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Silencing ANGPTL8 reduces mouse preadipocyte differentiation and insulin signaling. | LitMetric

AI Article Synopsis

  • * Research shows that reducing ANGPTL8 levels in mouse preadipocytes hampers their ability to differentiate into fat cells, slows down fat accumulation, and decreases fat breakdown when stimulated.
  • * The study found that ANGPTL8 knockdown disrupts early expression of important genes related to fat cell development and insulin signaling, indicating that ANGPTL8 has crucial intracellular roles beyond its known external functions.

Article Abstract

ANGPTL8, expressed mainly in the liver and adipose tissue, regulates the activity of lipoprotein lipase (LPL) present in the extracellular space and triglyceride (TG) metabolism through its interaction with ANGPTL3 and ANGPTL4. Whether intracellular ANGPTL8 can also exert effects in tissues where it is expressed is uncertain. ANGPTL8 expression was low in preadipocytes and much increased during differentiation. To better understand the role of intracellular ANGPTL8 in adipocytes and assess whether it may play a role in adipocyte differentiation, we knocked down its expression in normal mouse subcutaneous preadipocytes. ANGPTL8 knockdown reduced adipocyte differentiation, cellular TG accumulation and also isoproterenol-stimulated lipolysis at day 7 of differentiation. RNA-Seq analysis of ANGPTL8 siRNA or control siRNA transfected SC preadipocytes on days 0, 2, 4 and 7 of differentiation showed that ANGPTL8 knockdown impeded the early (day 2) expression of adipogenic and insulin signaling genes, PPARγ, as well as genes related to extracellular matrix and NF-κB signaling. Insulin mediated Akt phosphorylation was reduced at an early stage during adipocyte differentiation. This study based on normal primary cells shows that ANGPTL8 has intracellular actions in addition to effects in the extracellular space, like modulating LPL activity. Preadipocyte ANGPTL8 expression modulates their differentiation possibly via changes in insulin signaling gene expression.

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Source
http://dx.doi.org/10.1016/j.bbalip.2024.159461DOI Listing

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