organizing committee  

Cellular and Molecular Mechanisms of CLA Action
Martha A. Belury, Carol S. Kennedy Professor of Human Nutrition,
Ohio State University, Columbus, OH.


The incidence of type 2 diabetes mellitus is increasing in epidemic proportions in developed countries worldwide. Type 2 diabetes arises from a variety of etiological factors including environmental factors that affect obesity and dyslipidemia and non-modifiable factors including genetics, ethnicity and age. The delay of onset or therapy to reduce the severity of the disease through diet and other lifestyle approaches offers the possibility of reducing the severity of co-morbid disorders that contribute to morbidity and mortality. Co-morbid disorders that often exist with type 2 diabetes include cardiovascular disease, retinopathy and neuropathy. Numerous studies have shown that the dietary fatty acids, conjugated linoleic acids (CLA), reduce adiposity in experimental animals and recent studies suggest similar findings in humans. We have identified that dietary CLA delays the onset and improve lipid profiles in a rat model for type 2 diabetes. Subsequent studies have demonstrated that CLA may improve glucose metabolism by enhancing glucose uptake into muscle. Numerous investigators have shown CLA alters deposition of body fat in a depot-specific pattern. In non-diabetic animals that has also resulted in increased insulin resistance. We and others have found that CLA modulates numerous pathways involving lipid signaling and fatty acid oxidation. Pathways that may explain CLA's anti-adipogenic effects include D6-, D9 desaturase metabolism as well as pathways modified by the transcription factor, peroxisome proliferators-activated receptors (PPARs). The potential ability of different isomers of CLA at various doses and durations (short vs. long term) to alter metabolic pathways through altering gene expression to ultimately affect type 2 diabetes mellitus will be discussed.

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