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Crtc1 deficiency aggravates fat accumulation in the white adipose tissue

ABSTRACT: Crtc1 deficiency aggravates fat accumulation in the white adipose tissue

PROVIDER: PRJNA660732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12563954.fastq.gz	Fastqsanger.gz
	SRR12563955.fastq.gz	Fastqsanger.gz
	SRR12563956.fastq.gz	Fastqsanger.gz
	SRR12563957.fastq.gz	Fastqsanger.gz
	SRR12563958.fastq.gz	Fastqsanger.gz

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Crtc1 deficiency aggravates fat accumulation in the white adipose tissue

Project description:Obesity is described as excessive fat accumulation that drives the development of glucose and lipid metabolism disorders, which is linked to multiple diseases. Crtc1, known as a transducer to regulate Creb activity, plays an important role in several basic physiological functions. Previous studies have shown visible hyperappetite and obesity in Crtc1 knockout (Crtc1-/-) mice. To investigate the effect of Crtc1 on fat accumulation in different organs, we generated Crtc1-/- mice by CRISPR/Cas9 system and regarded Crtc1+/+ as control under the normal feeding conditions. Compared with Crtc1+/+ mice, Crtc1-/- mice exhibited increase of bodyweight which was resulted from the abnormal expansion of white adipocyte. In addition, Crtc1-/- mice were more prone to hyperglycemia and dyslipidemia, supported by the levels of plasma glucose and FABP4. The results of RNA-seq and qRT-PCR in liver and epididymal white adipose tissue (eWAT) showed that the fat accumulation caused by Crtc1 deletion was mainly related to the lipid metabolism of adipose tissue, not liver. Moreover, the up-regulation of lipid metabolism in eWAT induced by Crtc1 deficiency was closely related to the up-regulation of Pparγ signaling pathway. Our findings suggested that endogenous Crtc1 had a protective role in obesity development and Crtc1 deficiency aggravates the progression of fat accumulation and related co-morbidities, which introduced a new insight for treatment of obesity.

2020-09-05 | GSE157270 | GEO

Brown fat-specific YY1 deficiency effect on subcutaneous white adipose tissue

Project description:Analysis of visceral white adipose tissue (EWAT) from Yin Yang 1 adipose-specific knockout mice exposed to cold (4ºC) for 4 days.

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Brown fat-specific YY1 deficiency effect on subcutaneous white adipose tissue

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2015-11-10 | E-GEOD-70562 | biostudies-arrayexpress

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Project description:We compared gene expression between high fat diet (HFD)-fed Adipo-NDUFS4 knockout (KO) and WT mice in inguinal white adipose tissue (iWAT or scWAT).

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TP53INP2 knockout in inguinal white adipose tissue

Project description:Excessive fat accumulation is a major risk factor for the development of type 2 diabetes.To determine the mechanisms by wich TP53INP2 regulates adipogenesis, gene expression profile was performed in inguinal white adipose tissue fromTP53INP2-deficient mice.

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TP53INP2 knockout in perigonadal white adipose tissue

Project description:Excessive fat accumulation is a major risk factor for the development of type 2 diabetes.To determine the mechanisms by wich TP53INP2 regulates adipogenesis, gene expression profile was performed in perigonadal white adipose tissue fromTP53INP2-deficient mice.

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Gpnmb secreted from liver promotes lipogenesis in white adipose tissue and aggravates obesity and insulin resistance

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miRNA-22 deletion limits white adipose expansion and activates brown fat to attenuate high-fat diet-induced fat mass accumulation.

Project description:BackgroundObesity, characterized by excessive expansion of white adipose tissue (WAT), is associated with numerous metabolic complications. Conversely, brown adipose tissue (BAT) and beige fat are thermogenic tissues that protect mice against obesity and related metabolic disorders. We recently reported that deletion of miR-22 enhances energy expenditure and attenuates WAT expansion in response to a high-fat diet (HFD). However, the molecular mechanisms involved in these effects mediated by miR-22 loss are unclear.Methods and resultsHere, we show that miR-22 expression is induced during white, beige, and brown adipocyte differentiation in vitro. Deletion of miR-22 reduced white adipocyte differentiation in vitro. Loss of miR-22 prevented HFD-induced expression of adipogenic/lipogenic markers and adipocyte hypertrophy in murine WAT. In addition, deletion of miR-22 protected mice against HFD-induced mitochondrial dysfunction in WAT and BAT. Loss of miR-22 induced WAT browning. Gain- and loss-of-function studies revealed that miR-22 did not affect brown adipogenesis in vitro. Interestingly, miR-22 KO mice fed a HFD displayed increased expression of genes involved in thermogenesis and adrenergic signaling in BAT when compared to WT mice fed the same diet.ConclusionsCollectively, our findings suggest that loss of miR-22 attenuates fat accumulation in response to a HFD by reducing white adipocyte differentiation and increasing BAT activity, reinforcing miR-22 as a potential therapeutic target for obesity-related disorders.

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Ubiquitin independent degradation pathway regulates browning of white adipose tissue

Project description:Obesity is a significant risk factor for diabetes, cardiovascular diseases, and certain cancers, and manifests as excessive fat accumulation. The browning of white adipose tissue (WAT) represents one of the most promising strategies for preventing and treating obesity and metabolic diseases. To date, an increasing number of studies have focused on key molecular mechanisms regulating fat thermogenesis, laying the foundation for effective intervention strategies.We analyzed the differentially expressed proteins in white adipose tissue of the inguinal region using mass spectrometry.

2024-08-29 | PXD055441 |

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