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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Trends Biochem Sci. 2017 Nov 23;43(1):61–74. doi: 10.1016/j.tibs.2017.11.004

Figure 4. ACLY mediates a feed-forward mechanism to regulate GLUT4 levels in response to glucose uptake in adipocytes.

Figure 4

Adipocytes take up glucose in response to insulin via the GLUT4 glucose transporter. Glucose-dependent lipid synthesis and histone acetylation are ACLY-dependent, and GLUT4 expression is regulated in an ACLY-dependent manner in adipocytes[16,22,25]. Both adipocyte de novo lipogenesis and adipocyte GLUT4 expression are associated with improved systemic insulin sensitivity [35,36,38]. Since ACLY levels in adipocytes are suppressed by high fat feeding and obesity [25], it is plausible that low ACLY levels contribute to development of insulin resistance via ACLY’s dual roles in gene regulation and lipid synthesis.