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DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

ABSTRACT: DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

PROVIDER: PRJNA494786 | ENA |

REPOSITORIES: ENA

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DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:The differential DNA methylation in hepatocytes was compared between the KK.Cg-Ay/J mice and the KK-a/a mice, corresponding to the Diabetic strain and the wild-type known as control. The methylation microarrays were used to support gene expression for screening the candidates susceptibility to the pathogenesis of Type-2 Diabetes in the pre-development, early and development stages, corresponding to the 6, 16 and 42 weeks old. To determine the methylation-dependent biological processes and pathways contributing to development of Diabetic phenotypes in the KKAy mouse, we identified the candidates with the differential DNA methylation levels between the KKAy and KKa mice. The expression of methylation-dependent genes have relationship linkage to construct the networks for mechanistic explanation of the disease.

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Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:The differential gene expression in hepatocytes was compared between the KK.Cg-Ay/J mice and the KK-a/a mice, corresponding to the Diabetic strain and the control. The microarrays were used to screen the candidates supporting to the essential pathogenesis of Type-2 Diabetes in the pre-developing, early and developing stages, corresponding to the 6 weeks, 16 weeks and 42 weeks. To determine the significant biological processes and pathways contributing to development of Diabetic phenotypes in the KKAy mouse, we identified the candidates with the differential gene expression of the livers by comparison of the KKAy and KKa mice. These genes have relationship linkage to construct the networks for mechanistic explanation of the disease.

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Hepatic gene expression profiles in persimmon peel extract administrated KK-Ay mice

Project description:We have shown in a previous study that the intake of persimmon peel (PP) extract altered hepatic gene expression of insulin signaling and enhanced tyrosine phosphorylation of insulin receptors in nonobese type 2 diabetic Goto–Kakizaki rats. We also showed the alteration of gene expression in fatty acid synthesis and metabolism. To evaluate the effect of PP extract on obese diabetic KK-Ay mice, we fed them a diet mixed with 0.1% of the extract for 8 weeks. The plasma total ketone bodies level of the treated mice were significantly lower than that of the untreated mice. The hepatic gene expression profiles of treated mice indicated upregulation of fatty acid biosynthesis-associated gene expression. Hepatic nonesterified palmitic acid content was higher in treated mice than in untreated mice. These results suggest that the intake of PP extract enhances hepatic fatty acid biosynthesis of KK-Ay mice, reducing their plasma total ketone bodies level.

2018-10-01 | GSE67573 | GEO

Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:Gene expression profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

| PRJNA494787 | ENA

Gene expression and DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

Project description:Gene expression and DNA methylation profiles of KK.Cg-Ay/J (KKAy) mice and KK-a/a (KKa) mice

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Comparison of expression profiles of WT and Nrf2AY/AY mutant macrophages under electrophilic stress agent [RNA-Seq]

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Comparison of expression profiles of WT and Nrf2AY/AY mutant macrophages under electrophilic stress agent [ChIP-Seq]

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Comparison of expression profiles of WT and Nrf2AY/AY mutant macrophages under electrophilic stress agent [ChIP-Seq]

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Royal jelly improves hyperglycemia in obese/diabetic KK-Ay mice.

Project description:The study examined whether royal jelly (RJ) can prevent obesity and ameliorate hyperglycemia in type 2 diabetes. This study utilized obese/diabetic KK-Ay mice. RJ (10 mg/kg) was administered by oral gavage. Body weight, plasma glucose and insulin levels were measured. mRNA and protein levels were determined using quantitative reverse transcription polymerase chain reaction and western blotting, respectively. Four weeks of RJ administration improved hyperglycemia and partially suppressed body weight gain, although the latter effect did not reach statistical significance. In addition, RJ administration did not improve insulin resistance. RJ administration suppressed the mRNA expression of glucose-6-phosphatase (G6Pase), a key enzyme of gluconeogenesis, in the liver. Simultaneously, RJ administration induced adiponectin (AdipoQ) expression in abdominal fat, adiponectin receptor-1 (AdipoR1) expression in the liver and phosphorylated AMP-activated protein kinase (pAMPK) expression, which suppressed G6Pase levels in the livers of KK-Ay mice. pAMPK levels were also increased in skeletal muscle, but glucose transporter-4 (Glut4) translocation was not increased in the RJ supplementation group. The improvement in hyperglycemia due to long-term RJ administration may be because of the suppression of G6Pase expression through the upregulation of AdipoQ and AdipoR1 mRNA and pAMPK protein expressions.

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Project description:KK-Ay mice gene expression profile

| PRJNA395843 | ENA