Transcriptional regulation of adipocyte lipolysis by IRF2BP2

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipocyte lipolysis controls systemic energy levels and metabolic homeostasis. Lipolysis is regulated by posttranslational modifications of key lipolytic enzymes. However, less is known about the transcriptional mechanisms that regulate lipolysis. Here, we identify interferon regulatory factor-2 binding protein 2 (IRF2BP2) as a transcriptional repressor of adipocyte lipolysis. Deletion of IRF2BP2 in human adipocytes increases lipolysis without affecting glucose uptake, whereas IRF2BP2 overexpression decreases lipolysis. RNA sequencing, and chromatin immunoprecipitation sequencing analyses show that IRF2BP2 represses lipolysis-related genes, including LIPE , which encodes hormone sensitive lipase, the rate-limiting enzyme in lipolysis. Adipocyte-selective deletion of Irf2bp2 in mice increases Lipe expression and free fatty acid levels, resulting in adipose tissue inflammation and glucose intolerance. Together, these findings demonstrate that IRF2BP2 restrains adipocyte lipolysis and opens avenues to target lipolysis for the treatment of metabolic disease.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.