Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression Profiles of miRNAs in brown fat of mice at room temperature and cold exposure (8C)

ABSTRACT: microRNAs levels were measured in brown adipose tissue of male C57Bl6N mice that were kept at RT or during cold exposure (8Â°C) for 24 hrs. Several miRNAs including myomirs were identified to be regulated in response to cold. Brown adipose tissue from 2 groups of 8 weeks old male C57Bl6N mice at room temperature (n=3) or after cold exposure n=3) at 8Â°C for 24 hrs were excised and RNA was extracted using Trizol and the manufactureres recommended procedure. miRNA expression levels were determined using Agilent microRNA expression analysis platform.

ORGANISM(S): Mus musculus

SUBMITTER: Markus Stoffel

PROVIDER: E-GEOD-41306 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MyomiR-133 regulates brown fat differentiation through Prdm16.

Trajkovski Mirko M Ahmed Kashan K Esau Christine C CC Stoffel Markus M

Nature cell biology 20121201 12

Brown adipose tissue (BAT) uses the chemical energy of lipids and glucose to produce heat, a function that can be induced by cold exposure or diet. A key regulator of BAT is the gene encoding PR domain containing 16 (Prdm16), whose expression can drive differentiation of myogenic and white fat precursors to brown adipocytes. Here we show that after cold exposure, the muscle-enriched miRNA-133 is markedly downregulated in BAT and subcutaneous white adipose tissue (SAT) as a result of decreased ex ...[more]

PMID: 23143398

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Project description:Non-shivering thermogenesis in adipocytes is mediated by brown adipose tissue, purportedly through the sole action of uncoupling protein 1 (UCP1). The physiological relevance of UCP1-dependent thermogenesis has primarily been inferred from the attenuation of thermogenic output of mice genetically lacking Ucp1 from birth (germline Ucp1-/-). However, germline Ucp1-/- mice harbor secondary changes within brown adipose tissue beyond UCP1, such as reduced electron transport chain abundance. We show here that these secondary changes also encompass reduced expression of genes regulating fuel liberation, changes that would attenuate the capacity of any thermogenic pathway. Therefore, the quantitative contribution of UCP1-dependent and -independent thermogenesis is not fully understood. To mitigate the potentially confounding ancillary changes to brown adipose tissue of germline Ucp1-/- mice, we constructed mice with inducible adipocyte-selective disruption of Ucp1. We find that, while germline Ucp1-/- mice succumb to cold-induced hypothermia with complete penetrance, most mice with inducible deletion of Ucp1 maintain homeothermy in the cold. However, inducible adipocyte-selective co-deletion of Ucp1 and creatine kinase B (Ckb, an effector of UCP1-independent thermogenesis) exacerbates cold-intolerance, indicative of a negative genetic interaction and thus a parallel thermogenic function. We find no evidence for impairments in insulation or non-shivering thermogenesis in skeletal muscle that would drive this phenotype. Furthermore, following UCP1 deletion or UCP1/CKB co-deletion from mature adipocytes, moderate cold exposure triggers the regeneration of mature adipocytes that coordinately restore UCP1 and CKB to brown adipose tissue, providing further evidence of their parallel thermogenic relationship. Our findings suggest that thermogenic adipocytes utilize non-paralogous protein redundancy – through UCP1 and CKB – to promote cold-induced energy dissipation.

Dataset Information

Expression Profiles of miRNAs in brown fat of mice at room temperature and cold exposure (8C)

Publications

MyomiR-133 regulates brown fat differentiation through Prdm16.

Similar Datasets

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