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Gene expression altered by Chrebp deficiency and fructose treatment

ABSTRACT: Gene expression altered by Chrebp deficiency and fructose treatment

PROVIDER: PRJNA689855 | ENA |

REPOSITORIES: ENA

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Gene expression altered by Chrebp deficiency and fructose treatment

Project description:To identify hepatic genes specifically regulated by fructose-activated ChREBPα. Fgf21 is one of the genes activated by fructose dependent on ChREBP.

2021-01-06 | GSE164321 | GEO

Gene expression altered by high-fructose diet feeding and Chrebp deficiency

Project description:Epidemiologic and animal studies implicate overconsumption of fructose in the development of non-alcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remains largely unknown. We present evidence supporting the essential function of the lipogenic transcription factor ChREBP in mediating adaptation response to fructose and protecting against fructose-induced hepatotoxicity. High-fructose diet (HFrD) activates hepatic lipogenesis via a ChREBP-dependent manner in wildtype mice, while inducing steatohepatitis in Chrebp-KO mice. In Chrebp-KO mouse livers, HFrD reduces levels of molecular chaperones and activates the CHOP-dependent unfolded protein response, whereas administration of chemical chaperone or Chop shRNA rescues liver injury. Gene expression profiling revealed elevated expression of cholesterol biosynthesis genes in Chrebp-KO livers after HFrD, in parallel with increased abundance of nuclear SREBP2. genes expression were compared between livers of wildtype mice fed 70%-fructose-diet v.s. regular chow, and between livers of Chrebp-/- mice v.s. wildtype mice fed 70%-fructose-diet.

2017-03-21 | GSE96820 | GEO

Effect ofhepatocyte-specific Chrebp knockout on model of high-fructose diet during pregnancy

Project description:During pregnancy, a high-fructose diet (HFrD) exacerbates gestational insulin resistance and is associated with an increased risk of gestational diabetes. The relationship between liver ChREBP and gestational insulin resistance remains unknown. To address this question, we fed pregnant hChrebp-KO mice and wild-type mice a high-fructose diet, and on the 17th day of pregnancy, we extracted liver tissue from the mice and conducted comparative transcriptomic analysis to elucidate the role of liver ChREBP in gestational insulin resistance."

2024-02-18 | GSE248051 | GEO

Expression data of liver with ChREBP gene knockout from mice fed with 60% sucrose diet for 1 week.

Project description:Carbohydrate response element binding protein (ChREBP) is one of the major transcription factors regulating carbohydrate metabolism and lipogenesis.It expresses highly in several tissues including liver, adipose tissue, small intestine,kidney and muscles. Mice with global knockout of ChREBP exhibit intolerance to carbohydrate including glucose and fructose. However, the exact role of liver ChREBP in high carbohydrate stress is not well defined. We used microarrays to exame the changes of gene expression pfofile upon high sucrose (50% glucose and 50% fructose) stress when liver ChREBP was deleted.

2020-01-24 | GSE139937 | GEO

RNA-sequencing analysis of liver tissue from mice subjected to high-fructose or normal diets during pregnancy.

Project description:During pregnancy, a high-fructose diet (HFrD) exacerbates gestational insulin resistance and is associated with an increased risk of gestational diabetes. The relationship between liver ChREBP and gestational insulin resistance remains elusive. To address this question, we fed pregnant mice either a high-fructose diet or a normal diet. On the 17th day of pregnancy, we extracted liver tissue from the mice and conducted comparative transcriptomic analysis to elucidate the alterations in liver ChREBP during gestational insulin resistance.

2024-02-18 | GSE247892 | GEO

Mus musculus

Project description:Gene expression altered by high-fructose diet feeding and Chrebp deficiency

| PRJNA379821 | ENA

Proline hydroxylation of ChREBP

Project description:This project investigated proline hydroxylation of ChREBP. Proline hydroxylation was investigated in flag-IP enriched protein extracts from ChREBP-flag overexpressing HEK293 cells (A) and in ChREBP-IP enriched mouse liver protein (male, C57BL6/J) (B).

2020-10-19 | PXD019137 | Pride

DNA methylation profile for male SD Rats upon fructose treatment by RRBS

Project description:DNA methylation profile for male SD Rats upon fructose treatment by RRBS

2016-10-19 | GSE59893 | GEO

Gene expression profile for male SD Rats upon fructose treatment by RNA-Seq

Project description:Gene expression profile for male SD Rats upon fructose treatment by RNA-Seq

2016-07-13 | GSE59918 | GEO

Metformin Impairs Intestinal Fructose Metabolism

Project description:Objective: To investigate the effects of metformin on intestinal carbohydrate metabolism in vivo. Method: Male mice preconditioned with a high-fat, high-sucrose diet were treated orally with metformin or a control solution for two weeks. Fructose metabolism, glucose production from fructose, and production of other fructose-derived metabolites were assessed using stably labeled fructose as a tracer. Results: Metformin treatment decreased intestinal glucose levels and reduced incorporation of fructose-derived metabolites into glucose. This was associated with decreased intestinal fructose metabolism as indicated by decreased enterocyte F1P levels and diminished labeling of fructose-derived metabolites. Metformin also reduced fructose delivery to the liver. Proteomic analysis revealed that metformin coordinately down-regulated proteins involved carbohydrate metabolism including those involved in fructolysis and glucose production within intestinal tissue. Conclusion: Metformin reduces intestinal fructose metabolism, and this is associated with broad-based changes in intestinal enzyme and protein levels involved in sugar metabolism indicating that metformin's effects on sugar metabolism are pleiotropic.

2024-04-27 | PXD041833 | JPOST Repository

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