| 1. |
- Hellsten, Sofie V., et al.
(författare)
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The gene expression of the neuronal protein, SLC38A9, changes in mouse brain after in vivo starvation and high-fat diet
- 2017
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Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 12:2
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Tidskriftsartikel (refereegranskat)abstract
- SLC38A9 is characterized as a lysosomal component of the amino acid sensing RagulatorRAG GTPase complex, controlling the mechanistic target of rapamycin complex 1 (mTORC1). Here, immunohistochemistry was used to map SLC38A9 in mouse brain and staining was detected throughout the brain, in cortex, hypothalamus, thalamus, hippocampus, brainstem and cerebellum. More specifically, immunostaining was found in areas known to be involved in amino acid sensing and signaling pathways e.g. piriform cortex and hypothalamus. SLC38A9 immunoreactivity co-localized with both GABAergic and glutamatergic neurons, but not with astrocytes. SLC38A9 play a key role in the mTORC1 pathway, and therefore we performed in vivo starvation and high-fat diet studies, to measure gene expression alterations in specific brain tissues and in larger brain regions. Following starvation, Slc38a9 was upregulated in brainstem and cortex, and in anterior parts of the brain (Bregma 3.2 to -2.1mm). After high-fat diet, Slc38a9 was specifically upregulated in hypothalamus, while overall downregulation was noticed throughout the brain (Bregma 3.2 to -8.6mm).
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| 2. |
- Jacobsson, Josefin A., et al.
(författare)
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The impact of intronic single nucleotide polymorphisms and ethnic diversity for studies on the obesity gene FTO
- 2012
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Ingår i: Obesity Reviews. - 1467-7881 .- 1467-789X. ; 13:12, s. 1096-1109
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Forskningsöversikt (refereegranskat)abstract
- In 2007, the first common genetic variants were identified, which undoubtedly affect our susceptibility to obesity. These variants are located in the fat mass and obesity-associated gene FTO. Since then, over 50 loci for common obesity have been identified. As the research on these loci is still at an early stage, there is a great need to review, for clarification purposes, the current research on FTO, as this is likely to influence future studies. Based on the current knowledge, FTO seems to be directly involved in the regulation of energy intake, but there is an urgent need for the identification of regulatory polymorphisms. Thus, herein, we discuss current knowledge and highlight putative functional regions in FTO based on published data and computer-based analysis.
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| 3. |
- Tripathi, Rekha, PhD student, 1985-, et al.
(författare)
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Integrated analysis of transcriptomic and metabolic profiling of SLC38A10 knockout primary cortex cells
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Solute carrier transporter responsible protein to transfer of biological membrane and act as a vital regulator of transporter of amino acid, sugar, ion, and drug. Members of the glutamine transporters SLC38 family have played a key role in regulating the Glutamate/GABA-glutamine cycle (GGG) and nutrient-sensing mTOR pathway. Membrane-bound SLC38A10 transporters regulate the flow of glutamine, glutamate, aspartic acid, and alanine and play a vital role in regulating neurotransmission. This study aimed to understand the possible role of SLC38A10 in brain metabolism and nutrient-sensing pathway. We have used primary cortex cultured from SLC38 Knockout mice and performed nutrient starvation and refed experiment. Here we used the omics approach to integrate data derived from transcriptomic and metabolomics. Differentially expressed genes and changed metabolites were submitted in ingenuity pathway analysis (IPA) to elucidate the cellular function and disease resulting from the absence of SLC38A10 in primary cortex cells.Further, the effect of nutrient deprivation on KO PCCs cells was studied, and associated cellular pathway and bio function indicated towards disease. Our findings relevel that KO cells increase neurotransmission, GABA receptor signalling, Synaptic transmission, Neurotransmission of cerebral cortex cells, Differentiation of oligodendrocytes, neuroglia, branching of neurons, apoptosis and degeneration of neurons, Sprouting, Branching of neurites, dendritic growth/branching and Concentration of lipid. The overall conclusion suggests that SLC38A10 removal results in damaged neuronal morphology and nervous system morphology and functionality, linked with neurodevelopmental and neurological disease.
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