Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
1,089
datasets available to search
ShareScore release 0.9.0
Dataset results
1,089 results for “metabolic syndrome”
Gestational Cd exposure in the CD-1 mouse induces sex-specific hepatic insulin insensitivity, obesity and metabolic syndrome in adult female offspring
<p>There is compelling evidence that developmental exposure to some toxic metals increases risk for obesity and obesity-related morbidity including cardiovascular disease and type 2 diabetes in adults. To explore the hypothesis that developmental Cd exposure increased risk of obesity later in life, male and female CD-1 mice were maternally exposed to 500 ppb CdCl<sub>2</sub> in drinking water during a human gestational equivalent period (GD0 - PND10). Hallmark indicators of metabolic disruption, hepatic steatosis, and metabolic syndrome were evaluated prior to birth through adulthood. Blood Cd levels in dams were similar to those observed in human pregnancy cohorts. There were no observed impacts of exposure on dams or pregnancy-related outcomes. Results of glucose and insulin tolerance testing revealed that Cd-exposure impaired glucose homeostasis in young adult offspring. Exposure-related increases in circulating triglycerides and hepatic steatosis were apparent only in females. By PND120, Cd-exposed females had become 30% heavier with 700% more perigonadal fat than unexposed control females. There was no evidence of dyslipidemia, steatosis, increased weight gain, nor increased adiposity in Cd-exposed male offspring. Hepatic transcriptome analysis at PND1, PND21, and PND42 revealed evidence for female-specific increases in oxidative stress and mitochondrial dysfunction with significant early disruption of retinoic acid signaling and altered insulin receptor signaling consistent with hepatic insulin sensitivity in adult females. The observed steatosis and metabolic syndrome-like phenotypes resulting from exposure to 500 ppb CdCl<sub>2</sub> during the pre- and perinatal period of development equivalent to human gestation indicate that Cd acts developmentally as a sex-specific delayed obesogen.</p>
Unveiling Pathophysiological Insights: Serum Metabolic Dysregulation in Acute Respiratory Distress Syndrome Patients with Acute Kidney Injury
<p>The uploaded data is an Excel sheet obtained after performing the binning of 1H CPMG NMR spectra acquired using 800 MHz NMR on the serum samples of ARDS patients and ARDS with AKI patients. </p>
Data from: Additive effects of developmental acclimation and physiological syndromes on lifetime metabolic and water loss rates of a dry-skinned ectotherm
<p>Data sets from the paper: "Additive effects of developmental acclimation and physiological syndromes on lifetime metabolic and water loss rates of a dry-skinned ectotherm" by Dezetter et al. in Functional Ecology.</p> <p> </p> <p> </p>
Study of Semaglutide for Non-Alcoholic Fatty Liver Disease (NAFLD), a Metabolic Syndrome With Insulin Resistance, Increased Hepatic Lipids, and Increased Cardiovascular Disease Risk (The SLIM LIVER St
ClinicalTrials.gov study NCT04216589. IPD Sharing: YES. Countries: 2. Publications: 2.
Effects of Pioglitazone on Insulin and Glucose Metabolism in Women With Polycystic Ovary Syndrome (PCOS)
ClinicalTrials.gov study NCT00868140. IPD Sharing: NO. Countries: 2. Publications: 1.
Gestational Cd exposure in the CD-1 mouse induces sex-specific hepatic insulin insensitivity, obesity and metabolic syndrome in adult female offspring
Open the record for dataset details and reuse information.
Metabolic syndrome for the prognosis of postoperative complications after open pancreatic surgery in Chinese adult: a propensity score matching study
<p><strong>Background: </strong>To investigate the relationship between metabolic syndrome (MS) and postoperative complications in Chinese adults after open pancreatic surgery.</p> <p><strong>Methods: </strong>Relevant data were retrieved from the Medicalsystem® database of Changhai hospital (MDCH). All patients who underwent pancreatectomy from January 2017 to May 2019 were included, and relevant data were collected and analyzed. A propensity score matching (PSM) and a multivariate generalized estimating equation were used to investigate the association between MS and composite compositions during hospitalization. Cox regression model was employed for survival analysis.</p> <p><strong>Results: </strong>1481 patients were finally eligible for this analysis. According to diagnostic criteria of Chinese MS, 235 patients were defined as MS, and the other 1246 patients were controls. After PSM, no association was found between MS and postoperative composite complications (OR: 0.958, 95%CI: 0.715-1.282, P=0.958). But MS was associated with postoperative acute kidney injury (OR: 1.730, 95%CI: 1.050-2.849, P=0.031). Postoperative AKI was associated with mortality in 30 days and 90 days after surgery (P<0.001).</p> <p><strong>Conclusions: </strong>MS is not an independent risk factor correlated with postoperative composite complications after open pancreatic surgery. But MS is an independent risk factor for postoperative AKI of pancreatic surgery in Chinese population, and AKI is associated with survival after surgery.</p>
Senescent preosteoclast secretome promotes metabolic syndrome-associated osteoarthritis through COX2-PGE2
<p><span>Metabolic syndrome–associated osteoarthritis (MetS-OA)</span><span> is a distinct osteoarthritis phenotype defined by the coexistence of MetS or its individual components. Despite the high prevalence of MetS-OA, its pathogenic mechanisms are unclear. Here, we report that humans and mice with MetS are more likely to develop osteoarthritis-related subchondral bone alterations than those without MetS. </span><span>MetS-OA mice exhibited</span><span> a rapid</span> <span>increase in joint </span><span>subchondral bone plate and trabecular thickness </span><span>before articular cartilage degeneration. Subchondral preosteoclasts undergo senescence </span><span>at the pre- or early</span><span>-osteoarthritis stage</span><span> and </span><span>acquire a unique secretome to</span><span> stimulate osteoblast differentiation and inhibit osteoclast differentiation. Antagonizing preosteoclast senescence markedly mitigates pathological subchondral alterations and osteoarthritis progression in MetS-OA mice. </span><span>At the molecular level,</span> <span>preosteoclast secretome activates </span><span>COX2-PGE2, resulting in stimulated differentiation of osteoblast progenitors for subchondral bone formation. Administration of a selective COX2 inhibitor attenuated subchondral bone alteration and osteoarthritis progression in MetS-OA mice. Longitudinal analyses of the human Osteoarthritis Initiative (OAI) cohort dataset also revealed that </span><span>COX2 inhibitor use, relative to non-selective nonsteroidal anti-inflammatory drug use</span><span>, is associated with less</span><span> progression of </span><span>osteoarthritis and subchondral bone marrow lesion worsening in participants with MetS-OA. Our findings suggest a central role of a senescent preosteoclast secretome-COX2/PGE2 axis in the pathogenesis of MetS-OA.</span></p>
Predictors of metabolic syndrome among adults in Ethiopia
<p><strong>Background</strong></p> <p>Available evidence showed that metabolic syndrome in the adult population is persistently elevated due to nutrition transition, genetic predisposition, individual-related lifestyle factors, and other environmental risks. However, in developing nations, the burden and scientific evidence on the pattern, and risk exposures for the development of the metabolic syndrome were not adequately investigated. Thus, the study aimed to measure the prevalence of metabolic syndrome and to identify specific risk factors among adult populations who visited Dessie Comprehensive Specialized Hospital, Ethiopia.</p> <p><strong>Methods</strong></p> <p>A hospital-based cross-sectional study was conducted among randomly selected 419 adults attending Dessie Comprehensive Specialized Hospital from January 25 to February 29, 2020. We used the WHO STEP-wise approach for non-communicable disease surveillance to assess participants' disease condition. Metabolic syndrome was measured using the harmonized criteria recommended by the International Diabetes Federation Task Force in 2009. Data were explored for missing values, outliers, and multicollinearity before presenting the summary statistics and regression results. Multivariable logistic regression was used to disentangle statistically significant predictors of metabolic syndrome expressed using an odds ratio with a 95% of uncertainty interval. All statistical tests were managed using SPSS version 26. A non-linear dose-response analysis was performed to show the relationships between metabolic syndrome with potential risk factors.</p> <p><strong>Results</strong></p> <p>The overall prevalence of metabolic syndrome among adults was 35.0 %( 95% CI, (30.5, 39.8)). Women were more affected than men (i.e. 40.3% vs 29.4%). After adjusting for other variables, being female [OR=1.85; 95% CI (1.01, 3.38)], urban residence [OR=1.94; 95% CI (1.08, 3.24)], increased age [OR= 18.23; 95% CI (6.66, 49.84)], shorter sleeping durations [OR= 4.62; 95% CI (1.02, 20.98)], sedentary behaviour[OR=4.05; 95% CI (1.80, 9.11)], obesity[OR=3.14; 95% CI (1.20, 8.18) and alcohol drinking[OR=2.85; 95% CI (1.27,6.39)] were positively associated with the adult metabolic syndrome. Whilst have no formal education [OR=0.30; 95% CI (0.12, 0.74)] was negatively associated with metabolic syndrome.</p> <p><strong>Conclusions</strong></p> <p>The prevalence of the adult metabolic syndrome is found to be high. Metabolic syndrome has linear relationships with BMI, physical activity, sleep duration, and level of education. The demographic and behavioral factors are strongly related to the risk of metabolic syndrome. Since most of the factors are modifiable, there should be urgent large-scale community intervention programs focusing on increased physical activity, healthy sleep, weight management, minimizing behavioral risk factors, and healthier food interventions targeting a lifecycle approach. The existing policy should be evaluated whether due attention has been given to prevention strategies of NCDs.</p>
Pace-of-life syndrome: linking personality, metabolism and colour ornamentation in male guppies
<p>Within populations, there commonly exists consistent among-individual differences in behaviour. As a potential mechanism maintaining this variation, the pace-of-life-syndrome (POLS) hypothesis posits that consistent differences in the behaviour of individuals (i.e. 'personality') are intercorrelated and have coevolved with consistent individual differences in metabolism and life-history traits. Here, using adult male guppies, <em>Poecilia reticulata</em>, we tested under laboratory conditions (1) whether behavioural and metabolic traits vary consistently among individuals over time (≤ 7 days) and (2) the POLS prediction that repeatable behavioural traits should be intercorrelated with each other and with repeatable metabolic rate at the among-individual level. Furthermore, based on indicator models of sexual selection, we expected that sexually selected male colour ornamentation would predict individual personality and metabolic rate. We repeatedly assayed three behavioural traits (sociability, boldness, exploration) and three metabolic traits (resting metabolic rate, maximal metabolic rate, aerobic scope) in a set of males that varied in body size and colour ornamentation. All behavioural trait measures were repeatable, consistent with individual personality. Of the three metabolic traits, only resting metabolic rate (RMR) was repeatable. Behavioural trait measures were significantly intercorrelated and thus integrated in a behavioural syndrome. More 'proactive' males were bolder, more exploratory and more sociable than 'reactive' ones. However, contrary to the POLS hypothesis, <span>RMR</span>was not significantly correlated with any of the behavioural trait measures, suggesting that consistent individual differences in RMR do not drive or support differences in personality, or vice versa. Male colour ornamentation did not covary with behaviour or RMR and thus does not appear to be a reliable predictor of either behavioural or metabolic phenotypes. We therefore did not find any compelling support for the POLS hypothesis, suggesting that <span>individual differences in metabolism do not underlie the evolution and maintenance of among-individual behavioural variation in our study population.</span></p>
Metabolic syndrome severity score and associated cardiovascular risk in postmenopausal women of Bangladesh
<p>This data help to construct metabolic syndrome severity score and seek its association with absolute cardiovascular risk.</p>
Central obesity, body mass index, metabolic syndrome and mortality in Mediterranean breast cancer patients
<p>Importance: Obesity and metabolic disorders have been associated with an increased risk of cancer and with poorer outcomes in many cohorts of breast cancer (BC) patients, with poor evidence from Mediterranean cohorts. <br> Objective: To investigate the prognostic potential of anthropometric variables, namely body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), as well as Metabolic Syndrome (MetS) and its components, in early BC patients living in a Southern Mediterranean region of Italy.<br> Design: Prospective cohort study enrolling consecutive early BC patients who were treated between January 2009 and December 2013 in Southern Italy. Median follow-up was 11.8 years and ended on June 15th 2022. Physicians who measured the study variables were blinded to patient groupings.<br> Setting: Multicenter study enrolling consecutive, early BC patients referred to specialized cancer centers.<br> Participants: A total of 955 early BC patients consecutively treated at the Istituto Nazionale dei Tumori, “G. Pascale” and at the Policlinico University Hospital “Federico II”, Naples, Italy, were enrolled. All study subjects provided written informed consent to participate. <br> Intervention(s) (for clinical trials) and exposure (for observational studies): Anthropometric measurements and indices (BMI, hip circumference and WC) were collected. MetS was defined according to NCEP-ATP III criteria. MetS components were categorized as 0, 1-2 or ≥3. <br> Main Outcomes and Measures: Overall survival and BC-specific survival. <br> Results: Mean age was 55.3 years (±12.5 years); 61% of patients were post-menopausal. At the end of follow-up, 208 (22%) patients had died, 131 (14%) of whom from BC. Obesity (BMI≥30 kg/m2) was found in 29% of enrolled patients (14% in pre- and 38% in post-menopause); 24% of patients met the criteria for a diagnosis of MetS (7% in pre- and 36% in post-menopause), whereas 1-2 MetS criteria were found in 53% of patients<br> High WC or WHR were associated with a moderately increased risk of all-cause mortality (WC ≥ 88 cm, HR=1.39, 95%CI: 1.00-1.94; WHR > 0.85, HR=1.62, 95%CI: 1.12-2.37). Furthermore, an increased risk of all-cause mortality was observed with the presence of MetS (HR=1.61, 95%CI: 1.12-2.32). An increased BC-specific mortality risk was found in obese patients (BMI≥30 kg/m2, HR=1.72, 95%CI: 1.06-2.78) and in those with WC ≥88 (HR=1.71, 95%CI: 1.12-2.61). High WHR was also associated with increased risk of BC-specific mortality, both when evaluated as a categorical variable (WHR>0.85, HR=1.80, 95%CI: 1.13-2.86) and as a continuous variable (for each 0.1-U increase in WHR, HR=1.33, 95%CI: 1.08-1.63). The presence of MetS was associated with an 81% increased risk of BC-specific mortality (HR=1.81, 95%CI: 1.51-2.85). <br> These associations varied according to menopausal status. In particular, in pre-menopausal patients higher BMI was associated with an increased risk of both all-cause and BC-specific mortality (HR=1.43 and HR=1.58, respectively). In post-menopausal women an increased risk of all-cause mortality was found only in the presence of ≥3 MetS components (HR=2.77, 95%CI: 1.09-7.06). The associations among anthropometric variables and all-cause and BC-specific mortality also varied according to BC subtype. Triple negative BC was the only disease subtype that wasn’t independently associated with BMI, WC, WHR or MetS or all-cause and BC-specific mortality.<br> Conclusions and Relevance: Central obesity and metabolic disorders result in a highly increased risk of BC death. The magnitude of this effect suggests that obesity may nullify the benefit of effective BC therapies. Active lifestyle interventions to maintain optimal body weight and to prevent MetS should be recommended for several expected beneficial effects, including a potential reduction in BC-specific mortality.</p>
Effects of Hyperuricemia Reversal on Features of the Metabolic Syndrome
ClinicalTrials.gov study NCT01654276. IPD Sharing: NO. Countries: 1. Publications: 1.
Effect of Banaba (Lagerstroemia Speciosa) on Metabolic Syndrome, Insulin Secretion and Insulin Sensitivity
ClinicalTrials.gov study NCT02767869. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Topiramate for Cryptogenic Sensory Peripheral Neuropathy in Metabolic Syndrome (CSPN)
ClinicalTrials.gov study NCT02878798. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Effects of Colchicine in Non-Diabetic Adults With Metabolic Syndrome
ClinicalTrials.gov study NCT02153983. IPD Sharing: YES. Countries: 1. Publications: 7.
Effects of Restricted-time and Psychochrononutritional Feeding in People With Metabolic Syndrome
ClinicalTrials.gov study NCT07389603. IPD Sharing: NO. Countries: 1. Publications: 1.
Exercise, Statins, and the Metabolic Syndrome
ClinicalTrials.gov study NCT01700530. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Exercise and Pioglitazone for HIV-Metabolic Syndromes
ClinicalTrials.gov study NCT00639457. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Inflammation and the Metabolic Syndrome in Humans
ClinicalTrials.gov study NCT00954824. IPD Sharing: Not stated. Countries: 1. Publications: 9.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.