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Glycan changes caused by insulin-deficient diabetes in the mouse liver

ABSTRACT: To determine the effect of insulin deficiency on global changes to expression of glycan related genes in the liver. See: Joseph R. Bishop,‡ Erin Foley,‡§ Roger Lawrence,‡ and Jeffrey D. Esko‡1 (2010) Insulin-dependent Diabetes Mellitus in Mice Does Not Alter Liver Heparan Sulfate* J Biol Chem. 2010 May 7; 285(19): 14658–14662. We are studying the glycan changes caused by insulin-deficient diabetes in the mouse liver. We would like to determine whether insulin-deficiency causes global changes to expression of glycan-related genes in the liver. Male C57BL/6 mice (4 weeks of age) were purchased from Jackson Laboratory and maintained in a temperature-controlled (25 °C) facility with a 12-h light/dark cycle. The derivation and genotyping of Ndst1f/fAlbCre+ mice have been described previously (16). Mice were fed laboratory rodent chow (Harlan-Teklad) ad libitum except when fasting blood specimens were obtained. Mice were made diabetic by administering 50 mg/kg body weight of streptozotocin (STZ; Sigma) intraperitoneally for 5 consecutive days. Because of variations in plasma triglycerides in females, only male mice were used in this study.

ORGANISM(S): Mus musculus

PROVIDER: GSE31989 | GEO | 2011/09/08

SECONDARY ACCESSION(S): PRJNA145159

REPOSITORIES: GEO

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Glycan changes caused by insulin-deficient diabetes in the mouse liver

Project description:To determine the effect of insulin deficiency on global changes to expression of glycan related genes in the liver. See: Joseph R. Bishop,‡ Erin Foley,‡§ Roger Lawrence,‡ and Jeffrey D. Esko‡1 (2010) Insulin-dependent Diabetes Mellitus in Mice Does Not Alter Liver Heparan Sulfate* J Biol Chem. 2010 May 7; 285(19): 14658–14662. We are studying the glycan changes caused by insulin-deficient diabetes in the mouse liver. We would like to determine whether insulin-deficiency causes global changes to expression of glycan-related genes in the liver. Male C57BL/6 mice (4 weeks of age) were purchased from Jackson Laboratory and maintained in a temperature-controlled (25 °C) facility with a 12-h light/dark cycle. The derivation and genotyping of Ndst1f/fAlbCre+ mice have been described previously (16). Mice were fed laboratory rodent chow (Harlan-Teklad) ad libitum except when fasting blood specimens were obtained. Mice were made diabetic by administering 50 mg/kg body weight of streptozotocin (STZ; Sigma) intraperitoneally for 5 consecutive days. Because of variations in plasma triglycerides in females, only male mice were used in this study. Our preliminary results suggest glycosaminoglycan enzymes may be down-regulated, which may affect the turnover of lipids in the plasma. Liver RNA samples from 3 diabetic mice will be compared to 3 wildtype samples for properly controlled analysis.

2011-09-07 | E-GEOD-31989 | biostudies-arrayexpress

Mus musculus

Project description:Glycan changes caused by insulin-deficient diabetes in the mouse liver

| PRJNA145159 | ENA

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.

2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress

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."

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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.

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Gene expression profile in the liver of insulin-deficient mice with icv leptin administration

Project description:Analysis of gene expression in the liver of insulin-deficient mice regulated by icv leptin administration. Control group received icv PBS administration. Icv leptin administration ameliorates hyperglycemia in insulin-deficient mice. Our transcriptome data provides important aspects of the leptin’s anti-type 1 diabetes action.

2013-09-03 | GSE48598 | GEO

Transcription profiling of mice overexpressing spermidine/spermine N1-acetyltransferase (SSAT)

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Disruption of the phosphate transporter Pit1 in hepatocytes improves glucose metabolism and insulin signalling by modulating the USP7/IRS1 interaction.

Project description:The liver plays a central role in whole-body lipid and glucose homeostasis. Increasing dietary fat intake results in increased hepatic fat deposition, which is associated with a risk for development of insulin resistance and type 2 diabetes. In this study, we demonstrate a role for the phosphate inorganic transporter 1 (PiT1/SLC20A1) in regulating metabolism. Specific knockout of Pit1 in hepatocytes significantly improved glucose tolerance and insulin sensitivity, enhanced insulin signalling, and decreased hepatic lipogenesis. We identified USP7 as a PiT1 binding partner and demonstrated that Pit1 deletion inhibited USP7/IRS1 dissociation upon insulin stimulation. This prevented IRS1 ubiquitination and its subsequent proteasomal degradation. As a consequence delayed insulin negative feedback loop and sustained insulin signalling were observed. Moreover, PiT1-deficient mice were protected against high fat diet-induced obesity and diabetes. Our findings indicate that PiT1 has potential as a therapeutic target in the context of metabolic syndrome, obesity, and diabetes.

2016-08-25 | E-MTAB-4989 | biostudies-arrayexpress

Proteomic analysis of liver tissue from a pig model of mutant INS gene induced diabetes of youth (MIDY)

Project description:To evaluate functional consequences of insulin-deficient diabetes mellitus for the liver, we used a genetically engineered pig model of mutant INS gene induced diabetes of youth (MIDY). Liver samples of MIDY pigs and wild-type (WT) littermate controls were analyzed by label-free proteomics to reveal pathways and key drivers significantly affected by chronic insulin deficiency and hyperglycemia.

2019-11-12 | PXD011536 | Pride

SMOC1 as a therapeutic target for type 2 diabetes

Project description:Inter-tissue communication is a fundamental feature of systemic metabolic regulation and the liver is central to this process. We have identified sparc-related modular calcium-binding protein 1 (SMOC1) as a glucose-responsive hepatokine and potent regulator of glucose homeostasis. Acute administration of recombinant SMOC1 improves glycemic control and insulin sensitivity, independent of changes in insulin secretion. SMOC1 exerts its favourable glycemic effects by inhibiting cAMP-PKA-CREB signaling in the liver, leading to decreased gluconeogenic gene expression and suppression of hepatic glucose output. Over expression of SMOC1 in the liver or once-weekly injections of a stabilized SMOC1-FC fusion protein induces durable improvements in glucose tolerance and insulin sensitivity in db/db mice, without significant adverse effects on adiposity, liver histopathology or inflammation. Furthermore, SMOC1 correlates with systemic insulin sensitivity and is decreased in obese, insulin resistant humans. Together, these findings identify SMOC1 as a potential pharmacological target for the management of glycemic control in type 2 diabetes.

2020-08-21 | PXD015767 | Pride

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