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Clore Laboratory: News
Diabetes, Obesity and Metabolic Research
12 September 2005 – Jon Arch presents work on 11β-hydroxysteroid dehydrogenase inhibitor at EASD meeting
Jon Arch, Deputy Director of Metabolic Research, Clore Laboratory, University of Buckingham, UK, presented work on an inhibitor of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD-1) at the 41st Annual Meeting of the European Association for the Study of Diabetes (EASD), held in Athens, Greece, 10–15 September 2005.
Excessive stimulation of glucocorticoid receptors may be one cause of insulin resistance and other features of the metabolic syndrome. 11βHSD-1 produces active glucocorticoids from inactive precursors in insulin sensitive tissues. Inhibitors of 11βHSD-1 are therefore being evaluated as treatments for type 2 diabetes.
Jon Arch described work on the 11βHSD-1 inhibitor BVT.2733 in diet-induced obese and insulin resistant mice. BVT.2733 not only improved glucose handling, but it also had an anti-obesity effect. The anti-obesity effect was partly due to reduced food intake, but BVT.2733 also increased energy expenditure. Reduced food intake did not explain the improved blood glucose control. Increased energy expenditure, particularly fat oxidation, may, however, have contributed to the well-established insulin sensitising effect of reduced glucocorticoid receptor stimulation.
These insights may help in the planning and evaluation of clinical studies on 11βHSD inhibitors, which are being developed by several companies as treatments for obesity, type 2 diabetes and the metabolic syndrome.
The full reference to the abstract is:
Arch JRS, Wang SJY, Birtles S, Smith DM, Turnbull A. Effects of an inhibitor of 11beta-hydroxysteroid dehydrogenase type 1 inhibitor on energy balance and glucose homeostasis in diet-induced obesity. Diabetologia 2005 48(Suppl 1): A238, Abs 650