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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice injected with control, Mafg and LncIRS2 LNA.

ABSTRACT: A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice injected with control, Mafg and LncIRS2 LNA.

PROVIDER: PRJNA497097 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8064900_1.fastq.gz	Fastqsanger.gz
	SRR8064900_2.fastq.gz	Fastqsanger.gz
	SRR8064910_1.fastq.gz	Fastqsanger.gz
	SRR8064910_2.fastq.gz	Fastqsanger.gz
	SRR8064901_1.fastq.gz	Fastqsanger.gz

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice injected with control, Mafg and LncIRS2 LNA.

Project description:Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcrips with elusive functions in metabolism. Here we report that an unexpectedly high fraction of lncRNAs, but not protein-coding mRNAs, is repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation specifically induced lncRNAs in mouse liver. Similarly, lncRNAs were lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirmed that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in primary hepatocytes and in vivo elicited a fasting-like expression profile, improved glucose metabolism, derepressed lncRNAs and prevented mammalian target of rapamycin (mTOR)-driven protein translation. We found that obesity-repressed lincIRS2 is controlled by MAFG and observed that genetic and RNAi-mediated lincIRS2 loss causes hyperglycemia, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a novel MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.

Project description:A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: RNA profiles of metabolically active tissues.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of obese and lean mice.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of mice treated with adenoviruses expressing either Mafg cDNA or empty vector.

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Gene expression profiles in the striatum of the R6/2 mouse model of Huntington's disease injected with LNA-oligonucleotides complementary to the CAG repeats (LNA-CTG)

Project description:We investigated gene expression signatures in the striatum of wild-type mice injected with a control/scrambeled LNA-oligonucleotide (LNA-SCB) and R6/2 mice injected with LNA-SCB or LNA-CTG. Five mice were used per condition. Each group of mice received two consecutive intrastriatal injections of LNA-CTG or LNA-SCB (0.05 nmols per injection, separated by 3 days) at 11 weeks of age , when motor symptoms appeared in the R6/2 mice. Injection of LNA-CTG resulted in a signifficant attenuation of the R6/2 mice motor defficits, as early as one week after administration (12 weeks of age) and persisted for at least 4 additional weeks (15 weeks of age). Overal gene expression in each group was evaluated short before motor improvement was observed (5 days post-injection), to detect gene expression changes and signalling pathway alterations underlying the benefficial effects. Gene expression was assessed with Agilent SurePrint G3 Mouse GE 8 × 60K Microarray. Target genes were validated using real-time quantitative PCR.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.

Project description:Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcripts with elusive functions in metabolism. Here we show that a high fraction of lncRNAs, but not protein-coding mRNAs, are repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation induced lncRNAs in mouse liver. Similarly, lncRNAs are lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirm that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profile, improves glucose metabolism, de-represses lncRNAs and impairs mammalian target of rapamycin (mTOR) activation. We find that obesity-repressed LincIRS2 is controlled by MAFG and observe that genetic and RNAi-mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.

| S-EPMC6994702 | biostudies-literature

A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of lean non-diabetic, obese non-diabetic as well as obese diabetic humans.

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Comparison of gene expression profiles of MafF-/-: MafG-/-: MafK-/- embryos and MafF-/-: MafG+/+: MafK-/- embyos

Project description:MafF-/-: MafG+/+: MafK-/- mice are viable, while MafF-/-: MafG-/-: MafK-/- mice are embryonic lethal. To get an insight into the cause of the lethality of small Maf triple knockout mice, transcriptome analysis was performed using whole embyos of MafF-/-: MafG-/-: MafK-/- at E10.5 and those of MafF-/-: MafG+/+: MafK-/- at E9.5 or E10.5. Because MafF-/-: MafG-/-: MafK-/- embryos exhibit growth retardation, the gene expression profile of MafF-/-: MafG-/-: MafK-/- embryos at E10.5 was compared with that of MafF-/-: MafG+/+: MafK-/- embyos at E9.5. The gene expression profile of MafF-/-: MafG+/+: MafK-/- embryos at E10.5 was also examined as an alternative control. Total RNA was prepared from pooled three embryos for each sample.

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