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Dietary conjugated linoleic acid and insulin sensitivity and resistance in rodent models^1,2,3,4

¹ From the Departments of Human Nutritional Sciences (CGT) and Physiology (PZ), University of Manitoba, and the Institute of Cardiovascular Sciences, St Boniface Research Centre (PZ), Winnipeg, Canada

ABSTRACT

Dietary conjugated linoleic acid (CLA) is being investigated for beneficial effects for disease prevention and treatment in a variety of experimental models, including obesity and type 2 diabetes. To date, rodent studies suggest that trans-10,cis-12 (t10,c12) CLA is associated with greater insulin resistance, despite lower body fat, and that a CLA mixture (and perhaps c9,t11) could be beneficial for the management of insulin resistance. Studies investigating the mechanisms by which CLA operates at the cellular level show that the primary targets for CLA are members of the nuclear receptor family, particularly the lipostat transcription factors peroxisome proliferator-activated receptor (PPAR), PPAR, sterol regulatory element-binding protein 1c, and liver X receptor . Consequently, the effects of CLA on glucose metabolism are likely secondary effects mediated through factors such as PPAR coactivator 1 that are controlled by these nuclear receptors. The different responses of normal compared with insulin-resistant obese rodents suggest that interactions of CLA isomers with the cellular components that contribute to development of metabolic syndrome require further investigation.

Key Words: CLA • insulin resistance • rats • mice

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