Abstract
The extraction of RNA and lipids from a large number of biological samples is time-consuming and costly with steps required for both transcriptomic and lipidomic approaches. Most protocols rely on independent extraction of nucleic acids and lipids from a single sample, thereby increasing the need for biological material and inducing variability in data analysis. We investigated whether it is possible to use a standard RNA extraction procedure to analyze not only RNA levels, but also lipids in a single liver sample. We show that the organic phase obtained when using standard reagents for RNA extraction can be used to analyze lipids, including neutral lipids and fatty acids, by gas chromatography. We applied this technique to an analysis of lipids and the associated gene expression pattern in mice with hepatic steatosis induced by pharmacological activation of nuclear receptor LXR.
Highlights
The extraction of RNA and lipids from a large number of biological samples is time-consuming and costly with steps required for both transcriptomic and lipidomic approaches
We used liver tissue and hepatic cell lines to assess the method we developed and validated the protocol by analyzing samples from wild-type mice and transgenic mice lacking liver X receptor (LXR) α and β (NR1H3 and NR1H2, respectively)[4], two transcription factors known to play a central role in cholesterol and fatty acid metabolism[5]
By administering T0901317, a pharmacological agonist of both LXRs6, we induced hepatic steatosis in wild-type mice but not LXR−/− mice[4,6]. This steatosis occurs through an important increase in the expression of genes involved in fatty acid synthesis[6], called de novo lipogenesis
Summary
The extraction of RNA and lipids from a large number of biological samples is time-consuming and costly with steps required for both transcriptomic and lipidomic approaches. We show that the organic phase obtained when using standard reagents for RNA extraction can be used to analyze lipids, including neutral lipids and fatty acids, by gas chromatography We applied this technique to an analysis of lipids and the associated gene expression pattern in mice with hepatic steatosis induced by pharmacological activation of nuclear receptor LXR. By administering T0901317, a pharmacological agonist of both LXRs6, we induced hepatic steatosis in wild-type mice but not LXR−/− mice[4,6] This steatosis occurs through an important increase in the expression of genes involved in fatty acid synthesis[6], called de novo lipogenesis. Sample-specific networks[8] were analyzed, indicating Dgat[2] as an atypical LXR-sensitive gene involved in triglyceride synthesis[9,10] and down-regulated by pharmacological activation of LXR
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