Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity

Background. Glucocorticoid excess has been linked to clinical observations associated with the pathophysiology of metabolic syndrome. The intracellular glucocorticoid levels are primarily modulated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme that is highly expressed in key metabolic...

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Main Authors: Thirumurugan Rathinasabapathy, Kimberly Marie Palatini Jackson, Yiwen Thor, Ayuba Sunday Buru, Debora Esposito, Xu Li, Mallikarjuna Rao Pichika, Ahmad Sazali Hamzah, Slavko Komarnytsky
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Journal of Chemistry
Online Access:http://dx.doi.org/10.1155/2017/3182129
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author Thirumurugan Rathinasabapathy
Kimberly Marie Palatini Jackson
Yiwen Thor
Ayuba Sunday Buru
Debora Esposito
Xu Li
Mallikarjuna Rao Pichika
Ahmad Sazali Hamzah
Slavko Komarnytsky
author_facet Thirumurugan Rathinasabapathy
Kimberly Marie Palatini Jackson
Yiwen Thor
Ayuba Sunday Buru
Debora Esposito
Xu Li
Mallikarjuna Rao Pichika
Ahmad Sazali Hamzah
Slavko Komarnytsky
author_sort Thirumurugan Rathinasabapathy
collection DOAJ
description Background. Glucocorticoid excess has been linked to clinical observations associated with the pathophysiology of metabolic syndrome. The intracellular glucocorticoid levels are primarily modulated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme that is highly expressed in key metabolic tissues including fat, liver, and the central nervous system. Methods. In this study we synthesized a set of novel tetrahydrothiazolopyridine derivatives, TR-01–4, that specifically target 11β-HSD1 and studied their ability to interfere with the glucocorticoid and lipid metabolism in the 3T3-L1 adipocytes. Results. Based on the docking model and structure-activity relationships, tetrahydrothiazolopyridine derivatives TR-02 and TR-04 showed the highest potency against 11β-HSD1 by dose-dependently inhibiting conversion of cortisone to cortisol (IC50 values of 1.8 μM and 0.095 μM, resp.). Incubation of fat cells with 0.1–10 μM TR-01–4 significantly decreased cortisone-induced lipid accumulation in adipocytes and suppressed 11β-HSD1 mRNA expression. Observed reduction in adipocyte fat stores could be partially explained by decreased expression levels of adipogenic markers (PPAR-γ, aP2) and key enzymes of lipid metabolism, including fatty acid synthase (FAS), hormone sensitive lipase (HSL), and lipoprotein lipase (LPL). Conclusions. The tetrahydrothiazolopyridine moiety served as an active pharmacophore for inhibiting 11β-HSD1 and offered a novel therapeutic strategy to ameliorate metabolic alterations found in obesity and diabetes.
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spelling doaj-art-d2322e16bf87477e88a0d38f6e77bb872025-08-20T03:24:07ZengWileyJournal of Chemistry2090-90632090-90712017-01-01201710.1155/2017/31821293182129Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase ActivityThirumurugan Rathinasabapathy0Kimberly Marie Palatini Jackson1Yiwen Thor2Ayuba Sunday Buru3Debora Esposito4Xu Li5Mallikarjuna Rao Pichika6Ahmad Sazali Hamzah7Slavko Komarnytsky8Department of Pharmaceutical Chemistry, School of Pharmacy, International Medical University, 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000 Kuala Lumpur, MalaysiaPlants for Human Health Institute, North Carolina State University, North Carolina Research Campus, 600 Laureate Way, Kannapolis, NC 28081, USADepartment of Food, Bioprocessing, and Nutrition Sciences, North Carolina State University, 400 Dan Allen Drive, Raleigh, NC 27695, USADepartment of Pharmaceutical Chemistry, School of Pharmacy, International Medical University, 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000 Kuala Lumpur, MalaysiaPlants for Human Health Institute, North Carolina State University, North Carolina Research Campus, 600 Laureate Way, Kannapolis, NC 28081, USAPlants for Human Health Institute, North Carolina State University, North Carolina Research Campus, 600 Laureate Way, Kannapolis, NC 28081, USADepartment of Pharmaceutical Chemistry, School of Pharmacy, International Medical University, 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000 Kuala Lumpur, MalaysiaCenter for Synthesis and Chemical Biology, Institute of Science, Universiti Teknologi MARA, 40450 Shah Alam, Selangor Darul Ehsan, MalaysiaPlants for Human Health Institute, North Carolina State University, North Carolina Research Campus, 600 Laureate Way, Kannapolis, NC 28081, USABackground. Glucocorticoid excess has been linked to clinical observations associated with the pathophysiology of metabolic syndrome. The intracellular glucocorticoid levels are primarily modulated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme that is highly expressed in key metabolic tissues including fat, liver, and the central nervous system. Methods. In this study we synthesized a set of novel tetrahydrothiazolopyridine derivatives, TR-01–4, that specifically target 11β-HSD1 and studied their ability to interfere with the glucocorticoid and lipid metabolism in the 3T3-L1 adipocytes. Results. Based on the docking model and structure-activity relationships, tetrahydrothiazolopyridine derivatives TR-02 and TR-04 showed the highest potency against 11β-HSD1 by dose-dependently inhibiting conversion of cortisone to cortisol (IC50 values of 1.8 μM and 0.095 μM, resp.). Incubation of fat cells with 0.1–10 μM TR-01–4 significantly decreased cortisone-induced lipid accumulation in adipocytes and suppressed 11β-HSD1 mRNA expression. Observed reduction in adipocyte fat stores could be partially explained by decreased expression levels of adipogenic markers (PPAR-γ, aP2) and key enzymes of lipid metabolism, including fatty acid synthase (FAS), hormone sensitive lipase (HSL), and lipoprotein lipase (LPL). Conclusions. The tetrahydrothiazolopyridine moiety served as an active pharmacophore for inhibiting 11β-HSD1 and offered a novel therapeutic strategy to ameliorate metabolic alterations found in obesity and diabetes.http://dx.doi.org/10.1155/2017/3182129
spellingShingle Thirumurugan Rathinasabapathy
Kimberly Marie Palatini Jackson
Yiwen Thor
Ayuba Sunday Buru
Debora Esposito
Xu Li
Mallikarjuna Rao Pichika
Ahmad Sazali Hamzah
Slavko Komarnytsky
Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
Journal of Chemistry
title Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
title_full Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
title_fullStr Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
title_full_unstemmed Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
title_short Thiazolopyridines Improve Adipocyte Function by Inhibiting 11 Beta-HSD1 Oxoreductase Activity
title_sort thiazolopyridines improve adipocyte function by inhibiting 11 beta hsd1 oxoreductase activity
url http://dx.doi.org/10.1155/2017/3182129
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