highest on the first drug night and attenuated over the course of the next 6 days. Three subjects reported transient restless legs symptoms.ConclusionsMirtazapine provoked PLMS in 67% of young healthy males. The effect was most pronounced in the first days. The possible role of serotonergic, noradrenergic and histaminergic mechanisms in mirtazapine-induced PLMS is discussed.
| S-EPMC3624820 | biostudies-literature
Project description:Study objectivesSleep is increasingly recognized to influence a growing array of physiological processes. The relationship between sleep duration and testis size, a marker of male reproductive potential, has not been studied.MethodsThis was a preliminary cross-sectional analysis of the baseline data from 92 healthy men (mean ± standard deviation, age 33 ± 6 years, body mass index [BMI] 24.7 ± 6.1 kg/m2), of whom 66 underwent at-home actigraphy and 47 underwent in-laboratory polysomnography. Sleep duration and architecture were measured by actigraphy and polysomnography, testicular volume by Prader orchidometer, total testosterone by liquid chromatography tandem mass spectrometry, free testosterone by equilibrium dialysis, and luteinizing hormone and follicle-stimulating hormone (FSH) by immunochemiluminometric assay.ResultsSleep duration was correlated with testicular volume (r = .31, P = .046) and with FSH (r = -.30, P = .035), and rapid eye movement sleep was correlated with FSH (r = .44, P = .006). The significance of these findings did not change after adjustment for age and BMI, and were confirmed nonparametrically by resampling. A putative inverse U-shaped relationship between testicular volume and sleep duration was observed by polynomial regression (P = .049), but not with resampling (P = .068).ConclusionsThere is a positive linear and a possible inverse U-shaped relationship between sleep duration and testis volume. Longitudinal or interventional studies manipulating sleep are required to better define causality, and ultimately to establish how much sleep is needed to maximize male reproductive potential.Clinical trial registrationTitle: Hormonal Mechanisms of Sleep Restriction, Registry: ClinicalTrials.gov, Identifier: NCT02256865, URL: https://clinicaltrials.gov/ct2/show/NCT02256865.
| S-EPMC6175801 | biostudies-literature