Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA358202 | ENA |
REPOSITORIES: ENA
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Project description:Adiponectin is known as a key molecule to ameliorate symptoms of the type 2 diabetes mellitus and disorder of lipid metabolism. In this study, we investigated whether hot water extracts of some livestock by-products induced expression of adiponectin using 3T3-L1 adipocytes. Out of 11 extracts tested, pig testis extracts (PT) enhanced adiponectin mRNA expression and secretion of adiponectin protein from 3T3-L1 cells. Furthermore, simultaneous treatment with PT and daidzein, soy phytoestrogen, enhanced synergistically adiponectin secretion. Moreover, pretreatment with an estrogen receptor β (ERβ) antagonist (PHTPP) diminished adiponectin secretion in daidzein treated cell, but not in PT treated cells. Transcriptome analyses revealed that daidzein and PT commonly regulated PPAR signaling pathway, although gene expression was differently regulated in PT-treated cells and daidzein-treated cells. The expression of 476 and 380 genes significantly up-regulated in daidzein and PT treatment, although commonly regulated genes were only 86 genes. These results suggested that PT may ameliorate lipid metabolic dysfunction via promote adipocytes differentiation and enhance adiponectin secretion through different mechanism from daidzein.
2017-06-30 | GSE92630 | GEO
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2012-04-04 | E-GEOD-18600 | biostudies-arrayexpress
Project description:Cebpa is a critical transcription factor gene for adipocyte differentiation and adipose tissue development. However, mechanisms controlling Cebpa expression during adipogenic differentiation remain largely unknown. Here, we generated the high-resolution chromatin interaction maps of Cebpa in 3T3-L1 preadipocytes (3T3-L1) and 3T3-L1 adipocytes (3T3-L1-AD) using circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq), and characterized differences in their chromatin interactomes and chromatin status of the interaction sites during adipogenic differentiation. We performed a 4C-seq experiment on inguinal white adipose tissue (iWAT) to evaluate whether chromatin interaction between Cebpa-L1-AD-En2 and Cebpa promoters in 3T3-L1 adipocytes also exists in mouse adipose tissue.
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Project description:Aims/Hypothesis. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Methods. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high fat diet (HFD). The effects of eWAT transduction on metabolic parameters were evaluated 10 weeks later. To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain- or loss of LMO3 expression, respectively. Results. AAV transduction of eWAT results in strong and stable Lmo3 expression specifically in the adipocyte fraction over a course of 10 weeks with HFD feeding. Lmo3 expression in eWAT significantly improved glucose clearance and insulin sensitivity in diet-induced obesity, paralleled by increased serum adiponectin. On a molecular level, LMO3 expression in eWAT increased pathways indicative of adipogenesis and PPARg signaling as well as mitochondrial activity, paralleled by a suppression of adipose tissue fibrosis. In vitro, Lmo3 expression in 3T3-L1 adipocytes increased insulin-stimulated GLUT4 translocation and glucose uptake as well as mitochondrial oxidative capacity in addition to fatty acid oxidation. LMO3 overexpression promoted, while silencing of LMO3 suppressed, mitochondrial oxidative capacity in human mature adipocytes. Conclusions. LMO3 expression in visceral adipose tissue regulates multiple genes that preserve adipose tissue functionality during obesity, such as glucose tolerance, insulin sensitivity and adiponectin secretion. Together with increased PPARγ activity, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. These data add LMO3 as a novel regulator improving visceral adipose tissue function during obesity.
2021-08-24 | GSE139162 | GEO
Project description:Aims/Hypothesis. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Methods. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high fat diet (HFD). The effects of eWAT transduction on metabolic parameters were evaluated 10 weeks later. To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain- or loss of LMO3 expression, respectively. Results. AAV transduction of eWAT results in strong and stable Lmo3 expression specifically in the adipocyte fraction over a course of 10 weeks with HFD feeding. Lmo3 expression in eWAT significantly improved glucose clearance and insulin sensitivity in diet-induced obesity, paralleled by increased serum adiponectin. On a molecular level, LMO3 expression in eWAT increased pathways indicative of adipogenesis and PPARg signaling as well as mitochondrial activity, paralleled by a suppression of adipose tissue fibrosis. In vitro, Lmo3 expression in 3T3-L1 adipocytes increased insulin-stimulated GLUT4 translocation and glucose uptake as well as mitochondrial oxidative capacity in addition to fatty acid oxidation. LMO3 overexpression promoted, while silencing of LMO3 suppressed, mitochondrial oxidative capacity in human mature adipocytes. Conclusions. LMO3 expression in visceral adipose tissue regulates multiple genes that preserve adipose tissue functionality during obesity, such as glucose tolerance, insulin sensitivity and adiponectin secretion. Together with increased PPARγ activity, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. These data add LMO3 as a novel regulator improving visceral adipose tissue function during obesity.
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