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TCTP participate in hepatic metabolism with regulate the gene expression involved in insulin resistance

ABSTRACT: TCTP participate in hepatic metabolism with regulate the gene expression involved in insulin resistance

PROVIDER: PRJNA600396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10867677_1.fastq.gz	Fastqsanger.gz
	SRR10867677_2.fastq.gz	Fastqsanger.gz
	SRR10867678_1.fastq.gz	Fastqsanger.gz
	SRR10867678_2.fastq.gz	Fastqsanger.gz
	SRR10867679_1.fastq.gz	Fastqsanger.gz

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TCTP participate in hepatic metabolism with regulate the gene expression involved in insulin resistance

Project description:The translationally controlled tumor protein (TCTP) has various cellular functions and molecular interactions, many related to its growth promoting and antiapoptotic properties. Recently, TCTP highly increased expression in high-fat diet-fed mice with insulin-resistant states. Despite TCTP is a multifunction protein, but its role in liver metabolism is still unknown. Here, we investigated the function and mechanism of TCTP in HepG2 cells. Knock-down the TCTP regulated 287 differentially expressed genes and these genes are highly associated with the cellular apoptosis and stress, NF-kB, Glycolysis/Gluconeogenesis, insulin resistance. TCTP deletion selectively downregulated the expression of PCK1 and G6PC in glucose metabolism. Furthermore, TCTP regulated the alternative splicing of genes enriched in phospholipid biosynthetic process, and glycerophospholipid metabolism. Our results implied that TCTP regulates liver cell transcriptome at both the transcriptional and alternative splicing levels. The TCTP regulatory network predicts the biological functions of TCTP in glycometabolism and lipid metabolism, which may be associated with liver metabolism and induces fatty liver disease through enhanced insulin resistant signaling.

2021-01-13 | GSE143409 | GEO

The Effect of Fatty Acids in Hepatic Insulin Resistance - Part 1

Project description:Monounsaturated fatty acid (MUFA) oleic acid (OA) has been reported to restore saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, the detailed molecular mechanism remains elusive. In addition, -3 polyunsaturated fatty acid (PUFA) such as Eicosapentaenoic acid (EPA) has also exerted opposite effects to PA in muscle IR. But whether it plays the same role in hepatic IR and the possible mechanism involved needs to be further explored. Here, we compared the proteome change of HepG2 cells after different fatty acids treatment.

2019-07-11 | PXD012065 | Pride

Treatment with ginseng flower buds extract prevents hepatic steatosis by ameliorating hepatic inflammation and insulin resistance

Project description:Background: Ginseng flower bud (GFB) is a part of ginseng with high content of ginsenosides, the known active components of ginseng. While the scientific data for the pharmacological activity of ginseng roots are accumulating, the therapeutic potential of GFB have been neglected. The current study aimed to examine the therapeutic effect of GFB on hepatic steatosis and to elucidate the underlying mechanisms. Methods: HepG2 cells treated with free fatty acids mixture and hepatocytes isolated from rats after 3 weeks of HFD feeding were used as in vitro models of hepatic steatosis for evaluation of anti-steatotic effect of GFB. The effect of GFB was further investigated in pathological conditions of hepatic steatosis induced by 12 weeks of HFD feeding in C57BL/6J mice. We performed systematical analyses on hepatic gene expression profiles in GFB treated mice. The effect of GFB on the expression profile of selected genes was validated by quantitative PCR. Results: GFB treatment markedly reduced oil red O stained lipid droplets and intracellular triglyceride levels in HepG2 cells and rat hepatocytes. In HFD-fed mice, GFB (500 mg/kg) treatment markedly reduced histological signs of hepatic steatosis and decreased hepatic triglyceride content by 34.1% compared to those of HFD. These changes by GFB treatment were accompanied by improved insulin signaling. Global gene expression analysis revealed that hepatic gene expression in the steatotic liver was reversed by GFB treatment, and the GFB-regulated genes are involved in immune process, insulin response and lipid storage. Conclusion: These findings provide a substantial evidence for the medicinal use of GFB in prevention or treatment of NAFLD through suppression of hepatic inflammation and fatty acid uptake while sensitizing hepatic insulin signaling

2021-01-01 | GSE142059 | GEO

A Novel Factor Associating with Hepatic Insulin Sensitivity in Humans with Nonalcoholic Fatty Liver Disease

Project description:We comprehensively searched for the factors that may attribute to hepatic insulin sensitivity in the patients with NAFLD. Forty-three NAFLD patients were assessed for putative biomarkers in blood and urine, body composition, tissue lipid content, tissue insulin sensitivity by hyperinsulinemic-euglycemic clamp, hepatic histology and gene expressions using liver biopsies, and life styles. In results, the higher levels of plasma adiponectin, muscle insulin sensitivity, and adipose tissue insulin sensitivity positively, but the higher levels of HbA1c, ALT, and log converted high-sensitive CRP negatively correlated with hepatic insulin sensitivity. Interestingly, whole liver volume and hepatic lean volume corrected by body surface area (cm3/m2) showed significant negative correlation with hepatic insulin sensitivity, specifically in patients with T2DM.

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Hepatic follistatin increases basal metabolic rate and attenuates diet-induced obesity during hepatic insulin resistance

Project description:Insulin resistance not compensated by secretion reduces energy storage, but little is known about its effect upon energy expenditure (EE). Insulin receptor substrates Irs1 and Irs2 mediate signaling in all tissues, resulting in the inhibition of FoxO transcription factors. We found that hepatic disruption of Irs1 and Irs2 (LDKO mice) attenuated high-fat diet (HFD)-induced obesity and increased whole-body EE in a FoxO1-dependent manner. Hepatic disruption of Fst (follistatin), a FoxO1-regulated hepatokine, normalized EE in LDKO mice and restored adipose mass during HFD consumption. Moreover, hepatic Fst disruption alone increased fat mass accumulation, whereas hepatic overexpression of Fst attenuated high HFD-induced obesity. Excess circulating Fst in overexpressing mice neutralized Mstn (myostatin), activating mTORC1-promoted pathways of nutrient uptake and EE in skeletal muscle. Similar to Fst overexpression, direct activation of muscle mTORC1 also reduced adipose mass. We conclude that Fst-promoted EE in muscle attenuates obesity during hepatic insulin resistance.

2024-02-29 | GSE260531 | GEO

Identify factors associated with preserved hepatic insulin sensitivity despite of hepatic steatosis.

Project description:Among all the evaluated factors, only adipose tissue insulin sensitivity (assessed by clamped % suppression of serum free fatty acid), serum concentration of high molecular weight adiponectin, and plasma concentration of TCA cycle metabolites such as citric acid and cis-aconitic acid (assessed by metabolome analysis), associated significantly and positively with hepatic insulin sensitivity in NAFLD.

2016-12-23 | GSE92746 | GEO

Molecular studies on sex-different control of the hepatic metabolism in relations to insulin sensitivity

Project description:This SuperSeries is composed of the following subset Series: GSE23808: Molecular studies on sex-different control of the hepatic metabolism in relations to insulin sensitivity (set 1) GSE23809: Molecular studies on sex-different control of the hepatic metabolism in relations to insulin sensitivity (set 2) Refer to individual Series

2011-08-09 | E-GEOD-23810 | biostudies-arrayexpress

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

2014-04-01 | E-GEOD-48815 | biostudies-arrayexpress

Follistatin dysregulates systemic glucose homeostasis during hepatic insulin resistance

Project description:Follistatin dysregulates systemic glucose homeostasis during hepatic insulin resistance

| PRJNA438228 | ENA

Hypermethylation of hepatic mitochondrial ND6 provokes systemic insulin resistance

Project description:Hypermethylation of hepatic mitochondrial ND6 provokes systemic insulin resistance

| PRJNA438900 | ENA