AI Article Synopsis

  • Chronic sleep restriction (CSR) is linked to various health issues, and this study evaluates its effects on metabolic processes in white adipose tissue (WAT) using young male mice.
  • Research found that CSR significantly increased the expression of sirtuin 1 (SIRT1) and its target genes which are crucial for lipid metabolism and adipose tissue development, while genes promoting fat cell formation were downregulated.
  • The study suggests that SIRT1 pathways may help mitigate weight gain associated with CSR, providing new insights into how sleep deprivation impacts energy balance at a molecular level.

Article Abstract

Chronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic homeostasis at the level of white adipose tissue (WAT) remain poorly understood. Therefore, this study aimed to investigate the influence of CSR on sirtuin 1 (SIRT1) and the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway in the WAT of young male mice. Both genes interact with specific targets involved in multiple metabolic processes, including adipocyte differentiation, browning, and lipid metabolism. The quantitative PCR (qPCR) results demonstrated a significant upregulation of SIRT-1 and some of its target genes associated with the transcriptional regulation of lipid homeostasis (i.e., PPARα, PPARγ, PGC-1α, and SREBF) and adipose tissue development (i.e., leptin, adiponectin) in CSR mice. On the contrary, DNA-binding transcription factors (i.e., CEBP-β and C-myc), which play a pivotal function during the adipogenesis process, were found to be down-regulated. Our results also suggest that the induction of SIRT1-dependent molecular pathways prevents weight gain. Overall, these findings offer new, valuable insights into the molecular adaptations of WAT to CSR, in order to support increased energy demand due to sleep loss.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10969409PMC
http://dx.doi.org/10.3390/cimb46030138DOI Listing

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