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An overfeeding-induced obesity mouse model reveals necessity for Sin3a in postnatal peak β cell mass acquisition

ABSTRACT: An overfeeding-induced obesity mouse model reveals necessity for Sin3a in postnatal peak β cell mass acquisition

PROVIDER: PRJNA821919 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18575425.fastq.gz	Fastqsanger.gz
	SRR18575426.fastq.gz	Fastqsanger.gz
	SRR18575427.fastq.gz	Fastqsanger.gz
	SRR18575428.fastq.gz	Fastqsanger.gz
	SRR18575429.fastq.gz	Fastqsanger.gz

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An overfeeding-induced obesity mouse model reveals necessity for Sin3a in postnatal peak β cell mass acquisition

Project description:The increase of functional β cell mass is paramount to maintain glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow β cell mass adaptation may allow discovery of therapeutically actionable control nodes. In this study, we report the rapid and robust β cell hyperplasic effect in a mouse model of overfeeding-induced obesity (OIO) based on direct gastric caloric infusion. By performing RNA sequencing in islets isolated from OIO mice, we identified Sin3a as a novel transcriptional regulator of β cell mass adaptation. β cell-specific Sin3a knockout animals showed profound diabetes, due to defective acquisition of postnatal β cell mass. These findings reveal a novel regulatory pathway in β cell proliferation, and validate OIO as a model for discovery of other mechanistic determinants to β cell adaptation.

2022-11-09 | GSE199907 | GEO

An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak β-Cell Mass Acquisition.

Project description:The increase of functional β-cell mass is paramount to maintaining glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow β-cell mass adaptation may allow for the discovery of therapeutically actionable control nodes. In this study, we report the rapid and robust β-cell hyperplasic effect in a mouse model of overfeeding-induced obesity (OIO) based on direct gastric caloric infusion. By performing RNA sequencing in islets isolated from OIO mice, we identified Sin3a as a novel transcriptional regulator of β-cell mass adaptation. β-Cell-specific Sin3a knockout animals showed profound diabetes due to defective acquisition of postnatal β-cell mass. These findings reveal a novel regulatory pathway in β-cell proliferation and validate OIO as a model for discovery of other mechanistic determinants of β-cell adaptation.

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Baseline body fat percentage is related with weight and fat mass gain from high-fat overfeeding over a period of 8 weeks

Project description:Epidemiological data suggest that lean individuals resist exposure to the obesogenic environment better than those with obesity. To test this, we analyzed the relationship between overfeeding-induced weight and fat mass gains with baseline body mass index (BMI) and body fat percentage. In this controlled intervention study, 34 young men (BMI: 25.5±2.4 kg/m2, body fat [DXA]: 19.3±5.1%) consumed for 8 weeks 40% more energy than needed at weight maintenance. The energy costs of weight and fat mass gain were calculated as the 8-week excess energy consumed (EEC) divided by weight or fat mass gain. Energy expenditure (baseline and after overfeeding) was determined using a metabolic chamber and doubly labeled water. Transcriptomic analysis was conducted from abdominal subcutaneous adipose tissue samples

2025-04-28 | GSE294614 | GEO

SIN3A Acetylation Complex - Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal

Project description:Sin3a is the central scaffold protein of the prototypical Hdac1/2 chromatin repressor complex, crucially required during early embryonic development for the growth of pluripotent cells of the inner cell mass. Here, we explore the endogenous composition of the Sin3a-Hdac complex in pluripotent embryonic stem (ES) and differentiated cells. To do this, we established an endogenous double immunoprecipitation strategy coupled with quantitative mass spectrometry (ENDIP-MS) allowing us to define the precise composition of the Sin3a complex in multiple cell types. We identify the Fam60a subunit as a key defining feature of a variant Sin3a complex present in ES cells, but not in differentiated cells. Fam60a co-occupies H3K4me3 positive promoters with Sin3a and is essential to maintain it on chromatin. Consistent with this, Fam60a depletion phenocopies the loss of Sin3a, leading to decreased proliferation, an extended G1-phase and the deregulation of genes associated with differentiation. Taken together, our data characterise Fam60a as an essential core subunit of a variant Sin3a complex in ES cells required to promote rapid proliferation and to prevent unscheduled differentiation.

2017-05-19 | PXD005464 | Pride

Murine Testes: Germ Cell-Specific Sin3a Knockout vs. Hemizygous vs. Wild Type at Postnatal Day 0

Project description:Chromatin modifier Swi-independent 3a (SIN3A), together with associated histone deacetylases, influences gene expression during development and differentiation through multiple transcription factors in a cell-specific manner. Sin3a is essential for the maintenance of inner cell mass cells of mouse blastocysts, embryonic fibroblasts, and myoblasts, but is not required for the survival of trophectoderm or Sertoli cells. To better understand how this transcriptional regulator modulates cells at different developmental stages within a single lineage, we used conditional gene targeting in mice to ablate Sin3a from perinatal quiescent male gonocytes and from postnatal differentiating spermatogonia. Gene expression in the whole testes of age-matched Ddx4(Vasa/Mvh)-cre mediated conditional Sin3a gene-targeted(VSKO) mice, germ cell-specific Sin3a hemizygous (HEMI) mice, and wild type (WT) mice was measured at postnatal day 0. Two biological replicate animals were used for each condition.

2012-10-01 | E-GEOD-38096 | biostudies-arrayexpress

Murine Testes: Germ Cell-Specific Sin3a Knockout vs. Hemizygous vs. Wild Type at Postnatal Day 0

2012-10-01 | GSE38096 | GEO

Protection against overfeeding-induced weight gain in mice is preserved in obesity but does not require FGF21 or MC4R

Project description:Experimental overfeeding triggers homeostatic compensatory mechanisms that counteract weight gain. Here, we utilized intragastric overfeeding in mice to investigate the physiological and molecular responses to forced weight gain. Both lean and diet-induced obese (DIO) mice exhibited a potent and prolonged lowering of voluntary food intake following overfeeding-induced weight gain. Although overfeeding resulted in a marked increase in circulating fibroblast growth factor 21 (FGF21), experiments with FGF21 knockout (KO) mice demonstrated that FGF21 is dispensable for the homeostatic defense against experimental weight gain. Targeted proteomics unveiled novel circulating factors linked to overfeeding, including the protease legumain (LGMN). Notably, administration of recombinant LGMN lowered body weight and food intake in DIO mice. The protection against weight gain was also associated with reduced vascularization in the hypothalamus and sustained reductions in transcript levels of the orexigenic neuropeptides, Npy and AgRP, suggesting a role of hypothalamic signaling in the homeostatic recovery from overfeeding. Overfeeding of melanocortin 4 receptor (MC4R) KO mice showed that these mice can suppress voluntary food intake and counteract the enforced weight gain, although their rate of weight recovery is impaired. Collectively, these findings demonstrate that the defense against overfeeding-induced weight gain remains intact in obesity and involves mechanisms independent of both FGF21 and MC4R.

2024-01-12 | GSE247825 | GEO

Epigenetic analysis of healthy young men following a control and high-fat overfeeding diet

Project description:Genome-wide DNA methylation profiling of healthy young men following a control and high-fat overfeeding diet using Illumina's Infinium 27k Human DNA methylation Beadchip v. 1.2. DNA methylation profiles were obtained for 27,578 CpG sites in human skeletal muscle. Randomized cross-over desgin, where all subjects receieved both treatments (control and high-fat overfeeding diet). Biopsies were obtained from 23 different individuals amounting to 22 samples following the control diet and 22 samples following the high-fat overfeeding diet (paired n=21). Bisulphite converted DNA from the 44 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip.

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Sin3A mutant pancreatic islets

Project description:Sin3A null islet cells compared with wild type

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Sin3A mutant pancreatic islets

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