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Articles in PresS, published online ahead of print December 10, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00348.2002
Submitted on August 7, 2002
Accepted on December 8, 2002
/
activation provides enhanced improvement of insulin sensitivity and glycemic control in ZDF rats
1 Research and Development, Novo Nordisk A/S, Bagsvaerd, Denmark
2 Diabetes and Metabolism Research Program, Garvan Institute of Medical Research, Sydney, Australia
* To whom correspondence should be addressed. E-mail: clbr{at}novonordisk.com.
Improvement of insulin sensitivity and lipid and glucose metabolism by co-activation of both nuclear Peroxisome Proliferator Activated Receptor (PPAR)
and
PPAR
potentially provides beneficial effects over existing PPAR- and -preferential drugs, respectively, in treatment of type 2 diabetes. We examined the effects of the dual PPAR/ agonist, ragaglitazar, on hyperglycemia and whole body insulin sensitivity in early and late diabetes stages in Zucker Diabetic Fatty (ZDF) rats and compared to treatment with the PPAR-preferential agonist, rosiglitazone. Despite normalization of hyperglycemia and HbA1c and reduction of plasma triglycerides by both compounds in both prevention and early intervention studies, ragaglitazar treatment resulted in overall reduced
circulating insulin and improved insulin sensitivity to a greater extent than after treatment with rosiglitazone. In late intervention therapy, ragaglitazar reduced HbA1c by 2.3 percent compared to 1.1 percent by rosiglitazone. Improvement of insulin sensitivity caused by the dual PPAR/ agonist ragaglitazar seemed to have beneficial impact over that of the PPAR-preferential activator, rosiglitazone, on glycemic control in frankly diabetic ZDF rats.
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