Gene expression altered by Chrebp deficiency and fructose treatment
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ABSTRACT:
PROVIDER: PRJNA689855 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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
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
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
Project description:Intramuscular fat (IMF) content is one of the key factors affecting meat quality. Carbohydrate response element binding protein (ChREBP) can promote glucose metabolism and fat synthesis by activating the expression of glycolysis and lipogenesis-related genes, but its function and regulatory mechanism in IMF are still unclear. This study evaluated the correlation between TG content and ChREBP expression level in muscles of different species to reveal the relationship between ChREBP and IMF. RNA-seq analysis showed that overexpressing ChREBP in C2C12 cells can significantly up-regulate fatty acid synthesis pathways, while significantly down-regulate the expression levels of muscle development pathways and related genes. In vivo, we found that overexpression of ChREBP or activation by fructose significantly increased the triglyceride content of the tibialis anterior muscle (TA) and the IMF content of yellow feather chicken leg and breast muscle in mice. And lipidomics data also found that feeding fructose can change the lipid composition of yellow feather broiler breast muscle and improve the flavor substances. This study demonstrated that ChREBP is a key gene regulating IMF deposition, providing a new target for genetic selection and nutritional regulation of IMF content.
2024-08-08 | GSE228899 | GEO
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
Project description:Gene expression altered by high-fructose diet feeding and Chrebp deficiency
| PRJNA379821 | ENA
Project description:Effect ofhepatocyte-specific Chrebp knockout on model of high-fructose diet during pregnancy
| PRJNA1041456 | ENA
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
Project description:Muscle performance and fatigability are determined by the structural and metabolic properties of the specialized myofibers. Skeletal muscle demonstrates significant plasticity, with myofiber types and energy metabolic functions undergoing adaptive remodeling in response to physiological or pathophysiological stimuli. The transcription factor carbohydrate-responsive element-binding protein (ChREBP) is recognized as a crucial glucose-sensing regulator involved in glucose and lipid metabolism. However, However, the precise role of ChREBP in influencing myofiber composition and energy metabolism within muscle tissue remains ambiguous. Here, utilizing skeletal muscle-specific knockout mice, we demonstrated that ChREBP deletion did not substantially alter muscle fiber composition or metabolic function, nor did it play a role in skeletal muscle adaptive remodeling under hypoxic or high-fructose dietary conditions. Interestingly, the absence of ChREBP was associated with a modest enhancement in aerobic exercise capacity, although it markedly impaired lipid transport function and led to a reduction in triglyceride content. Furthermore, we observed that upregulation of ChREBP expression significantly increased the number of newly formed myofibers and their cross-sectional area. Taken together, this study elucidates the role of ChREBP in skeletal muscle and its adaptive remodeling, while also identifying a significant promotive function of ChREBP in the repair of skeletal muscle injuries.
2026-07-01 | GSE319093 | GEO