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Overactivation of intestinal SREBP2 in mice increases serum cholesterol

Ke Ma1, Pooja Malhotra1, Vinay Soni1

  • 1Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America.

Plos One
|January 28, 2014
PubMed

Insights

Activating intestinal Sterol Response Element Binding Protein 2 (SREBP2) increases cholesterol levels. This highlights the intestine's crucial role in maintaining body cholesterol homeostasis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Sterol Response Element Binding Protein 2 (SREBP2) is a key regulator of cholesterol homeostasis.
  • Statins activate intestinal SREBP2, potentially counteracting their cholesterol-lowering effects.
  • The impact of intestinal SREBP2 activation on plasma cholesterol was previously unknown.

Purpose of the Study:

  • To investigate the effect of intestine-specific overexpression of active SREBP2 on cholesterol metabolism.
  • To determine if activating intestinal SREBP2 alone is sufficient to alter plasma cholesterol levels.

Main Methods:

  • Generation of a novel transgenic mouse model (ISR2) with intestine-specific active SREBP2 overexpression using the villin promoter.
  • Microarray analysis of jejunal RNA to assess gene expression changes.
  • Quantification of cholesterol and triglyceride levels in jejunum, liver, and serum.

Main Results:

  • ISR2 mice exhibited specific overexpression of active SREBP2 in the intestine.
  • Increased expression of genes involved in fatty acid and cholesterol synthesis in the jejunum.
  • Elevated cholesterol and triglyceride levels in the jejunum and liver of ISR2 mice compared to wild-type.
  • Increased serum cholesterol in VLDL and LDL fractions, with decreased serum triglycerides in ISR2 mice.

Conclusions:

  • Intestine-specific activation of SREBP2 is sufficient to raise plasma cholesterol levels.
  • This study underscores the critical role of the intestine in maintaining overall body cholesterol homeostasis.
  • Findings suggest potential therapeutic implications for managing cholesterol disorders.

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