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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse liver and brown adipose tissue from KRAP deficient mice

ABSTRACT: KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. This SuperSeries is composed of the following subset Series:; GSE13582: Expression data from BAT of the KRAP deficient mice; GSE13583: Expression data from liver of the KRAP deficient mice Experiment Overall Design: Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: takahiro fujimoto

PROVIDER: E-GEOD-13585 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.

Fujimoto Takahiro T Miyasaka Kyoko K Koyanagi Midori M Tsunoda Toshiyuki T Baba Iwai I Doi Keiko K Ohta Minoru M Kato Norihiro N Sasazuki Takehiko T Shirasawa Senji S

PloS one 20090121 1

Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiological roles remain unknown. Here we demonstrate that KRAP-deficient (KRAP(-/-)) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. K ...[more]

PMID: 19156225

Similar Datasets

Transcription profiling of brown adipose tissue from KRAP deficient animals

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Experiment Overall Design: Total RNA was extracted from BAT of three pairs of littermates (KO1 vs. WT1, KO2 vs. WT2 and KO3 vs. WT3) fed normal chow.

2009-01-30 | E-GEOD-13582 | biostudies-arrayexpress

Expression data from liver of the KRAP deficient mice

2009-01-22 | GSE13583 | GEO

Expression data from BAT of the KRAP deficient mice

2009-01-22 | GSE13582 | GEO

Expression data from BAT and liver of the KRAP deficient mice

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. This SuperSeries is composed of the SubSeries listed below.

2009-01-22 | GSE13585 | GEO

Transcription profiling of mous eliver of the KRAP deficient animals

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Experiment Overall Design: Total RNA was extracted from livers of three pairs of littermates (KO1 vs. WT1, KO2 vs. WT2 and KO3 vs. WT3) fed normal chow.

2009-02-07 | E-GEOD-13583 | biostudies-arrayexpress

Proteome imbalance of mitochondrial electron transport chain in brown adipocytes leads to metabolic benefits

Project description:Adaptive thermogenesis of brown adipose tissue (BAT) is critical for thermoregulation and contributes to total energy expenditure. However, whether BAT has non-thermogenic functions is largely unknown. Here, we describe that mice with a BAT-specific Liver kinase b1 deletion (Lkb1BKO mice) exhibited impaired mitochondrial respiration and thermogenesis in BAT, but reduced adiposity and liver triglyceride accumulation under high-fat-diet feeding at room temperature. Importantly, these metabolic benefits were also present in Lkb1BKO mice at thermoneutrality, where BAT thermogenesis was not required. Mechanistically, decreased mRNA levels of mtDNA-encoded electron transport chain (ETC) subunits and ETC proteome imbalance led to impaired mitochondrial respiration in BAT of Lkb1BKO mice. Furthermore, reducing mtDNA gene expression directly in BAT by removing mitochondrial transcription factor A (Tfam) in BAT also showed ETC proteome imbalance and the tradeoff between BAT thermogenesis and systemic metabolism at both room temperature and thermoneutrality. Collectively, our data demonstrates that ETC proteome imbalance in BAT regulates systemic metabolism independently of BAT thermogenic capacity.

2018-07-12 | PXD008599 | Pride

Gene expression data of brown-like adipocytes from Lgr4 homozygous mutant SVF

2013-11-07 | GSE47760 | GEO

Rdh1 supresses adiposity by promoting brown adipose adaptation to fasting and re-feeding

Project description:Rdh1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Here we show that Rdh1-null mice fed low-fat diet gain more weight as adiposity thann wild-type mice by 20 weeks old, despite neither consuming more calories nor decreasing activity. RNAseq revealed dysregulation of 424 BAT genes in null mice, with segregated predominantly into differences after fasting vs after re-feeding. Rdh1-generated atRA in BAT regulates multiple genes that promote BAT adaptation to whole-body energy status, such as fasting and re-feeding.

2019-03-20 | GSE128631 | GEO

Gene expression data of brown-like adipocytes from Lgr4 homozygous mutant SVF

Project description:Obesity has become a global health problem. Brown adipose tissue (BAT), specialized for energy expenditure through thermogenesis, potently counteracts obesity. Recently, BAT is also identified in human adults. We found that Lgr4 homozygous mutant (Lgr4m/m) mice display reduced adiposity and exhibit brown-like adipocytes in their WAT depots with higher expression of uncoupling protein 1 (Ucp1). Furthermore, Lgr4 ablation potentiates brown adipocyte differentiation from stromal vascular fraction (SVF) of epididymal WAT (eWAT) in vitro. We used microarrays to emxamine the gene expression profiles of the brown-like adipocytes differentiated from SVF of wild-type and Lgr4 mutant mice. We identified distinct gene expression profiles of these two groups. To demonstrate Lgr4 ablation can potentiate the differentiation of SVF from eWAT toward brown-like adipocytes in vitro, we isolated SVF from epididymal white adipose tissue (eWAT) of wild-type (WT) and Lgr4 mutant mice. We then plated SVF cells in 12-well plate, and differentiated them to brown adipocytes, followed by RNA extraction and hybridization with Affymetrix microarrays.

2013-11-07 | E-GEOD-47760 | biostudies-arrayexpress

Architecture of the outbred brown fat proteome defines regulators of metabolic physiology

Project description:Obesity is a polygenic disorder with variable penetrance in the general population. Brown adipose tissue (BAT) is a major regulator of energy expenditure and metabolic physiology due to a specialized proteome that orchestrates futile metabolic cycles, which could be leveraged to treat obesity. However, nearly all mechanistic studies of BAT protein function occur in a single inbred mouse strain, which has limited understanding of generalizable mechanisms of BAT regulation over metabolism. Here we perform deep quantitative multiplexed proteomics of BAT across a cohort of 163 genetically defined Diversity Outbred (DO) mice, a model that parallels the genetic and phenotypic variation found in the human population. Leveraging the high variation afforded by this model, we define the functional architecture of the outbred BAT proteome, comprising 10,479 proteins. In doing so, we assign novel co-operative functions to 2,578 proteins with 780 established protein networks. We demonstrate that this analytic framework enables systematic discovery of regulators of BAT function, exemplified by uncovering SFXN5 and LETMD1 as modulators of UCP1-dependent thermogenesis. We also identify 638 proteins that underlie protection from, or sensitivity to, at least one parameter of metabolic disease. From this basis, we identify the Na+/K+- ATPase α2 subunit as an inhibitor of BAT energy expenditure, that increases adiposity through antagonism of calcium influx-dependent activation of thermogenic effectors. We provide this Outbred Proteomic Architecture as a resource for understanding conserved mechanisms of BAT regulation over metabolic physiology.

2022-11-08 | PXD036947 | Pride

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