Multi-organ transcriptome changes in response to acute cold exposure
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE290875 | GEO | 2025/09/30
REPOSITORIES: GEO
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Project description:Understanding how species adapt to changing environments is a major goal in evolutionary biology and can elucidate the impact of climate change. Climate imposes inevitable effects on the geographical distribution of insects as their body temperature primarily depends on the environment. The vinegar fly Drosophila ananassae expanded from its tropical ancestral range to more temperate regions, which requires adaptation to colder temperatures. Transcriptome and genome-wide association studies focusing on the ancestral-range population identified the targets of selection related to ionoregulatory tissues. However, how cosmopolitan D. ananassae adapted to colder environments, where low temperatures last longer, is still unknown. Here, we present a study on the effect of long-term cold exposure on D. ananassae, examining the gene expression variation in the whole body and the ionoregulatory tissues, namely the hindgut and the Malpighian tubule. To elucidate molecular mechanisms of cold adaptation during species expansion, we included cold-tolerant and cold-sensitive strains from the ancestral species range and cold-tolerant strains from the derived species range. We show that cold acclimation improves cold tolerance and results in differential expression of more than half of the transcriptome in the ionoregulatory tissues and the whole body. Notably, we provide complementary insight into molecular processes at four levels: strains, populations, phenotypes, and tissues. By determining the biochemical pathways of phenotypic plasticity underlying cold tolerance, our results enhance our understanding of how environmental changes affect thermal adaptation in natural populations.
2025-04-14 | GSE270239 | GEO
Project description:The physiological adaptation to cold environmental temperatures involves the remodeling of energy-storing white adipose tissue (WAT) into an energy-burning thermogenic phenotype, characterized by the emergence of multi-locular beige adipocytes. To date, the full array of cold-responsive cells within WAT that mediate thermogenic remodeling remain undefined. Here, we demonstrate that distinct perivascular PDGFRb+ adipocyte precursor cell (APC) subpopulations are differentially sensitive to cold temperatures in vivo. One day of cold exposure elicits striking transcriptional changes in DPP4+ PDGFRb+ APCs, whereas committed DPP4- PDGFRb+ preadipocytes appear comparatively much less responsive. This adaptation includes beta-adrenergic receptor mediated induction in the expression of the pro-thermogenic cytokine, IL-33. DPP4+ PDGFRb+ cells represent the sole source of IL-33 within inguinal WAT of adult mice. Doxycycline-inducible deletion of Il33 in PDGFRb+ cells at the onset of cold exposure significantly compromises the thermogenic remodeling of WAT without directly impacting the differentiation capacity of APCs per se. Together, these studies reveal the presence of a cold-responsive progenitor cell subpopulation in adult WAT and highlight their ability to regulate tissue plasticity through the production of immunological factors.
2021-11-09 | GSE165974 | GEO
Project description:The physiological adaptation to cold environmental temperatures involves the remodeling of energy-storing white adipose tissue (WAT) into an energy-burning thermogenic phenotype, characterized by the emergence of multi-locular beige adipocytes. To date, the full array of cold-responsive cells within WAT that mediate thermogenic remodeling remain undefined. Here, we demonstrate that distinct perivascular PDGFRb+ adipocyte precursor cell (APC) subpopulations are differentially sensitive to cold temperatures in vivo. One day of cold exposure elicits striking transcriptional changes in DPP4+ PDGFRb+ APCs, whereas committed DPP4- PDGFRb+ preadipocytes appear comparatively much less responsive. This adaptation includes beta-adrenergic receptor mediated induction in the expression of the pro-thermogenic cytokine, IL-33. DPP4+ PDGFRb+ cells represent the sole source of IL-33 within inguinal WAT of adult mice. Doxycycline-inducible deletion of Il33 in PDGFRb+ cells at the onset of cold exposure significantly compromises the thermogenic remodeling of WAT without directly impacting the differentiation capacity of APCs per se. Together, these studies reveal the presence of a cold-responsive progenitor cell subpopulation in adult WAT and highlight their ability to regulate tissue plasticity through the production of immunological factors.
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Project description:Transcriptomic analysis on white adipose tissues (WAT), brown adipose tissues (BAT), skeletal muscles and liver from cold-exposed obese mice treated with KPT-330 or DMSO, and those from obese mice housed at ambient temperature indicated that KPT-330 profoundly modulates immune responses in these thermogenic tissues and organs.
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Project description:<p>Glucose uptake is essential for cancer glycolysis and is involved in non-shivering thermogenesis of adipose tissues. Most cancers use glycolysis to harness energy for their infinite growth, invasion and metastasis. Activation of thermogenic metabolism in brown adipose tissue (BAT) by cold and drugs instigates blood glucose uptake in adipocytes. However, the functional effects of the global metabolic changes associated with BAT activation on tumour growth are unclear. Here we show that exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers. Mechanistically, cold-induced BAT activation substantially decreases blood glucose and impedes the glycolysis-based metabolism in cancer cells. The removal of BAT and feeding on a high-glucose diet under cold exposure restore tumour growth, and genetic deletion of Ucp1-the key mediator for BAT-thermogenesis-ablates the cold-triggered anticancer effect. In a pilot human study, mild cold exposure activates a substantial amount of BAT in both healthy humans and a patient with cancer with mitigated glucose uptake in the tumour tissue. These findings provide a previously undescribed concept and paradigm for cancer therapy that uses a simple and effective approach. We anticipate that cold exposure and activation of BAT through any other approach, such as drugs and devices either alone or in combination with other anticancer therapeutics, will provide a general approach for the effective treatment of various cancers.</p>
2022-08-12 | MTBLS4856 | MetaboLights
Project description:This study explored the proteomic basis of cold adaptation, quantifying 11,394 proteins across 6 metabolic tissues and plasma. Systems level analysis revealed an enrichment for proteins involved in metabolism. In brown adipose tissue (BAT), cold adaptation was associated with enhanced glucose utilisation, including select remodelling of upper glycolysis to enhance superoxide production and UCP1 activity, and a downregulation of proteins involved in fatty acid oxidation. Strikingly, opposite changes were observed in liver and white adipose tissues, including upregulation of proteins involved in gluconeogenesis and lipolysis, respectively. This suggests that coordinated changes in many organs are required for maximal BAT thermogenesis. This coordination also associated with cold-regulated alterations to the plasma proteome, including elevated Fetuin A that is consistent with enhanced lipolysis in white adipose. Finally, overlapping but inverse changes in cold-exposed and diet-induced obese mice support impaired BAT activity as a driver of obesity.
2025-04-22 | PXD055965 | Pride
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.
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Project description:In the last decades, adipose tissue has been defined to play a central role in the control of energy balance. Furthermore, the proven endocrine and thermogenic functions of adipocytes have renewed interest in the study of this tissue, as the activation of non-shivering thermogenesis may hold great potential for the future treatment of obesity and T2D. Cold exposure has defined to activate this process. Here, the miRNA transcriptomic response of epididymal and inguinal white adipose depots (eWAT and iWAT, respectively) as well as that of the interscapular brown adipose depot (iBAT) of C57Bl/6 mice either exposed to 22ºC or 4ºC for the period of 4 days were examined. This in-detail study of the adaptation of each depot to cold exposure has allowed unraveling depot-specific regulatory molecular mechanisms.
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