Story ideas from the Journal of Lipid Research

May 29, 2007

Articles to be published in the June 2007 issue of the Journal of Lipid Research (Vol. 48, No. 6)


New insight into how low HDL causes heart disease

Researchers have found that one of the reasons people with low HDL - a molecule that helps eliminate excess cholesterol from arteries - are at risk of developing heart disease could be a defective version of a protein called ABCA1.

People with familial low HDL, or hypolipoproteinemia, have an impaired ability to transport cholesterol out of their cells, which leads to an accumulation of cholesterol in many tissues. For some of these individuals, the disease is due to mutations in proteins called ATP-binding cassettes (ABCs) that transport lipids and other molecules inside and outside cells, but for many affected individuals, the causes of the disease is still not well known.

Marja-Riitta Taskinen and colleagues examined how the first steps of the transport of cholesterol into the liver were disturbed in individuals with familial low HDL. The scientists compared the gene expression of ABC proteins in low HDL and control subjects and found that the genetic expression of ABC proteins was increased in low HDL subjects, indicating that these ABC proteins may be abnormally produced in the affected individuals.

Article: "Common ABCA1 variants, HDL levels and cellular cholesterol efflux in subjects with Familial low-HDL," by Aino Soro-Paavonen1, Jussi Naukkarinen, Miriam Lee-Rueckert, Hiroshi Watanabe, Elina Rantala, Sanni Soderlund, Anne Hiukka, Petri T Kovanen, Matti Jauhiainen, Leena Peltonen, and Marja-Riitta Taskinen

MEDIA CONTACT: Marja-Riitta Taskinen, Helsinki University Central Hospital, Helsinki, Finland; e-mail:

Too much of a key protein observed in type 2 diabetes patients

Researchers have shown that key chemicals that carry cholesterol and fats in the blood accumulate in people with type 2 diabetes, which may help improve treatment of this disease.

Type 2 diabetes is a condition in which blood sugar is higher than it should be and too much insulin is produced to counter this blood sugar increase. Patients with this disease have increased levels of triglycerides - the most important type of fat - in their blood and high levels of a chemical called triglyceride-rich lipoprotein (TRL) that carries cholesterol and fats in the blood and is produced in the intestines. But how TRL accumulates in the blood is not well understood.

Patrick Couture and colleagues discovered that overaccumulation of TRL is due to an increased production of lipoproteins that contain proteins called apolipoprotein B-48 and apolipoprotein B-100, which are known to cause heart disease. The scientists also showed that the breakdown of these proteins was reduced, further contributing to their build-up. These results may help devise treatments that reduce the production of apolipoprotein B-48 and apolipoprotein B-100 in type 2 diabetes patients, thus reducing their risks of developing heart disease.

Article: "Evidence of Increased Secretion of Apolipoprotein B-48-Containing Lipoproteins in Subjects with Type 2 Diabetes and Severe Hypertriglyceridemia," by Jean-Charles Hogue, Benoit Lamarche, Andre J Tremblay, Jean Bergeron, Claude Gagne, and Patrick Couture

MEDIA CONTACT: Patrick Couture, Laval University Medical Center, Quebec City, Canada; e-mail:

The following article is the first in a series of nine reviews on "adipocyte biology" or the biology of fat tissue. The other articles in the series will appear in future issues of the journal. All thematic review articles and can be accessed at: (under "Thematic Reviews").

How fat tissue works

Jaswinder K. Sethi and Antonio J. Vidal-Puig review current knowledge on how fat tissue works in our bodies. They describe the biochemicals released by fat tissue and how they help keep the internal environment of the body stable by either storing fat or burning it to produce energy.

The scientists also review the latest research showing how too much fat tissue can lead to chronic diseases such as cardiovascular disease, diabetes, osteoarthritis, and some cancers. They explain that, in overweight or obese people, nutrients leak from fat tissue and accumulate in other organs, fat tissue releases abnormal quantities of biochemicals, and the distribution of fat tissue among various organs is altered.

The scientists also give ideas for therapeutic strategies that could help overweight and obese individuals lose their excessive amount of fat tissue. They suggest treatments that would affect the distribution of fat tissue throughout the body and that would alter the way the biochemicals produced by the fat tissue interact with other organs.

Article: "Adipose Tissue Function and Plasticity Orchestrate Nutritional Adaptation," by Jaswinder K. Sethi and Antonio J. Vidal-Puig

MEDIA CONTACT: Jaswinder K. Sethi, University of Cambridge, Cambridge, United Kingdom; e-mail:

MEDIA CONTACT: Antonio J. Vidal-Puig, University of Cambridge, Cambridge, United Kingdom; e-mail:
The American Society for Biochemistry and Molecular Biology is a nonprofit scientific and educational organization with over 11,900 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions and industry. The Society's student members attend undergraduate or graduate institutions.

Founded in 1906, the Society is based in Bethesda, Maryland, on the campus of the Federation of American Societies for Experimental Biology. The Society's purpose is to advance the science of biochemistry and molecular biology through publication of the Journal of Biological Chemistry, the Journal of Lipid Research, and Molecular and Cellular Proteomics, organization of scientific meetings, advocacy for funding of basic research and education, support of science education at all levels, and promoting the diversity of individuals entering the scientific work force.

For more information about ASBMB, see the Society's Web site at

American Society for Biochemistry and Molecular Biology

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