scholarly journals Estrogen Reduces 11β-Hydroxysteroid Dehydrogenase Type 1 in Liver and Visceral, but Not Subcutaneous, Adipose Tissue in Rats

Obesity ◽  
2010 ◽  
Vol 18 (3) ◽  
pp. 470-475 ◽  
Author(s):  
Therése Andersson ◽  
Ingegerd Söderström ◽  
Kotryna Simonyté ◽  
Tommy Olsson
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Subcutaneous Adipose

11β-Hydroxysteroid Dehydrogenase Type 1 mRNA is Increased in Both Visceral and Subcutaneous Adipose Tissue of Obese Patients*

Obesity ◽  
2006 ◽  
Vol 14 (5) ◽  
pp. 794-798 ◽  
Author(s):  
Raoul Desbriere ◽  
Vincent Vuaroqueaux ◽  
Vincent Achard ◽  
Sandrine Boullu-Ciocca ◽  
Martin Labuhn ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Obese Patients ◽  
Subcutaneous Adipose

11β-Hydroxysteroid Dehydrogenase Type 1 is Overexpressed in Subcutaneous Adipose Tissue of Morbidly Obese Patients

2008 ◽  
Vol 19 (6) ◽  
pp. 764-770 ◽  
Author(s):  
Rodrigo Muñoz ◽  
Cristian Carvajal ◽  
Alex Escalona ◽  
Camilo Boza ◽  
Gustavo Pérez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Subcutaneous Adipose

Rosiglitazone decreases 11?-hydroxysteroid dehydrogenase type�1 in subcutaneous adipose tissue

2007 ◽  
Vol 67 (3) ◽  
pp. 419-425 ◽  
Author(s):  
Knut Mai ◽  
Janin Andres ◽  
Thomas Bobbert ◽  
Christiane Maser-Gluth ◽  
Matthias Möhlig ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Subcutaneous Adipose

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

2010 ◽  
Vol 9 (1) ◽  
pp. 132 ◽  
Author(s):  
Sakamuri SS Vara Prasad ◽  
Anamthathmakula Prashanth ◽  
Chodavarapu Pavan Kumar ◽  
Sirisha J Reddy ◽  
Nappan V Giridharan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Rat Model ◽  
Subcutaneous Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Subcutaneous Adipose

The role and regulation of 11β-hydroxysteroid dehydrogenase type 1 in obesity and the metabolic syndrome

2013 ◽  
Vol 15 (2) ◽  
Author(s):  
Roland H. Stimson ◽  
Brian R. Walker
Keyword(s):  
Metabolic Disease ◽  
Adipose Tissue ◽  
Selective Inhibition ◽  
Hydroxysteroid Dehydrogenase ◽  
The Metabolic Syndrome ◽  
Specific Regulation ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

AbstractThe cortisol regenerating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) amplifies tissue glucocorticoid levels, particularly in the liver and adipose tissue. The importance of this enzyme in causing metabolic disease was highlighted by transgenic mice which over- or under-expressed 11β-HSD1; consequently, selective 11β-HSD1 inhibitors have been widely developed as novel agents to treat obesity and type 2 diabetes mellitus (T2DM). This review focuses on the importance of 11β-HSD1 in humans which has been more difficult to ascertain. The recent development of a deuterated cortisol tracer has allowed us to quantify in vivo cortisol production by 11β-HSD1. These results have been surprising, as cortisol production rates by 11β-HSD1 are at least equivalent to that of the adrenal glands. The vast majority of this production is by the liver (>90%) with a smaller contribution from subcutaneous adipose tissue and possibly skeletal muscle, but with no detectable production from visceral adipose tissue. This tracer has also allowed us to quantify the tissue-specific regulation of 11β-HSD1 observed in obesity and obesity-associated T2DM, determine the likely basis for this dysregulation, and identify obese patients with T2DM as the group most likely to benefit from selective inhibition of 11β-HSD1. Some of these inhibitors have now reached Phase II clinical development, demonstrating efficacy in the treatment of T2DM. We review these results and discuss whether selective 11β-HSD1 inhibitors are likely to be an important new therapy for metabolic disease.

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