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Related Concept Videos

Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

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Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
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Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

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Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
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Overview of Fatty Acid Metabolism01:28

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Lipids also are sources of energy that power cellular processes. Like carbohydrates, lipids are composed of carbon, hydrogen, and oxygen, but these atoms are arranged differently. Most lipids are nonpolar and hydrophobic. Major types include fats and oils, waxes, phospholipids, and steroids.
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Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
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Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
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Updated: Aug 16, 2025

Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
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Butyrate Lowers Cellular Cholesterol through HDAC Inhibition and Impaired SREBP-2 Signalling.

Stephanie Bridgeman1, Hon Chiu Woo1, Philip Newsholme1

  • 1Curtin Health Innovation Research Institute and Curtin Medical School, Curtin University, Bentley, WA 6102, Australia.

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|December 23, 2022
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Summary

Histone deacetylase (HDAC) inhibitors like sodium butyrate lower cholesterol by downregulating SREBP-2 signaling, unlike statins. This mechanism raises questions about butyrate

Keywords:
HDAC inhibitorsLDLSREBP-2butyratecholesterolstatins

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Histone deacetylase (HDAC) inhibitors, including butyrate, show potential in animal models for reducing cholesterol and protecting against diabetes.
  • The precise mechanisms underlying these effects, particularly concerning cholesterol metabolism, remain largely unelucidated in human cell systems.

Purpose of the Study:

  • To compare the effects of HDAC inhibitors (butyrate, valproate, trichostatin A) with statins on cholesterol metabolism.
  • To investigate the underlying molecular mechanisms, focusing on HepG2 hepatic cells and SREBP-2 signaling pathways.

Main Methods:

  • Treatment of HepG2 cells and other cell lines with sodium butyrate, sodium valproate, trichostatin A, and statins.
  • Analysis of cholesterol content, gene expression (HMGCR, LDL receptor), protein expression (ABCA1, SRB1), and SREBP-2 pathway activity.

Main Results:

  • HDAC inhibitors, including sodium butyrate, significantly reduced cholesterol content in HepG2 cells.
  • HDAC inhibition downregulated SREBP-2 target genes (HMGCR, LDL receptor), contrasting with statins that upregulate these processes.
  • Sodium butyrate did not increase cholesterol uptake and reduced ABCA1/SRB1 expression in HepG2 cells, though with cell-type variability.

Conclusions:

  • HDAC inhibition, exemplified by sodium butyrate, lowers cellular cholesterol primarily through impaired SREBP-2 signaling.
  • This mechanism differs fundamentally from statin action.
  • The findings question the potential efficacy of butyrate for reducing human serum LDL cholesterol.