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Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle [RNA-seq]

ABSTRACT: Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle [RNA-seq]

PROVIDER: PRJNA754599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15459500_1.fastq.gz	Fastqsanger.gz
	SRR15459500_2.fastq.gz	Fastqsanger.gz
	SRR15459600_1.fastq.gz	Fastqsanger.gz
	SRR15459600_2.fastq.gz	Fastqsanger.gz
	SRR15459501_1.fastq.gz	Fastqsanger.gz

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Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle

Project description:Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle

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Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle [Affymetrix]

Project description:Circadian rhythms are generated by an auto-regulatory feedback loop composed of transcriptional activators and repressors. Disruption of circadian rhythms contributes to Type 2 diabetes (T2D) pathogenesis. We elucidated whether altered circadian rhythmicity of clock genes is associated with metabolic dysfunction in T2D. Transcriptional cycling of core clock genes BMAL1, CLOCK, and PER3 was altered in skeletal muscle from individuals with T2D and this was coupled with reduced number and amplitude of cycling genes and disturbed circadian oxygen consumption. Inner-mitochondria associated genes were enriched for rhythmic peaks in NGT, but not T2D, and positively correlated with insulin sensitivity. ChIP-sequencing identified CLOCK and BMAL1 binding to inner-mitochondrial genes associated with insulin sensitivity, implicating regulation by the core clock. Inner-mitochondria disruption altered core-clock gene expression and free-radical production, phenomena that were restored by resveratrol treatment. We identify bi-directional communication between mitochondrial function and rhythmic gene expression, processes which are disturbed in diabetes.

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Disrupted circadian oscillations in type 2 diabetes are linked to altered rhythmic mitochondrial metabolism in skeletal muscle.

Project description:Circadian rhythms are generated by an autoregulatory feedback loop of transcriptional activators and repressors. Circadian rhythm disruption contributes to type 2 diabetes (T2D) pathogenesis. We elucidated whether altered circadian rhythmicity of clock genes is associated with metabolic dysfunction in T2D. Transcriptional cycling of core-clock genes BMAL1, CLOCK, and PER3 was altered in skeletal muscle from individuals with T2D, and this was coupled with reduced number and amplitude of cycling genes and disturbed circadian oxygen consumption. Inner mitochondria–associated genes were enriched for rhythmic peaks in normal glucose tolerance, but not T2D, and positively correlated with insulin sensitivity. Chromatin immunoprecipitation sequencing identified CLOCK and BMAL1 binding to inner-mitochondrial genes associated with insulin sensitivity, implicating regulation by the core clock. Inner-mitochondria disruption altered core-clock gene expression and free-radical production, phenomena that were restored by resveratrol treatment. We identify bidirectional communication between mitochondrial function and rhythmic gene expression, processes that are disturbed in diabetes.

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