The white adipose tissue transcriptional response to withdrawal of vitamin B3
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ABSTRACT:
PROVIDER: PRJNA478790 | ENA |
REPOSITORIES: ENA
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Project description:Distinct markers for early, mild vitamin B3 deficiency are lacking. To identify these, we examined the molecular responses of white adipose tissue to vitamin B3 withdrawal. We performed a dietary intervention in male C57Bl/6JRcc mice. A diet with a low but adequate level of tryptophan without nicotinamide riboside (NR) was compared to the same diet with NR at the recommended vitamin B3 (30 mg NR per kg diet). Physiological and circulating parameters were determined and global transcriptomics, qRT-PCR and histology of epididymal white adipose tissue (eWAT) were done. We observed a decreased insulin sensitivity and a shift from carbohydrate to fatty acid oxidation. This was consistent with molecular changes in eWAT, where we observed an altered MEK/ERK signalling, a lowering of glucose utilization markers and an increase in makers of fatty acid catabolism, which may be related to the consistent reduction of mitochondrial OXPHOS Complex I (mRNAs and protein). The synthesis pathway of tetrahydropteridine (BH4), an essential cofactor for neurotransmitter synthesis, was found to be increased. Based on our results, we propose the technically validated downregulation of Anp32a, Tnk2 and the upregulation of Mapk1, Map2k1, Mthfs, Mthfsl and Qdpr as a WAT transcriptional signature marker for mild vitamin B3 deficiency.
2019-05-06 | GSE116483 | GEO
Project description:Transcriptional profiling of mouse white adipose tissues The objective of this study is to explore the relationship between vitamin B6 activity and chronic inflammation of white adipose tissue in mice fed a high-fat diet. Twenty-four CD-1 mice were divided into two groups (n = 12) and fed either a 1 mg pyridoxine (PN) HCl /kg diet or a 35 mg PN HCl /kg diet for 8 weeks. We isolated total RNA from epididymal white adipose tissue of each group and compared gene expression profiles by DNA microarray data analysis. Noriyuki Yanaka
2013-01-12 | E-GEOD-43465 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse white adipose tissues The objective of this study is to explore the relationship between vitamin B6 activity and chronic inflammation of white adipose tissue in mice fed a high-fat diet. Twenty-four CD-1 mice were divided into two groups (n = 12) and fed either a 1 mg pyridoxine (PN) HCl /kg diet or a 35 mg PN HCl /kg diet for 8 weeks. We isolated total RNA from epididymal white adipose tissue of each group and compared gene expression profiles by DNA microarray data analysis.
2013-01-12 | GSE43465 | GEO
Project description:ScopeDistinct markers for mild vitamin B3 deficiency are lacking. To identify these, the molecular responses of white adipose tissue (WAT) to vitamin B3 withdrawal are examined.Methods and resultsA dietary intervention is performed in male C57BL/6JRccHsd mice, in which a diet without nicotinamide riboside (NR) is compared to a diet with NR at the recommended vitamin B3 level. Both diets contain low but adequate level of tryptophan. Metabolic flexibility and systemic glucose tolerance are analyzed and global transcriptomics, qRT-PCR, and histology of epididymal WAT (eWAT) are performed. A decreased insulin sensitivity and a shift from carbohydrate to fatty acid oxidation in response to vitamin B3 withdrawal are observed. This is consistent with molecular changes in eWAT, including an activated MEK/ERK signaling, a lowering of glucose utilization markers, and an increase in makers of fatty acid catabolism, possibly related to the consistent lower expression of mitochondrial electron transport complexes. The synthesis pathway of tetrahydropteridine (BH4), an essential cofactor for neurotransmitter synthesis, is transcriptionally activated. Genes marking these processes are technically validated.ConclusionThe downregulation of Anp32a, Tnk2 and the upregulation of Mapk1, Map2k1, Qdpr, Mthfs, and Mthfsl are proposed as a WAT transcriptional signature marker for mild vitamin B3 deficiency.
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