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A mitochondrial long-chain fatty acid oxidation defect in a mouse leads to dysregulation of plasma long-chain acylcarnitines, dysregulation of plasma amino acids, and an increased reliance on glucocorticoid signaling to maintain euglycemia during fasting

ABSTRACT: A mitochondrial long-chain fatty acid oxidation defect in a mouse leads to dysregulation of plasma long-chain acylcarnitines, dysregulation of plasma amino acids, and an increased reliance on glucocorticoid signaling to maintain euglycemia during fasting

PROVIDER: PRJNA774961 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16596000.fastq.gz	Fastqsanger.gz
	SRR16596001.fastq.gz	Fastqsanger.gz
	SRR16596002.fastq.gz	Fastqsanger.gz
	SRR16596003.fastq.gz	Fastqsanger.gz
	SRR16596004.fastq.gz	Fastqsanger.gz

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A mitochondrial long-chain fatty acid oxidation defect in a mouse leads to dysregulation of plasma long-chain acylcarnitines, dysregulation of plasma amino acids, and an increased reliance on glucocorticoid signaling to maintain euglycemia during fasting

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