Browse
Submit Data
Databases
API
Help

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Negative legacy of obesity.

ABSTRACT: Obesity promotes excessive inflammation, which is associated with senescence-like changes in visceral adipose tissue (VAT) and the development of type 2 diabetes (T2DM) and cardiovascular diseases. We have reported that a unique population of CD44hi CD62Llo CD4+ T cells that constitutively express PD-1 and CD153 exhibit cellular senescence and cause VAT inflammation by producing large amounts of osteopontin. Weight loss improves glycemic control and reduces cardiovascular disease risk factors, but its long-term effects on cardiovascular events and longevity in obese individuals with T2DM are somewhat disappointing and not well understood. High-fat diet (HFD)-fed obese mice were subjected to weight reduction through a switch to a control diet. They lost body weight and visceral fat mass, reaching the same levels as lean mice fed a control diet. However, the VAT of weight reduction mice exhibited denser infiltration of macrophages, which formed more crown-like structures compared to the VAT of obese mice kept on the HFD. Mechanistically, CD153+ PD-1+ CD4+ T cells are long-lived and not easily eliminated, even after weight reduction. Their continued presence maintains a self-sustaining chronic inflammatory loop via production of large amounts of osteopontin. Thus, we concluded that T-cell senescence is essentially a negative legacy effect of obesity.

SUBMITTER: Shirakawa K

PROVIDER: S-EPMC5657997 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

The Legacy of Parental Obesity: Mechanisms of Non-Genetic Transmission and Reversibility.

Project description:While a dramatic increase in obesity and related comorbidities is being witnessed, the underlying mechanisms of their spread remain unresolved. Epigenetic and other non-genetic mechanisms tend to be prominent candidates involved in the establishment and transmission of obesity and associated metabolic disorders to offspring. Here, we review recent findings addressing those candidates, in the context of maternal and paternal influences, and discuss the effectiveness of preventive measures.

| S-EPMC9599218 | biostudies-literature

Neuroimaging biomarkers to associate obesity and negative emotions.

Project description:Obesity is a serious medical condition highly associated with health problems such as diabetes, hypertension, and stroke. Obesity is highly associated with negative emotional states, but the relationship between obesity and emotional states in terms of neuroimaging has not been fully explored. We obtained 196 emotion task functional magnetic resonance imaging (t-fMRI) from the Human Connectome Project database using a sampling scheme similar to a bootstrapping approach. Brain regions were specified by automated anatomical labeling atlas and the brain activity (z-statistics) of each brain region was correlated with body mass index (BMI) values. Regions with significant correlation were identified and the brain activity of the identified regions was correlated with emotion-related clinical scores. Hippocampus, amygdala, and inferior temporal gyrus consistently showed significant correlation between brain activity and BMI and only the brain activity in amygdala consistently showed significant negative correlation with fear-affect score. The brain activity in amygdala derived from t-fMRI might be good neuroimaging biomarker for explaining the relationship between obesity and a negative emotional state.

| S-EPMC5550465 | biostudies-other

Legacy of MESA.

Project description:The MESA (Multi-Ethnic Study of Atherosclerosis) was initiated to address unresolved questions about subclinical cardiovascular disease and its progression to clinically overt cardiovascular disease in a diverse population-based sample, incorporating emerging imaging technologies for better evaluation of subclinical disease and creating a population laboratory for future research. MESA's recruited (from 2000 to 2002) cohort comprised >6,000 adults from 4 racial/ethnic groups, ages 45 to 84 years, who were free of cardiovascular disease at baseline. Extensive cohort data have been collected over 5 exams (through 2011) with additional exam components added through extramurally funded ancillary study grants, and through regular phone follow-up contacts. Over 1,000 MESA papers have been published to date. Exam 6 will incorporate components that use novel wearable, imaging, and other technologies to address new research questions. MESA investigators have and continue to seek opportunities for collaboration with other researchers on a wide variety of topics to further expand the science of MESA.

| S-EPMC5134741 | biostudies-literature

Mercury's complex legacy.

Project description: Not available

| S-EPMC10433272 | biostudies-literature

Transcriptional legacy in the armadillo

Project description:Longitudinal study of armadillo transcription.

2023-10-10 | GSE141951 | GEO

A museum for Cajal's Legacy.

Project description: Not available

| S-EPMC7116571 | biostudies-literature

Legacy of a 10-Year Multidomain Lifestyle Intervention on the Cognitive Trajectories of Individuals with Overweight/Obesity and Type 2 Diabetes Mellitus.

Project description:IntroductionWeight loss and increased physical activity interventions are commonly recommended for individuals with type 2 diabetes (T2D) and overweight or obesity. We examined the impact of randomization to an intensive lifestyle intervention (ILI) on trajectories of cognitive function over 10 years in a cohort of participants in a randomized clinical trial who had T2D and overweight/obesity at baseline.MethodsParticipants aged 45-76 years were enrolled in 2001-2004 and were randomized to the ILI or a diabetes support and education (DSE) condition. Cognitive function was assessed in 3,938 participants at up to 4 time points 8-18 years after randomization. General linear mixed effects models examined cognitive trajectories over time. Subgroup analyses focused on sex, individuals with baseline body mass index >30, those carrying the APOE ε4 allele, and those with a baseline history of cardiovascular disease (CVD).ResultsOverall, there were no differences in the rate of cognitive decline by intervention arm. Subgroup analyses showed that participants who had a baseline history of CVD and were randomized to the ILI arm of the study performed significantly worse on the Stroop Color Word Test than those in the DSE arm.Discussion/conclusionsThe ILI did not result in preserved cognitive function or slower rates of cognitive decline in this cohort of individuals who had T2D and were overweight or obese at baseline.

| S-EPMC8530880 | biostudies-literature

Socioeconomic legacy yields an invasion debt.

Project description:Globalization and economic growth are widely recognized as important drivers of biological invasions. Consequently, there is an increasing need for governments to address the role of international trade in their strategies to prevent species introductions. However, many of the most problematic alien species are not recent arrivals but were introduced several decades ago. Hence, current patterns of alien-species richness may better reflect historical rather than contemporary human activities, a phenomenon which might be called "invasion debt." Here, we show that across 10 taxonomic groups (vascular plants, bryophytes, fungi, birds, mammals, reptiles, amphibians, fish, terrestrial insects, and aquatic invertebrates) in 28 European countries, current numbers of alien species established in the wild are indeed more closely related to indicators of socioeconomic activity from the year 1900 than to those from 2000, although the majority of species introductions occurred during the second half of the 20th century. The strength of the historical signal varies among taxonomic groups, with those possessing good capabilities for dispersal (birds, insects) more strongly associated with recent socioeconomic drivers. Nevertheless, our results suggest a considerable historical legacy for the majority of the taxa analyzed. The consequences of the current high levels of socioeconomic activity on the extent of biological invasions will thus probably not be completely realized until several decades into the future.

| S-EPMC3017203 | biostudies-literature

The Environmental Legacy of Modern Tropical Deforestation.

Project description:Tropical deforestation has caused a significant share of carbon emissions and species losses, but historical patterns have rarely been explicitly considered when estimating these impacts [1]. A deforestation event today leads to a time-delayed future release of carbon, from the eventual decay either of forest products or of slash left at the site [2]. Similarly, deforestation often does not result in the immediate loss of species, and communities may exhibit a process of "relaxation" to their new equilibrium over time [3]. We used a spatially explicit land cover change model [4] to reconstruct the annual rates and spatial patterns of tropical deforestation that occurred between 1950 and 2009 in the Amazon, in the Congo Basin, and across Southeast Asia. Using these patterns, we estimated the resulting gross vegetation carbon emissions [2, 5] and species losses over time [6]. Importantly, we accounted for the time lags inherent in both the release of carbon and the extinction of species. We show that even if deforestation had completely halted in 2010, time lags ensured there would still be a carbon emissions debt of at least 8.6 petagrams, equivalent to 5-10 years of global deforestation, and an extinction debt of more than 140 bird, mammal, and amphibian forest-specific species, which if paid, would increase the number of 20(th)-century extinctions in these groups by 120%. Given the magnitude of these debts, commitments to reduce emissions and biodiversity loss are unlikely to be realized without specific actions that directly address this damaging environmental legacy.

| S-EPMC5004800 | biostudies-other

Metabolically activated adipose tissue macrophages link obesity to triple-negative breast cancer.

Project description:Obesity is associated with increased incidence and severity of triple-negative breast cancer (TNBC); however, mechanisms underlying this relationship are incompletely understood. Here, we show that obesity reprograms mammary adipose tissue macrophages to a pro-inflammatory metabolically activated phenotype (MMe) that alters the niche to support tumor formation. Unlike pro-inflammatory M1 macrophages that antagonize tumorigenesis, MMe macrophages are pro-tumorigenic and represent the dominant macrophage phenotype in mammary adipose tissue of obese humans and mice. MMe macrophages release IL-6 in an NADPH oxidase 2 (NOX2)-dependent manner, which signals through glycoprotein 130 (GP130) on TNBC cells to promote stem-like properties including tumor formation. Deleting Nox2 in myeloid cells or depleting GP130 in TNBC cells attenuates obesity-augmented TNBC stemness. Moreover, weight loss reverses the effects of obesity on MMe macrophage inflammation and TNBC tumor formation. Our studies implicate MMe macrophage accumulation in mammary adipose tissue as a mechanism for promoting TNBC stemness and tumorigenesis during obesity.

| S-EPMC6547867 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data