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. 2010 Nov 17:9:132.
doi: 10.1186/1476-511X-9-132.

A novel genetically-obese rat model with elevated 11 beta-hydroxysteroid dehydrogenase type 1 activity in subcutaneous adipose tissue

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A novel genetically-obese rat model with elevated 11 beta-hydroxysteroid dehydrogenase type 1 activity in subcutaneous adipose tissue

Sakamuri S S Vara Prasad et al. Lipids Health Dis. .

Abstract

11 β-hydroxysteroid dehydrogenase type 1 (11 β-HSD1) catalyzes the conversion of inactive glucocorticoids to active glucocorticoids and plays an important role in the development of obesity and metabolic syndrome. 11 β-HSD1 activity is lower in liver and higher in omental adipose tissue of obese rodent models like obese zucker rats, Ob/Ob and db/db mice. Here, we report the 11 β-HSD1 activity in liver and adipose tissue of lean and obese rats of WNIN/Ob strain, a new genetic rat model of obesity. 11 β-HSD1 activity in liver, omental and subcutaneous adipose tissues of 3 month-old male WNIN/Ob lean and obese rats was assayed. As observed in other rodent models, 11 β-HSD1 activity was lower in liver and higher in omental adipose tissue. In contrast to other rodent obese models, WNIN/Ob obese rats had elevated 11 β-HSD1 activity in subcutaneous adipose tissue, which is in line with the observation in human obesity. Here, we conclude that dysregulation of 11 β-HSD1 in WNIN/Ob obese rat model is identical to human obesity, which makes it an excellent model for studying the effect of 11 β-HSD1 inhibitors in ameliorating obesity and metabolic syndrome.

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Figures

Figure 1
Figure 1
11β-HSD 1 activity in 3 month-old male WNIN/Ob lean and obese rats. (A). Omental fat. (B). Subcutaneous fat. (C). Liver. (D). Quadriceps muscle. Values are means ± S.E for 6 rats. Mean values with * mark are significant at P < 0.05 level (by student's t test). Comparisons were made between lean and obese phenotypes.

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