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Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene

Genetic disruption of glycosyltransferases has provided clear information on the roles of their reaction products in the body. Our group has studied the function of glycosphingolipids by genetic engineering of glycosyltransferases in cell culture and in mice, which has demonstrated both expected and...

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Autores principales: Furukawa, Koichi, Takamiya, Kogo, Ohmi, Yuhsuke, Bhuiyan, Robiul H., Tajima, Orie, Furukawa, Keiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10476564/
https://www.ncbi.nlm.nih.gov/pubmed/36999634
http://dx.doi.org/10.1002/2211-5463.13603
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author Furukawa, Koichi
Takamiya, Kogo
Ohmi, Yuhsuke
Bhuiyan, Robiul H.
Tajima, Orie
Furukawa, Keiko
author_facet Furukawa, Koichi
Takamiya, Kogo
Ohmi, Yuhsuke
Bhuiyan, Robiul H.
Tajima, Orie
Furukawa, Keiko
author_sort Furukawa, Koichi
collection PubMed
description Genetic disruption of glycosyltransferases has provided clear information on the roles of their reaction products in the body. Our group has studied the function of glycosphingolipids by genetic engineering of glycosyltransferases in cell culture and in mice, which has demonstrated both expected and unexpected results. Among these findings, aspermatogenesis in ganglioside GM2/GD2 synthase knockout mice was one of the most surprising and intriguing results. There were no sperms in testis, and multinuclear giant cells were detected instead of spermatids. Although serum levels of testosterone in the male mice were extremely low, testosterone accumulated in the interstitial tissues, including Leydig cells, and seemed not to be transferred into the seminiferous tubules or vascular cavity from Leydig cells. This was considered to be the cause of aspermatogenesis and low serum levels of testosterone. Patients with a mutant GM2/GD2 synthase gene (SPG26) showed similar clinical signs, not only in terms of the neurological aspects, but also in the male reproductive system. The mechanisms for testosterone transport by gangliosides are discussed here based on our own results and reports from other laboratories.
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spelling pubmed-104765642023-09-05 Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene Furukawa, Koichi Takamiya, Kogo Ohmi, Yuhsuke Bhuiyan, Robiul H. Tajima, Orie Furukawa, Keiko FEBS Open Bio Reviews Genetic disruption of glycosyltransferases has provided clear information on the roles of their reaction products in the body. Our group has studied the function of glycosphingolipids by genetic engineering of glycosyltransferases in cell culture and in mice, which has demonstrated both expected and unexpected results. Among these findings, aspermatogenesis in ganglioside GM2/GD2 synthase knockout mice was one of the most surprising and intriguing results. There were no sperms in testis, and multinuclear giant cells were detected instead of spermatids. Although serum levels of testosterone in the male mice were extremely low, testosterone accumulated in the interstitial tissues, including Leydig cells, and seemed not to be transferred into the seminiferous tubules or vascular cavity from Leydig cells. This was considered to be the cause of aspermatogenesis and low serum levels of testosterone. Patients with a mutant GM2/GD2 synthase gene (SPG26) showed similar clinical signs, not only in terms of the neurological aspects, but also in the male reproductive system. The mechanisms for testosterone transport by gangliosides are discussed here based on our own results and reports from other laboratories. John Wiley and Sons Inc. 2023-04-06 /pmc/articles/PMC10476564/ /pubmed/36999634 http://dx.doi.org/10.1002/2211-5463.13603 Text en © 2023 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Furukawa, Koichi
Takamiya, Kogo
Ohmi, Yuhsuke
Bhuiyan, Robiul H.
Tajima, Orie
Furukawa, Keiko
Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title_full Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title_fullStr Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title_full_unstemmed Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title_short Disordered testosterone transport in mice lacking the ganglioside GM2/GD2 synthase gene
title_sort disordered testosterone transport in mice lacking the ganglioside gm2/gd2 synthase gene
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10476564/
https://www.ncbi.nlm.nih.gov/pubmed/36999634
http://dx.doi.org/10.1002/2211-5463.13603
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