In vitro exploration of ACAT contributions to lipid droplet formation during adipogenesis

Mar 18, 2018Journal of lipid research

ACAT's role in fat droplet formation during fat cell development in the lab

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Abstract

Pharmacological inhibition of ACAT activity resulted in a 40% reduction in total adipocyte lipid content.

ACATs are identified as regulators of fat creation and lipid droplet formation in mouse fat cells.
Inhibition of ACAT activity led to lower levels of cholesterol and cholesteryl esters inside the cells.
Reduced ACAT activity decreased gene expression related to cholesterol uptake and release.
Inhibition of ACATs also suppressed the process of fat creation, as indicated by lower activity of specific proteins involved in fat metabolism.

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As adipose tissue is the major cholesterol storage organ and most of the intracellular cholesterol is distributed to lipid droplets (LDs), cholesterol homeostasis may have a role in the regulation of adipocyte size and function. ACATs catalyze the formation of cholesteryl ester (CE) from free cholesterol to modulate the cholesterol balance. Despite the well-documented role of ACATs in hypercholesterolemia, their role in LD development during adipogenesis remains elusive. Here, we identify ACATs as regulators of de novo lipogenesis and LD formation in murine 3T3-L1 adipocytes. Pharmacological inhibition of ACAT activity suppressed intracellular cholesterol and CE levels, and reduced expression of genes involved in cholesterol uptake and efflux. ACAT inhibition resulted in decreased de novo lipogenesis, as demonstrated by reduced maturation of SREBP1 and SREBP1-downstream lipogenic gene expression. Consistent with this observation, knockdown of eitherisoform reduced total adipocyte lipid content by approximately 40%. These results demonstrate that ACATs are required for storage ability of lipids and cholesterol in adipocytes. ACAT

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In vitro exploration of ACAT contributions to lipid droplet formation during adipogenesis

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