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Story ideas from the Journal of Lipid Research

Stories appearing in the Dec. 2007 Journal of Lipid Research (Vol. 48, No. 12)

  • Genetic Variants Affect Diet-Associated Cholesterol Metabolism
  • Crohns Disease Increases Progression of Atherosclerosis
  • Breaking the Vicious Cycle of Bile Acid Disorders

Genetic Variants Affect Weight-Associated Cholesterol Metabolism

Researchers have found that variants in two metabolic genes alter how the body adjusts cholesterol metabolism in response to weight loss, a finding that may lead to screening tools to identify the optimal method of reducing cholesterol levels in specific individuals.

Dietary intake clearly contributes to elevated cholesterol levels. However, inherited factors such as mutations in proteins that regulate how much dietary cholesterol is absorbed, specifically ABCG5 and ABCG8, also influence the effect of diet on cholesterol trafficking. Several variants of ABCG5 and ABCG8 exist in the general population, each with different metabolic properties.

To study how these variants affect cholesterol metabolism in response to changes in weight loss from diet and exercise, Peter Jones and colleagues performed a before and after analysis of 35 women with elevated cholesterol who lost an average of 25 pounds over 20 weeks. They found two variants that were linked to significant changes in cholesterol metabolism. People with the 604E variant of ABCG5 experienced far larger decreases in cholesterol absorption and consequently had increased cholesterol synthesis after weight loss, while individuals with a 54Y variant of ABCG8 exhibited lower post-weight loss cholesterol synthesis.

The researchers believe these results can lead to better therapy for overweight individuals. Knowing which variants are present will increase the understanding of how weight loss will affect cholesterol metabolism, and the best combination of diet, exercise, and medicine can be prescribed.

CORRESPONDING AUTHOR: Peter Jones, Richardson Centre for Functional Foods and Nutraceuticals, University of Manitoba, Winnipeg; Phone: 204.474.8883, email:

Crohns Disease Increases Progression of Atherosclerosis

While chronic inflammation is a known risk factor for atherosclerosis (hardening of the arteries) and heart disease, researchers have now shown that the sporadic but recurrent inflammation caused by Crohns disease also poses serious cardiovascular risk.

Sander van Leuven and his colleagues imaged 60 Crohns patients and 122 healthy controls for signs of arterial hardening; they found that the thickness of the carotid artery, a common marker for plaque buildup, was increased in Crohns disease.

They next examined the subjects HDL (high density lipoprotein, the good cholesterol) content. HDL helps prevent arterial hardening by shuttling cholesterol from blood vessels back to the liver as well as exerting anti-oxidant properties, and is often impaired during inflammation. They discovered that patients with active Crohns had profoundly reduced HDL levels compared to controls or Crohns patients in remission.

Interestingly, both active Crohns patients and those in remission had HDL with lower antioxidant potential than healthy individuals, revealing that acute inflammation episodes not only reduce total HDL, but alter the molecules biochemically, likely slowing down the recovery process during remission.

The researchers note their findings highlight the cardiovascular risks facing Crohns patients, even those who successfully manage their outbreaks, and suggest that early detection and prevention measures are critical.

CORRESPONDING AUTHOR: Sander I. van Leuven, Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, The Netherlands; Phone: +31-20-5668675, email:

Breaking the Vicious Cycle of Bile Acid Disorders

Researchers have found a potential new and improved avenue for treating defective bile acid absorption, a primary contributor to chronic diarrhea.

Liver-produced bile acids are intestinal detergents that break apart fats for easier absorption. Normally, most of the bile acids also reabsorb, but during certain conditions (e.g. infection or short bowel syndrome) excess bile acids enter the colon and impair water absorption, leading to diarrhea.

What makes bile acid malabsorption particularly insidious is that if enough bile acids dont reabsorb, the liver churns out even more acids to compensate, which produces even more problems.

Antonio Moschetta and colleagues targeted the intestinal receptor FXR to see if they could break this vicious cycle. When bile acids reenter intestinal cells, they attach to FXR, which in turn activates a hormone called FGF15 to helps suppress bile acid production.

The researchers fed a synthetic FXR target to engineered mice with defective bile absorption and found that treatment increased the FGF15 activation and reduced the total amount of bile acids present in both the liver and feces. They achieved similar results if they directly introduced FGF15 into the livers of the mice.

Moschetta and colleagues note that FXR drugs would be more beneficial than current treatments that use resins to sequester bile acids, which alleviates the diarrhea but doesnt solve the underlying absorption problem.

CORRESPONDING AUTHOR: David Mangelsdorf, Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas; Phone: 214-645-5957, email:


Contact: Nick Zagorski
American Society for Biochemistry and Molecular Biology

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