Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-seq of liver transcriptome of UCP1+ cell-ablated mice at room temperature and upon acute cold exposure

ABSTRACT: UCP1-expressing brown and beige adipocytes are known to play an important role in thermogenic adaptation in mammals. Recent studies have proposed that these cells also exert beneficial effects on metabolic health. Therefore, we aimed to identify the consequences of UCP1+ cell loss on the metabolism of adult mice under standard conditions and upon cold challenge. In this study, UCP1+ cells were ablated in adult mice, and liver tissue was collected at room temperature or following acute cold exposure. We intended to compare the transcriptional profile of the liver between control and UCP1+ cell-ablated mice in order to identify liver-specific adaptations to severe UCP1+ cell loss under basal conditions and during acute cold stress.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Lucille Lopez-Delisle

PROVIDER: E-MTAB-16705 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Similar Datasets

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

RNA-seq of liver transcriptome of UCP1+ cell-ablated mice at room temperature and upon acute cold exposure

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets