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Ablation of TET proteins in adipocytes protects against adiposity and metabolic dysfunction by potentiating energy expenditure

ABSTRACT: Ablation of TET proteins in adipocytes protects against adiposity and metabolic dysfunction by potentiating energy expenditure

PROVIDER: PRJNA740303 | ENA |

REPOSITORIES: ENA

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Ablation of TET proteins in adipocytes protects against adiposity and metabolic dysfunction by potentiating energy expenditure

Project description:Ten-eleven translocation (TET) proteins oxidize 5-methylcytosine in DNA to 5- hydroxymethylcytosine and further oxidized derivatives. Here we show that TET proteins are key epigenetic suppressors of adipocyte thermogenesis and energy expenditure in both white and brown adipose tissues in vivo. Tet expression in adipocytes decreases upon cold or adrenergic stimulation but increases following high-fat diet (HFD) consumption. Mice with triple deletion of all three Tet genes in adipocytes have higher energy expenditure due to enhanced fat browning and thermogenesis. They also show significantly enhanced lipolysis because of elevated expression of Adrb3 and key lipases including Atgl and Hsl. Consequently, the knockout mice display improved cold tolerance and are substantially resistant to obesity, inflammation, and associated metabolic complications including insulin resistance. Mechanistically, TET deficiency substantially prevents the HFD-induced transcriptional alterations in adipose tissues. TET proteins recruit histone deacetylases (HDACs) to the key thermogenic gene loci including Adrb3, Ppargc1a, and Ucp1, leading to transcriptional repression through histone deacetylation. Thus, the TET-HDAC axis may be therapeutically targeted to treat obesity and related metabolic diseases.

2021-11-01 | GSE178762 | GEO

Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure

Project description:Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure

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Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure

Project description:We investigated the effect of weight loss maintenance (WLM) and weight regain on skeletal muscle in rodents. In skeletal muscle of obesity prone rats, WLM reduced fat oxidative capacity and down-regulated genes involved in fat metabolism. After weight was regained in rats, the genes involved in fat metabolism were still reduced. Mice with skeletal muscle lipoprotein lipase overexpression (mCK-hLPL), which augments fat metabolism, were subjected to our WLM and weight regain paradigm. We found that mCK-hLPL attenuated weight regain by potentiating energy expenditure.Irrespective of genotype, weight regain suppressed dietary fat oxidation and down-regulated genes involved in fat metabolism in skeletal muscle. However, mCK-hLPL mice oxidized more fat throughout weight regain and had greater expression of genes involved in fat metabolism and lower expression of genes involved in carbohydrate metabolism during WLM and regain.

2021-03-24 | GSE154943 | GEO

Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity

Project description:Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity

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Adipocyte-Specific Ablation Of PU.1 Promotes Energy Expenditure and Ameliorates Metabolic Syndrome In Aging Mice

Project description:Adipocyte-Specific Ablation Of PU.1 Promotes Energy Expenditure and Ameliorates Metabolic Syndrome In Aging Mice

| PRJNA779077 | ENA

Adipocyte-Specific Ablation Of PU.1 Promotes Energy Expenditure and Ameliorates Metabolic Syndrome In Aging Mice

Project description:Here, we investigated the role of adipocyte PU.1 in the development of age-associated metabolic syndrome. We generated mice with adipocyte specific PU.1 knockout, assessed metabolic changes in young and aged PU.1fl/fl (control) and AdipoqCre PU.1fl/fl(aPU.1KO) mice, including body weight, body composition, energy expenditure and glucose homeostasis. We also performed transcriptional analyses using RNA-Sequencing of adipocytes from these mice.

2022-01-06 | GSE188497 | GEO

Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity [ChIP-seq]

Project description:Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity [ChIP-seq]

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Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity [RNA-seq]

Project description:Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity [RNA-seq]

| PRJNA451046 | ENA

EPAC1 enhances energy expenditure by selectively inducing brown and beige adipose tissue growth

Project description:Brown adipose tissue (BAT) is a central thermogenic organ that enhances energy expenditure (EE) and cardiometabolic health. However, regulators that specifically increase the number of thermogenic adipocytes are still an unmet need. Here, we show by phosphoproteomics that cAMP activates distinct signaling pathways in brown progenitors, with the cAMP-EPAC1 axis enhancing proliferation and differentiation of thermogenic but not white adipocytes. Further analysis revealed that a specific subpopulation of preadipocytes that are PDGFRα-positive express EPAC1. In vivo, pharmacological activation of EPAC1 enhances BAT growth and browning of white fat, leading to increased EE and reduced diet-induced adiposity. In contrast, mice lacking EPAC1 in PDGFRα-positive preadipocytes show the opposite phenotype. Importantly, EPAC1 activation enhances proliferation and differentiation of human brown adipocytes and human brown fat organoids. Interestingly, a coding variant in EPAC1 that positively correlates with BMI abolishes norepinephrine-induced proliferation of brown adipocytes. Thus, EPAC1 might be an attractive target to enhance thermogenic adipocyte number and EE to combat metabolic diseases.

2023-11-11 | PXD046709 | Pride

CIDR_Visceral Adiposity

Project description:CIDR_Visceral Adiposity

| PRJNA75481 | ENA