ArticleNpj biological timing and sleep2025
Deletion of Arntl, a component of the molecular clock, in adipocytes leads to cellular hypertrophy by increasing insulin sensitivity via FGF21.
Article in Npj biological timing and sleep, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- [Interactions among circadian rhythm, obesity, and inflammation and their regulation by exercise].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
Brain and muscle Arnt-like protein 1 (BMAL1), encoded by Aryl hydrocarbon receptor nuclear translocator like 1 (Arntl) gene, is a transcription factor that regulates the circadian rhythm of the expressions of several genes. The link between the loss of BMAL1 function in adipose tissue and obesity has been reported. Although these previous studies have suggested that dysregulation of lipolysis is a contributing factor, but the detailed mechanism has not been fully understood. This study aimed to elucidate the role of BMAL1 in adipocytes using adipocyte-specific Arntl deficient (AAKO) mice. Deletion of Arntl in adipocytes leads to increased cellular insulin sensitivity, which in turn, inhibited lipolysis in adipocytes and caused cellular hypertrophy. The expression levels of Fgf21 in adipose tissue were significantly elevated in AAKO mice compared to Arntl
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