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1/22/2022 7:08:04 AM | Browse: 628 | Download: 1743
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2021-07-08 07:17 |
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2021-07-09 10:38 |
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2022-01-13 05:35 |
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Accepted by Journal Editor-in-Chief |
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2022-01-14 06:34 |
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2022-01-14 06:34 |
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2021-12-01 02:24 |
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2022-01-19 17:20 |
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Publish the Manuscript Online |
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2022-01-22 06:08 |
ISSN |
1949-8454 (online) |
Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/ |
Copyright |
© The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved. |
Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
Website |
http://www.wjgnet.com |
Category |
Endocrinology & Metabolism |
Manuscript Type |
Basic Study |
Article Title |
Increased monoamine oxidase activity and imidazoline binding sites in insulin-resistant adipocytes from obese Zucker rats
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Manuscript Source |
Invited Manuscript |
All Author List |
Christian Carpéné, Luc Marti and Nathalie Morin |
Funding Agency and Grant Number |
Funding Agency |
Grant Number |
Recurrent Grants from Institut National de la Santé et de la Recherche Médicale to the INSERM U1048 |
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Corresponding Author |
Christian Carpéné, PhD, Senior Researcher, Institut des Maladies Métaboliques et Cardiovasculaires, INSERM, CHU Rangueil, Bat. L4, BP 84225 , Toulouse 31342, France. christian.carpene@inserm.fr |
Key Words |
Obesity; Adipocyte; Amine oxidases; Imidazoline binding sites; Creatine kinase B; Idazoxan; Lipogenesis; Hydrogen peroxide; Glucose uptake |
Core Tip |
The substrates of monoamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) partly reproduce the stimulatory effect of insulin on sugar entry in rat fat cells. Especially when combined with vanadium, tyramine and benzylamine mimic more than 70% of the insulin stimulation of glucose uptake. Unfortunately, such insulin activation of glucose utilization is strongly diminished in the genetically obese Zucker rat, an animal model of the metabolic syndrome. In this insulin-resistant and obese rat, the stimulation of glucose transport by tyramine is decreased as much as that of insulin, while the effect of benzylamine is even more altered. SSAO, responsible for benzylamine oxidation, is down-regulated in adipocytes from obese Zucker rats. In contrast, MAO, which predominantly supports the oxidation of tyramine, is increased, apparently not in a sufficient manner to reach the same hexose uptake activation seen in fat cells from lean rats. However, this greater ability to oxidize tyramine was found only in white adipocytes from obese rats since no change was found in the liver or skeletal muscle when compared to lean controls. Moreover, increased MAO activity in the large adipocytes of obese rats was accompanied by an enlarged number of imidazoline binding sites, previously described to be located on MAO. Since the repeated subcutaneous administration of tyramine plus vanadate is somewhat capable of reducing plasma glucose and triglycerides in obese rats, SSAO, MAO, and its associated imidazoline I2 sites deserve further studies with respect to their mimicking insulin action on glucose and lipid metabolism in fat cells. |
Publish Date |
2022-01-22 06:08 |
Citation |
Carpéné C, Marti L, Morin N. Increased monoamine oxidase activity and imidazoline binding sites in insulin-resistant adipocytes from obese Zucker rats. World J Biol Chem 2022; 13(1): 15-34 |
URL |
https://www.wjgnet.com/1949-8454/full/v13/i1/15.htm |
DOI |
https://dx.doi.org/10.4331/wjbc.v13.i1.15 |
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