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Comprehensive Proteomic Analysis of db/db Mice by LC-MSMS

ABSTRACT: This study focuses on the comprehensive analysis of the proteome in db/db mice, a model of type 2 diabetes mellitus (T2DM), using liquid chromatography coupled with mass spectrometry (LC-MSMS). The aim is to identify and quantify proteins present in tissues and fluids of db/db mice, providing insights into the pathophysiology of T2DM, related complications, and potential therapeutic targets. The data generated will contribute to a better understanding of the molecular mechanisms underlying diabetes and its complications, and may aid in the development of new diagnostic tools and treatment strategies for diabetes management.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: ji jiwoli

LAB HEAD: wanqing dong

PROVIDER: PXD062435 | Pride | 2025-05-20

REPOSITORIES: Pride

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			Action	DRS
	Dulaglutide1.raw	Raw
	Dulaglutide2.raw	Raw
	Dulaglutide3.raw	Raw
	Mazdutide1.raw	Raw
	Mazdutide2.raw	Raw

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Sex-specific epigenetics drive low GPER expression in gastrointestinal smooth muscles in Type 2 diabetic mice

Project description:Type 2 diabetes mellitus (T2DM) causes gastroparesis, delayed intestinal transit, and constipation, for unknown reasons. Complications are predominant in men and postmenopausal women, suggesting a female hormone-mediated mechanism. Low G-protein coupled estrogen receptor (GPER) expression from epigenetic modifications may explain it. We explored sexually differentiated GPER expression and gastrointestinal symptoms related to GPER alterations in wild-type (WT) and T2DM mice (db/db). GPER mRNA and protein expression, DNA methylation and histone modifications were measured from stomach and colon samples of db/db and WT mice. We found that WT female tissues have the highest GPER mRNA and protein expressions. The expression is lowest in all db/db. The lowest mRNA levels are in the male stomach and female colon. GPER downregulation is associated with promoter hypermethylation and reduced enrichment of H3K4me3 and H3K27ac marks around the GPER promoter. T2DM impairs gut GPER expression, and epigenetic sex-specific mechanisms matter in the downregulation.

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Profiling pancreatic islets from obese db/db and lean control db/+ mice

Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

2013-03-22 | E-GEOD-31953 | biostudies-arrayexpress

Profiling epididymal white adipose tissue (eWAT) from obese db/db and lean control db/+ mice

Project description:This program addresses the gene signature associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in adipose tissue of the db/db mice compared to the control db/+ mice? The db/db mice eWAT profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the eWAT of db/db mice compared to the corresponding db/+ controls.

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Topical estrogen application promotes cutaneous wound healing in db/db female mice with type 2 diabetes

Project description:Female sex hormones are beneficial effects for wound healing. However, till date, whether topical estrogen application can promote cutaneous wound healing in diabetes remains unclear. Therefore, the present study aimed to validate the effect of topical estrogen application on cutaneous wound healing in a type 2 diabetes db/db mice model. In total, 22 db/db female mice with type 2 diabetes and eight C57BL/6J female mice were subjected to two full-thickness wound injuries. The mice were divided into the db/db, db/db + estrogen, db/db + vehicle, and wild type (WT) groups. Wound healing was assessed until day 14. The db/db group had a significantly high wound area ratio (wound area/initial wound area) on days 3–14 and a significantly low re-epithelialization ratio on days 7 and 14. Moreover, their angiogenesis ratio was significantly low on day 7 and high on day 14. In contrast, compared with the db/db group, the db/db + estrogen group had a significantly lower wound area ratio on days 1–14 and angiogenesis ratio on day 14, thereby indicating early withdrawal of new blood vessels, as well as a significantly higher re-epithelialization ratio on days 7 and 14 and Ym1+ M2 macrophage/macrophage ratio on day 7. Moreover, microarray analysis showed that the top 10 upregulated or downregulated genes in the db/db group were reversed by estrogen treatment, particularly on day 14, in comparison with the WT group. Thus, topical estrogen application reduced the wound area, promoted re-epithelialization and angiogenesis, and increased the number of M2 macrophages in mice with type 2 diabetes. Furthermore, it improved the differential regulation of genes in db/db mice. Therefore, such treatment can enhance cutaneous wound healing in female mice with type 2 diabetes.

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Expression data from livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db)

Project description:In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS. To better understand the mechanisms contributing to metabolic dysfunction in obesity-induced diabetes, we used microarrays to comprehensively profile gene expression livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db) DBA/2J females were mated to C57BL/6 males carrying leptin receptor deficiency (db/+) and, F1 (db/+) offspring were interbred to produce F2 mice. Offspring deficient in leptin receptor (db/db) were fed on a chow diet until 5 weeks or 12 weeks of age and then euthanized for collection of liver tissue for RNA profiling along with other diabetes-related phenotypes.

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Project description:Eight-week-old C57BL/6J and T2DM db/db mice randomly divided into 4 groups of 8 based on equal bodyweight and fasting blood glucose (FBG) levels (mice were fasted for 6 h). The C57BL/6J mice (normal group) were treated with saline. The T2DM db/db mice were treated with saline, DLE (200 mg/kg), WTE (180 mg/kg), or pioglitazone (PGZ, 20 mg/kg) for 12 weeks, and were called the model group, DLE group, WTE group and PGZ group, respectively. All mice received oral administration of the indicated treatments once a day. After 12 weeks drug administration, liver aliquots from four randomly selected mice from the normal, model, PGZ and DLE groups were ground into powder in liquid nitrogen, followed by RNAseq for differentially expressed gene determination and pathway enrichment analysis.

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