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Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC β inhibitor, ruboxistaurin (RBX, or LY333531)

ABSTRACT: We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-β isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling. To further investigate the effect of high fat diet and specific PKC β inactivation on STZ-induced atherosclerosis using the PKC β inhibitor, ruboxistaurin (RBX, or LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression. The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings.

ORGANISM(S): Mus musculus

PROVIDER: GSE79623 | GEO | 2016/03/26

SECONDARY ACCESSION(S): PRJNA316467

REPOSITORIES: GEO

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Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC Î² inhibitor, ruboxistaurin (RBX, or LY333531)

Project description:We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-Î² isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling. To further investigate the effect of high fat diet and specific PKC Î² inactivation on STZ-induced atherosclerosis using the PKC Î² inhibitor, ruboxistaurin (RBX, or LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression. The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings. ApoE-/- mice were used as a rodent atherosclerosis model. Isolated total RNA from aortas of each ApoE-/- mouse fed with high fat diet for 10 weeks after STZ-induced diabetes or control groups were used for preparation and hybridization on Affymetrix microarrays. There were total 4 different mice groups, which were fed with high fat diet with or without RBX. Each group had four individual mouse (N=4).

2016-03-26 | E-GEOD-79623 | biostudies-arrayexpress

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

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

2016-06-29 | GSE79008 | GEO

Comparison of low-fat and high-fat diet on gene expression in muscle, liver and adipose tissue from mice of two genetic backgrounds

Project description:Diet-induced obesity is the primary determinant of the current epidemic of diabetes. We have explored the role of genetics in this phenomenon, using C57Bl/6 (B6) and 129S6/SvEvTac (129) mice on a low- or high-fat diet. Microarray analysis indicated significant changes in expression levels between B6 and 129 mice in the chromosomal area of Wnt5a and protein kinase C delta (PKC-delta). Thus, caloric efficiency, i.e., the “thrifty gene,” is a dominant-acting genetic determinant of diet-induced obesity in mice and can be linked to a locus on chromosome 14, including genes linked to adipose development and insulin sensitivity.

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Transforming growth factor beta-like stimulated clone 22 D4 promotes diabetic hyperglycemia and insulin resistance [abdominal fat]

Project description:Obesity-related insulin resistance represents the core component of the so-called Metabolic Syndrome, ultimately promoting glucose intolerance, pancreatic beta cell failure, and overt type 2 diabetes 1 2. Based on substantial side effects of existing pharmacological approaches, efficient and safe insulin sensitization and glucose control remain critical therapeutic aims to prevent diabetic late complications 3. Here, we identify Transforming Growth Factor beta-like Stimulated Clone (TSC) 22 D4 as a critical molecular determinant of insulin signaling and glucose handling. Hepatocyte-specific inactivation of TSC22D4 enhanced insulin signaling in liver and skeletal muscle, while hepatic TSC22D4 overexpression blunted insulin tissue responses. Consequently, hepatic TSC22D4 inhibition both prevented and reversed hyperglycemia, glucose intolerance, and insulin resistance in various diabetes mouse models, respectively. TSC22D4 was found to exert its effects on systemic glucose homeostasis - in large parts - through the transcriptional regulation of the small secretory protein lipocalin (LCN) 13 as demonstrated by chromatin recruitment and genetic rescue experiments in vivo. As hepatic TSC22D4 levels were found to be elevated in human diabetic patients, correlating with decreased insulin sensitivity and hyperglycemia, our results establish the inhibition of TSC22D4 as an attractive insulin sensitizing option in diabetes therapy. 28 BKS.Cg-Dock7m +/+ Leprdb/J (000642) mice (12 week old ) were divided to 4 forms of treatment (n=7 per treatment group) consisting of 4 different shRNA adenoviruses (reference sample: control shRNA), LCN13 (LCN13 shRNA), TSC22D4 (TSC22D4 shRNA), TSC22D4 plus LCN13 (TSC22D4+LCN13 shRNA). 1 week after shRNA injection animals were sacrificed, liver, abdominal fat tissue, gastrocnemius tissue was immediately snap frozen. 3 representative animals of each treatment group were selected for microarray analysis (abdominal fat tissue).

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Rat Liver HFD vs Chow, HFD vs PKCepsilon ASO

Project description:Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C epsilon (PKCÎµ), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCÎµ protects against high fat diet-induced hepatic insulin resistance. Here we employ a systems level approach to uncover additional signaling pathways involved in high fat diet-induced hepatic insulin resistance. We used quantitative phosphoproteomics to map global in vivo changes in hepatic protein phosphorylation in chow-fed, high fat-fed, and high fat-fed with PKCÎµ knockdown rats to distinguish the impact of lipid- and PKCÎµ-induced protein phosphorylation.

2018-08-30 | PXD010209 | Pride

Single-Cell Transcriptional Profiling of Mouse Islets Following Short-Term ObesogenicDietary Intervention

Project description:Obesity is closely associated with adipose tissue inflammation and insulin resistance. Dysglycemia and type 2 diabetes results when islet β cells fail to maintain appropriate insulin secretion in the face of insulin resistance. To clarify the early transcriptional events leading to β-cell failure in the setting of obesity, we fed male C57BL/6J mice an obesogenic, high fat diet (60% kcal from fat) or control diet (10% kcal from fat) for one week and islets from these mice (from 4 high fat- and 3 control-fed mice) were subjected to single cell RNA sequencing analysis. Islet endocrine cell types (α cells, β cells, δ cells, PP cells) and other resident cell types (macrophages, T cells) were annotated by transcript profiles and visualized using Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) plots. UMAP analysis revealed distinct cell sub-populations (11 for β cells, 5 for α cells, 3 for δ cells, PP cells, ductal cells, endothelial cells), emphasizing the heterogeneity of cell populations in the islet. We identified that distinct β cell populations downregulate genes associated with the endoplasmic reticulum stress response and upregulate genes associated with insulin secretion, while others upregulate genes that impair insulin secretion, cellular proliferation, and survival. Moreover, all β cell populations negatively regulate genes associated with immune response activation. Our data indicate that an early transcriptional response in islets to an obesogenic diet reflects an attempt by distinct populations of β cells to augment or impair cellular function, possible harbingers of ensuing insulin resistance.

2020-12-03 | GSE162512 | GEO

Transcriptomic profiling of diabetic rats treated with peripherical focused ultrasound (pFUS)

Project description:To better characterize the systemic response of diabetic rats to daily hepatoportal pFUS stimulation, we conducted transcriptomic profiling of different metabolic tissues by RNAseq. For this purpose, we included samples from liver, intestines, kidney, adipose, muscle, pancreas, hypothalamus and blood in the Zucker diabetic fatty (ZDF) and diet induced obese (DIO) rodent models. ZDF rats spontaneously develop type 2 diabetes (T2D) as a result of a missense mutation (fatty, fa) in the leptin receptor gene and develop moderate hyperglycemia spontaneously as a result of the insulin resistance and pancreatic insufficiency. DIO model uses a high fat/high carbohydrate diet to induce obesity and insulin resistance. Following development of obesity low dose streptozotocin (STZ) is used to induce a moderate level of pancreatic beta cell death which impairs insulin secretion similar to that seen in later stage T2D. Tissue samples were processed and analyzed after 3 days, 4 weeks, and 7 weeks of 3 minute per day pFUS treatments. All procedures performed were done in accordance with the National Institutes of Health (NIH) Guidelines under protocols approved by the Institutional Animal Care and Use Committee (IACUC) of GE Global Research.

2022-03-31 | GSE197097 | GEO

Effect of myostatin inhibition on skeletal muscle gene expression in high fat diet-fed mice

Project description:Myostatin (GDF8) is a member of the TGF-beta family of proteins which is predominantly expressed in skeletal muscle and acts as a negative regulator of muscle mass. Inhibition of myostatin leads to muscle hypertrophy and has been shown to mitigate insulin resistance in mouse models of type 2 diabetes, although the mechanisms underlying this effect are unclear. We found that myostatin inhibition by AAV-mediated overexpression of the myostatin propeptide improves skeletal muscle insulin sensitivity in mice made insulin-resistant by high fat diet feeding. To gain insight into potential gene expression changes responsible for this effect, we performed microarray analysis on skeletal muscle samples from high fat diet-fed mice with and without myostatin inhibition.

2020-05-29 | GSE130622 | GEO

Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers Elovl2 as a novel regulator of glucose-induced insulin secretion

Project description:Defective insulin secretion by pancreatic β cells underlies the development of type 2 diabetes (T2D). High fat diet-fed mice are commonly used to study diabetes progression, but studies are usually limited to a single strain, such as C57Bl/6J. Here, we use a systems biology approach to integrate large phenotypic and islet transcriptomic data sets from six commonly used strains fed a high fat or regular chow diet to identify genes associated with glucose intolerance and insulin secretion. One of these genes is Elovl2, encoding very long chain fatty acid elongase 2. ELOVL2 is responsible for the synthesis of the polyunsaturated fatty acid, docosahexaenoic acid (DHA). We show that DHA rescues glucose-induced insulin secretion and cytosolic Ca2+ influx impaired by glucolipotoxicity, and that Elovl2 over-expression is able to restore the insulin secretion defect under these conditions. We propose that increased endogenous DHA levels resulting from Elovl2 up-regulation counteracts the insulin secretion defect associated with glucolipotoxicity. Although we focus our experimental validation on Elovl2, the comprehensive data set and integrative network model we used to identify this candidate gene represents an important novel resource to dissect the molecular aetiology of β cell failure in murine models.

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