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Updated: Aug 5, 2026

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Integrin-linked kinase promotes hepatic fat accumulation via F-actin stabilization-dependent CD36 plasma membrane
Kakali Ghoshal1, Fabian Bock1,2, Nathan C Winn3,4
1Department of Medicine, Division of Nephrology and Hypertension, Vanderbilt University School of Medicine, Nashville, TN, USA.
Abstract:
Increased hepatic lipid accumulation occurs in high-fat diet (HFD)-induced insulin resistance. Integrin-linked kinase (ILK) contributes to HFD-induced hepatic insulin resistance by increasing hepatic triglyceride content. How ILK promotes HFD-induced hepatic fatty acid accumulation is underexplored. ILK favors the formation of F-actin bundling and is upregulated following HFD. Moreover, the fatty acid transporter CD36 localizes to membrane ruffles rich in F-actin following HFD. Thus, we investigated whether ILK-mediated F-actin stabilization and liver fatty acid uptake are mechanistically linked. HFD-fed mice lacking ILK in hepatocytes have reduced hepatic F-actin abundance, CD36 plasma membrane localization, and intracellular lipid accumulation. ILK-null cells treated with the F-actin stabilizer jasplakinolide increased cortical F-actin polymerization, plasma membrane-associated CD36, and intracellular lipid uptake. CD36 inhibition reduced lipid uptake in jasplakinolide-treated ILK-null cells, confirming that F-actin-induced CD36 plasma membrane localization promotes lipid accumulation. Thus, ILK regulates intracellular lipid transport by linking CD36 to an F-actin-rich cytoskeleton.
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