11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess

Recently, a specific peptide inhibitor for ATGL was isolated from white blood cells, specifically mononuclear cells. This peptide was originally identifed as being involved in the regulation of the G 0 to G 1 transition of the cell cycle . This peptide was, therefore, called G0G1 switch protein 2 (encoded by the G0S2 gene). The protein is found in numerous tissues, with highest concentrations in adipose tissue and liver. In adipose tissue G0S2 expression is very low during fasting but increases after feeding. Conversely, fasting or PPARα -agonists increase hepatic G0S2 expression. The protein has been shown to localize to LDs, cytoplasm, ER, and mitochondria. These different subcellular localizations likely relate to multiple functions for G0S2 in regulating lipolysis, the cell cycle , and, possibly, apoptosis via its ability to interact with the mitochondrial antiapoptotic factor Bcl-2. With respect to ATGL regulation, the binding of the enzyme to LDs and subsequent is dependent on a physical interaction between the N-terminal region of G0S2 and the patatin domain of ATGL.

CYP11B2 (Cytochrome P450 Family 11 Subfamily B Member 2) is a Protein Coding gene. Diseases associated with CYP11B2 include Corticosterone Methyloxidase Type I Deficiency and Corticosterone Methyloxidase Type Ii Deficiency . Among its related pathways are superpathway of steroid hormone biosynthesis and Metabolism . Gene Ontology (GO) annotations related to this gene include iron ion binding and oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen . An important paralog of this gene is CYP11B1 .

HSD11B1 (Hydroxysteroid 11-Beta Dehydrogenase 1) is a Protein Coding gene. Diseases associated with HSD11B1 include Cortisone Reductase Deficiency 2 and Hyperandrogenism Due To Cortisone Reductase Deficiency . Among its related pathways are Metabolism and Steroid hormone biosynthesis . Gene Ontology (GO) annotations related to this gene include oxidoreductase activity and 11-beta-hydroxysteroid dehydrogenase (NADP+) activity . An important paralog of this gene is HSD11B1L .

George T Griffing, MD  Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science , International Society for Clinical Densitometry , Southern Society for Clinical Investigation , American College of Medical Practice Executives , American Association for Physician Leadership , American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Heart Association , Central Society for Clinical and Translational Research , Endocrine Society

Disclosure: Nothing to disclose.

11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess

11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess

George T Griffing, MD  Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science , International Society for Clinical Densitometry , Southern Society for Clinical Investigation , American College of Medical Practice Executives , American Association for Physician Leadership , American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Heart Association , Central Society for Clinical and Translational Research , Endocrine Society

Disclosure: Nothing to disclose.

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11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess11 beta hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess

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