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Metabolic and behavioral parameters of mice with reduced expression of Syndecan-1

Energy balance is essential for all species. Ligand-receptor interactions mediate processes that regulate body activities like reproduction and metabolism based on the energy status. Such receptors are the heparan sulfate proteoglycans and specifically the family of syndecans. Therefore we investiga...

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Detalles Bibliográficos
Autores principales: Gougoula, Christina, Bielfeld, Alexandra Petra, Pour, Sarah Jean, Sager, Martin, Krüssel, Jan-Steffen, Benten, Wilhelm Peter M., Baston-Büst, Dunja Maria
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625734/
https://www.ncbi.nlm.nih.gov/pubmed/31299063
http://dx.doi.org/10.1371/journal.pone.0219604
Descripción
Sumario:Energy balance is essential for all species. Ligand-receptor interactions mediate processes that regulate body activities like reproduction and metabolism based on the energy status. Such receptors are the heparan sulfate proteoglycans and specifically the family of syndecans. Therefore we investigated the differences of metabolic parameters of heterozygous Syndecan 1 mice (Sdc1(+/-)) with reduced expression of Sdc1 and the corresponding wild type mice. Sdc1(+/-) mice have a reduced body weight although they show increased leptin and decreased corticosterone levels. Furthermore, their food and water intake is increased. This is accompanied with less adipose tissue, smaller adipocytes and thus an increased density of adipocytes. For the detailed analysis of the metabolism the automated PhenoMaster system has been used, which allowed continuous and undisturbed recording of food and water intake, energy expenditure and movement. The reason for the lower body weight was the higher energy expenditure of these animals compared to controls. Additionally, female Sdc1(+/-) mice showed an increased locomotor activity. Referring to organs, the intestine in Sdc1(+/-) mice was heavier and longer, but no differences at the cellular level could be observed. These findings were independent of normal mating or vice versa embryo transfers of Sdc1(+/-) and wild type embryos in recipient females of the other genotype. Herein we showed that the reduced expression of Sdc1 led to an altered metabolism on fetal as well as on maternal side, which may play a role in the growth restriction observed in human pregnancy pathologies and in mice lacking Sdc1.