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Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Bisulfite-Seq)

ABSTRACT: To investigate the effects of maternal adiposity and leptin on fetal brain development, fetal hippocampal brain tissue and DNA was collected at 0.9 term for targeted EM-Seq analysis

ORGANISM(S): Papio anubis

PROVIDER: GSE233720 | GEO | 2024/05/15

REPOSITORIES: GEO

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Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Targeted EM-Seq)

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Project description:The high prevalence of obesity has focused attention on defining the pathophysiological processes that underlie susceptibility or resistance to its deleterious metabolic consequences. Mice lacking translin (Tsn), a gene implicated in a variety of biological functions from transcription to microRNA degradation, display extremely high levels of adiposity, comparable to those found in well-known genetic models of obesity, such as melanocortin 4 receptor or leptin knockout (KO) mice. Although translin KO mice display increased adiposity they retain normal glucose tolerance. In contrast, wild-type (WT) mice placed on a high-fat diet until they match translin KO adiposity levels are glucose intolerant, as expected. Conversely, translin KO mice display prominent hepatic steatosis that is more severe than that of adiposity-matched WT mice. The ability of translin KO mice to retain normal glucose tolerance in the face of massive tissue expansion may be due to three factors: preferential accumulation of subcutaneous fat, reduced levels of TNF mRNA in both adipose and hepatic tissue, and elevated levels of plasma adiponectin. Further studies aimed at defining the molecular bases for these phenotypes may yield new approaches to limit the adverse metabolic consequences of obesity.

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Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus

Project description:This SuperSeries is composed of the SubSeries listed below.

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