CIDR_Visceral Adiposity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA75481 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The high prevalence of obesity has focused attention on defining the pathophysiological processes that underlie susceptibility or resistance to its deleterious metabolic consequences. Mice lacking translin (Tsn), a gene implicated in a variety of biological functions from transcription to microRNA degradation, display extremely high levels of adiposity, comparable to those found in well-known genetic models of obesity, such as melanocortin 4 receptor or leptin knockout (KO) mice. Although translin KO mice display increased adiposity they retain normal glucose tolerance. In contrast, wild-type (WT) mice placed on a high-fat diet until they match translin KO adiposity levels are glucose intolerant, as expected. Conversely, translin KO mice display prominent hepatic steatosis that is more severe than that of adiposity-matched WT mice. The ability of translin KO mice to retain normal glucose tolerance in the face of massive tissue expansion may be due to three factors: preferential accumulation of subcutaneous fat, reduced levels of TNF mRNA in both adipose and hepatic tissue, and elevated levels of plasma adiponectin. Further studies aimed at defining the molecular bases for these phenotypes may yield new approaches to limit the adverse metabolic consequences of obesity.
2020-04-10 | GSE114932 | GEO
Project description:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2α-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders. Differential gene expression profile between epididymal white adipose tissue of Nck2-/- and Nck2+/+ mice by RNA sequencing (Illumina HiSEq 2000)
2016-07-01 | E-GEOD-63510 | biostudies-arrayexpress
Project description:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2α-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders.
2016-07-01 | GSE63510 | GEO
Project description:Translin KO mice display elevated adiposity
| PRJNA473148 | ENA
Project description:Obesity is a pandemic health problem with poor solutions, especially for targeted treatment. Here we develop a polycation-based nanomedicine to selectively target visceral adiposity, the more metabolically detrimental and manipulation-resistant fat. We demonstrated that the polycationic polymer polyamidoamine (PAMAM) generation 3 (P-G3) was specifically enriched in the visceral fat due to its high charge density when delivered intraperitoneally. Moreover, P-G3 treatment of obese mice inhibited visceral adiposity, increased energy expenditure, prevented obesity, and alleviated the associated metabolic dysfunctions. In vitro adipogenesis models and single-cell RNA sequencing (scRNA-seq) revealed that P-G3 paradoxically uncouples the defining function of adipocyte - lipid synthesis and storage - from adipocyte development to create unique “dwarf” adipocytes that possess normal adipocyte functions but are deficient in hypertrophic growth at least through synergistically modulating NAD and mTOR pathways. The visceral fat distribution of P-G3 was further enhanced by modifying P-G3 with cholesterol to form lipophilic nanoparticles, which were also effective in treating obesity. Our study highlights an unexpected strategy to tackle visceral adiposity and champions a new direction of exploring cationic nanomaterials for treating metabolic diseases.
2022-09-19 | GSE209819 | GEO
Project description:Homozygous K107R mutation of PPARg in mice alters the expression of its downstream target genes and increases insulin sensitivity but not adiposity.
2018-11-13 | GSE120332 | GEO
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation. C57BL6 mice were divided into low-dose penicillin or control groups. Given antibiotics via drinking water after weaning. Sacrificed and liver sections collected for RNA extraction.
2012-06-30 | E-GEOD-38880 | biostudies-arrayexpress
Project description:Hypothalami from Fat (FL) and Lean lines (LL) of juvenile broiler chickens were obtained by divergent selection for high or low levels of abdominal fat at SRA-INRA, France. Gene expression patterns were measured during the development of adiposity at 1 to 7 weeks of age. Differentially expressed genes associated with line, age, or line-by-age were identified. Various phenotypic and metabolic alterations are present between the lines (i.e., abdominal fat, T3 levels and glycemia), however there are no alterations in ad libitum food intake between the lines. A balanced block hybrdization design and the Del-Mar 14K chicken integrated systems microarrays were used to measure gene expression during development. 561 genes were differentially expressed between line, and 442 genes were significant for line-by-age interactions. The greatest number of genes were differentially expressed at week 1 of age, prior to any divergence in adiposity between the two lines. Keywords: Chickens divergently selected for fatness or leanness, transcriptional profiling, differentially expressed genes
2008-01-03 | GSE10052 | GEO
Project description:Hypothalami from Fat (FL) and Lean lines (LL) of juvenile broiler chickens were obtained by divergent selection for high or low levels of abdominal fat at SRA-INRA, France. Gene expression patterns were measured during the development of adiposity at 1 to 7 weeks of age. Differentially expressed genes associated with line, age, or line-by-age were identified. Various phenotypic and metabolic alterations are present between the lines (i.e., abdominal fat, T3 levels and glycemia), however there are no alterations in ad libitum food intake between the lines. A balanced block hybrdization design and the Del-Mar 14K chicken integrated systems microarrays were used to measure gene expression during development. 561 genes were differentially expressed between line, and 442 genes were significant for line-by-age interactions. The greatest number of genes were differentially expressed at week 1 of age, prior to any divergence in adiposity between the two lines. Keywords: Chickens divergently selected for fatness or leanness, transcriptional profiling, differentially expressed genes Four biological replicates were used for each genotype (FL and LL) at four different ages (weeks 1, 3, 5 and 7). 20 micrograms of total RNA from each sample were analyzed using DEL-MAR 14K integrated systems microarrays in a reference design. Each experimental sample was labeled with Cy3 and then hybridized with an aliquot of the reference pool (Cy5). The reference pool of hypothalamic total RNA was generated from an equal aliquot of all the RNA samples (fat and lean lines, week 1, 3, 5, and 7).
2010-05-26 | E-GEOD-10052 | biostudies-arrayexpress
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation.
2012-07-01 | GSE38880 | GEO