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Comment
. 2020 Jun 1;130(6):2809-2810.
doi: 10.1172/JCI137050.

Insulin-stimulated lipogenesis gets an epigenetic makeover

Clarence R Manuel, Rebecca A Haeusler
Comment

Insulin-stimulated lipogenesis gets an epigenetic makeover

Clarence R Manuel et al. J Clin Invest. .

Abstract

Hepatic de novo lipogenesis is a major contributor to nonalcoholic fatty liver disease (NAFLD). In this issue of the JCI, Liu and Lin et al. identified Slug as an epigenetic regulator of lipogenesis. Their findings suggest that Slug is stabilized by insulin signaling, and that it promotes lipogenesis by recruiting the histone demethylase Lsd1 to the fatty acid synthase gene promoter. On the other hand, genetic deletion or acute depletion of Slug, or Lsd1 inhibition, reduced lipogenesis and protected against obesity-associated NAFLD and insulin resistance in mice. This study advances our understanding of how lipogenesis is regulated downstream of insulin signaling in health and disease.

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Conflict of interest statement

Conflict of interest: The authors have declared that no conflict of interest exists.

Figures

Figure 1
Figure 1. Model of insulin-stimulated lipogenesis.
Insulin stimulates protein kinase B (AKT), which activates mammalian target of rapamycin (mTORC1) and transcription factors/repressors (blue). Multiple glucose- and insulin-regulated transcription factors and chromatin remodelers (yellow) collaborate to regulate postprandial de novo lipogenesis in liver.
See this image and copyright information in PMC

Comment on

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