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Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet

ABSTRACT: Phloridzin is a dihydrochalcone typically contained in apples. A diet containing 0.5 % phloridzin significantly improves hyperglycemia but not hypoinsulinemia and tissue lipid peroxidation in streptozotocin (STZ)-induced diabetic mice after 14 days. The phloridzin diet has no effect on the alteration of hepatic gene expression in STZ-induced diabetic mice. A quantitative RT-PCR analysis showed a reversal of the STZ induction of the sodium/glucose cotransporter gene Sglt1 and the drug-metabolizing enzyme genes Cyp2b10 and Ephx1 in the small intestine of mice fed a 0.5% phloridzin diet. These mice also showed a reversal of the STZ-mediated renal induction of the glucose-regulated facilitated glucose transporter gene Glut2. Dietary phloridzin improved the abnormal elevations in blood glucose level and the overexpression of Sglt1, Cyp2b10 and Ephx1 in the small intestine of STZ-induced diabetic mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE38138 | GEO | 2012/05/30

SECONDARY ACCESSION(S): PRJNA167276

REPOSITORIES: GEO

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Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet

Project description:Phloridzin is a dihydrochalcone typically contained in apples. A diet containing 0.5 % phloridzin significantly improves hyperglycemia but not hypoinsulinemia and tissue lipid peroxidation in streptozotocin (STZ)-induced diabetic mice after 14 days. The phloridzin diet has no effect on the alteration of hepatic gene expression in STZ-induced diabetic mice. A quantitative RT-PCR analysis showed a reversal of the STZ induction of the sodium/glucose cotransporter gene Sglt1 and the drug-metabolizing enzyme genes Cyp2b10 and Ephx1 in the small intestine of mice fed a 0.5% phloridzin diet. These mice also showed a reversal of the STZ-mediated renal induction of the glucose-regulated facilitated glucose transporter gene Glut2. Dietary phloridzin improved the abnormal elevations in blood glucose level and the overexpression of Sglt1, Cyp2b10 and Ephx1 in the small intestine of STZ-induced diabetic mice. Six-week-old male mice were divided into 4 groups of 6 mice each, housed in groups of 3 per cage. After 1 week mice were intraperitoneally injected with STZ. Mice (n=6) in the untreated control group did not receive any treatment. After 1 week, 18 mice showing non-fasting blood glucose levels of 330-590 mg/dL were divided into 3 groups: one group was fed with AIN93G only (control group), the others with an AIN93G diet containing 0.1% or 0.5% phloridzin (Funakoshi, Tokyo, Japan) for 2 weeks.

2012-05-29 | E-GEOD-38138 | biostudies-arrayexpress

Hepatic gene expression in streptozotocin-induced diabetic mice fed a quercetin diet

Project description:Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury. We fed STZ-induced diabetic mice with diets containing 0.1% or 0.5% quercetin for 2 weeks and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). Six-week-old male mice were divided into 4 groups of 6 mice each, housed in groups of 3 per cage. After 1 week mice were intraperitoneally injected with STZ. Mice (n=6) in the untreated control group did not receive any treatment. After 1 week, 18 mice showing non-fasting blood glucose levels of 230-400 mg/dL were divided into 3 groups: one group was fed with AIN93G only (control group), the others with an AIN93G diet containing 0.1% or 0.5% quercetin (Funakoshi, Tokyo, Japan) for 2 weeks.

2012-05-22 | E-GEOD-38067 | biostudies-arrayexpress

Hepatic gene expression in streptozotocin-induced diabetic mice fed a quercetin diet

2012-05-23 | GSE38067 | GEO

Phloridzin reduces blood glucose levels and alters hepatic gene expression in normal BALB/c mice

Project description:We previously showed that a diet containing phloridzin suppressed the blood glucose levels in streptozotocin-induced diabetic mice most likely by inhibiting glucose absorption from the small intestine. In this study, we showed that 0.5% and 1% phloridzin diets significantly reduce the blood glucose levels in healthy normal BALB/c mice after 7 days of feeding. To understand the effect of the high continuing intake of dietary phloridzin on normal mouse livers, we analyzed the hepatic gene expressions in mice fed diets containing 0%, 0.1%, 0.5%, or 1% phloridzin for 14 days using DNA microarrays.

2012-05-18 | GSE37415 | GEO

Phloridzin reduces blood glucose levels and alters hepatic gene expression in normal BALB/c mice

2012-05-17 | E-GEOD-37415 | biostudies-arrayexpress

Hepatic gene expression in BALB/c mice fed a quercetin diet

Project description:We showed that diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). In this experiment, we determined the effect of quercetin on healthy control BALB/c mice that were fed the AIN93G diet containing 0, 0.1, 0.5 or 1% quercetin for 2 weeks. GSEA and one-way ANOVA did not detect any significant changes in hepatic gene expression in normal mice as a result of a quercetin diet. Using a linear modeling approach and the empirical Bayes statistics, we found that Ubc were significantly reduced by both the 0.5% and 1% quercetin.

2012-05-30 | GSE38136 | GEO

Hepatic gene expression in BALB/c mice fed a quercetin diet

2012-05-29 | E-GEOD-38136 | biostudies-arrayexpress

Integrated transcriptomic analyses identify altered nerve triglycerides in mouse models of prediabetes and type 2 diabetes

Project description:We employed high-fat diet (HFD)-induced prediabetes and HFD/streptozotocin (STZ)-induced type 2 diabetes mouse models that develop PN, which we compared to control mice maintained on standard diet (SD) and to HFD and HFD/STZ mice that were subject to SD dietary reversal (DR) half-way through the study. We performed gene expression profiling on sciatic nerves from SD, HFD, HFD-STZ, HFD-DR, and HFD-STZ-DR animal cohorts. Nerve transcriptomic profiles were integrated using complex correlation analyses, and biological meaning was inferred from known lipid-gene interactions in the literature

2019-11-12 | GSE140201 | GEO

N-glyco STZ mouse kidney - N-glycosylation proteome enrichment analysis in kidney reveals differences between diabetic mouse models

Project description:N-glycosylated proteome of STZ diabetic mice with diabetic nephropathy

2016-12-13 | PXD003196 | Pride

Liver adapts mitochondrial function to insulin-resistant and diabetic states in mice

Project description:Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls. Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis. We performed gene expression microarray analysis on liver tissue derived from mice treated with STZ or standard diet (control).

2013-12-10 | E-GEOD-39752 | biostudies-arrayexpress

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