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TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [ChIP-seq]

ABSTRACT: TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [ChIP-seq]

PROVIDER: PRJNA951644 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24046238_1.fastq.gz	Fastqsanger.gz
	SRR24046238_2.fastq.gz	Fastqsanger.gz
	SRR24046239_1.fastq.gz	Fastqsanger.gz
	SRR24046239_2.fastq.gz	Fastqsanger.gz
	SRR24046240_1.fastq.gz	Fastqsanger.gz

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TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1

Project description:TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1

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TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [RNA-seq]

Project description:TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [RNA-seq]

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TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1 [ChIP-seq]

Project description:Purpose: The goals of this study are to explore role of Tox3 in glucose homeostasis Methods: Tox3-activation was generated by adenovirus from Genechem.Successful activation of Tox3 was determined by mRNA and protein expression.

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Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention

Project description:Type 2 Diabetes (T2D) is a global health issue characterized by abnormal blood glucose levels and often associated with excessive hepatic gluconeogenesis. Increased circulating non-essential amino acids (NEAAs) are consistently observed in T2D individuals; however, the specific contribution of each amino acid to T2D pathogenesis remains less understood. Here, we reported an unexpected role of the NEAA proline in coordinating hepatic glucose metabolism by modulating paraspeckle, a nuclear structure scaffolded by the long noncoding RNA Neat1. Mechanistically, proline diminished paraspeckles in hepatocytes, liberating the retained mRNA species into cytoplasm for translation, including the mRNAs of Ppargc1a and Foxo1, contributing to enhanced gluconeogenesis and hyperglycemia. We further demonstrated that the proline-paraspeckle-mRNA retention axis existed in diabetic liver samples, and intervening this axis via paraspeckle restoration significantly alleviated hyperglycemia in both female and male diabetic mouse models. Collectively, our results not only delineated a previously unappreciated proline-instigated, paraspeckle-dependent mRNA retention mechanism regulating gluconeogenesis, but also spotlighted proline and paraspeckle as potential targets for managing hyperglycemia. This SuperSeries is composed of the SubSeries listed below.

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TOX3 drives hepatic gluconeogenesis and hyperglycemia by targeting FoxO1

Project description:This SuperSeries is composed of the SubSeries listed below.

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Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [lncRNA-Seq]

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Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [RIP-Seq]

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Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids

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Project description:In diabetes, the kidney contributes to the development of diabetic hyperglycemia by increasing glucose reabsorption from the primary urine and by upregulating gluconeogenesis in the proximal tubule. However, these two processes are also controlled by the circadian clock, a mechanism that synchronizes a large number of specific renal functions with environmental daily cycles. Here, we investigated the (patho)physiological role of intrinsic renal tubule circadian clocks in the diabetic kidney. We demonstrate that diabetic mice devoid of the circadian transcriptional regulator BMAL1 in the renal tubule exhibit additional enhancement of renal gluconeogenesis, exacerbated hyperglycemia, increased glucosuria, polyuria and renal hypertrophy. Collectively, our results suggest that diabetic hyperglycemia can be worsened by dysfunction or misalignment of intrinsic renal circadian clocks.

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