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A simple strategy effectively improves glucose homeostasis and prevents loss of islet beta cells in diabetic mice

ABSTRACT: Single cell sequencing revealed that the composition of islets cells were changed significantly in db/db mice, indicating diet intervention can shape islets cells and restore the function of endocrine cells in pancreases islets.

ORGANISM(S): Mus musculus

PROVIDER: GSE165267 | GEO | 2022/06/15

REPOSITORIES: GEO

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Paired box 6 gene delivery preserves beta cells and improves islet transplantation efficacy

Project description:Loss of pancreatic beta cells is the central feature of all forms of diabetes. Current therapies fail to halt the declined beta cell mass. Thus, strategies to preserve beta cells are imperatively needed. In this study, we identified paired box 6 (PAX6) as a critical regulator of beta cell survival. Under diabetic conditions, the human beta cell line EndoC-bH1, db/db mouse and human islets displayed dampened insulin and incretin signalings and reduced beta cell survival, which were alleviated by PAX6 overexpression. Adeno-associated virus (AAV)-mediated PAX6 overexpression in beta cells of streptozotocin-induced diabetic mice and db/db mice led to a sustained maintenance of glucose homeostasis. AAV-PAX6 transduction in human islets reduced islet graft loss and improved glycemic control after transplantation into immunodeficient diabetic mice. Our study highlights a previously unappreciated role for PAX6 in beta cell survival and raises the possibility that ex vivo PAX6 gene transfer into islets prior to transplantation might enhance islet graft function and transplantation outcome.

2023-10-13 | GSE242338 | GEO

A simple strategy effectively improves glucose homeostasis and prevents loss of islet beta cells in diabetic mice

Project description:A simple strategy effectively improves glucose homeostasis and prevents loss of islet beta cells in diabetic mice

| PRJNA693846 | ENA

Study of the tRNA-derived fragment expression profile in mouse pancreatic islets of pre-diabetic obese db/db mice

Project description:In this study, we discovered cytosolic and mitochondrial fragments resulting from tRNA and mt-tRNA cleavage, which may act as new regulators of cellular and metabolic functions. We analyzed hundreds of these fragments in the pancreatic islets of db/db mice and compared them to heterozygous control db/+ mice. At 16 weeks of age, db/db mice exhibit obesity, insulin resistance, and glucose intolerance. In our analysis, we identified 3858 tRFs in the islets of db/db mice, among which 342 exhibited significant changes (≥ 2 fold; adjusted p value ≤ 0.05) compared to controls. Of these, 199 tRFs showed increased levels, while 170 tRFs showed decreased levels in the pre-diabetic mice. Notably, a striking majority (147 out of 170) of the tRFs with reduced abundance in the islets of db/db mice were derived from the cleavage of tRNAs encoded by the mitochondrial genome. Our findings reveal a significant reshaping of mitochondrial tRFs in pre-diabetic conditions, coinciding with a well-established mitochondrial metabolic defect under these conditions. Specifically, we demonstrated that a fragment (named mt-tRF-LeuTAA) resulting from the cleavage of mt-tRNA-LeuTAA, encoded by the mitochondrial genome and found to be reduced in the islets of db/db mice, acts as a key regulator of mitochondrial OXPHOS functions, mitochondrial membrane potential, the insulin secretory capacity of ß-cells, and the insulin sensitivity of myotube muscle cells.

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Transcription profiling of islet of Langerhans from diabetic and non-diabetic patients

Project description:Diabetic islets

2009-06-30 | E-MEXP-1878 | biostudies-arrayexpress

Next-generation sequencing facilitates quantitative analysis of wild type and diabetic db/db mice islets transcriptomes

Project description:Long non-coding RNAs (LncRNAs) constitute an extensive fraction of the mammalian transcriptome. In this study, lncRNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. More than 1600 lncRNAs were detected using RNA sequencing, indicating that lncRNAs were abundant in islets. Among them, we found that lncRNA-Malat1 was significantly reduced in diabetic mouse islets. Further experiments suggested an involvement of lncRNA-Malat1 in lipotoxicity-induced β-cell dysfunction.

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CHIP-seq KAT2B in mouse isolated islet

Project description:The Endoplasmic Reticulum (ER) unfolded protein response (UPRer) pathway plays an important role for pancreatic β cells to adapt their cellular responses to environmental cues and metabolic stress. Although altered UPRer gene expression appears in rodent and human type 2 diabetic (T2D) islets, the underlying molecular mechanisms remain unknown. We show here that germ-line and β-cell specific disruption of the lysine acetyltransferase 2B (Kat2b) gene in mice leads to impaired insulin secretion and glucose intolerance. Genome wide analysis of Kat2b-regulated genes and functional assays revealed a critical role for KAT2B in maintaining UPRer gene expression and subsequent β-cell function. Importantly, Kat2b expression was decreased in db/db and in human T2D islets and correlated with UPRer genes in normal human islets. In conclusion, KAT2B is a crucial transcriptional regulator for adaptive β-cell function during metabolic stress by controlling UPRer and represents a promising target for T2D prevention and treatment

2016-05-03 | GSE78860 | GEO

Expression analysis in pancreatic and liver tissues of diabetic db/db mice in response to dietary supplementation with selenate

Project description:Investigation of gene expression level changes in pancreatic and liver tissues of diabetic db/db mice supplemented with selenate, compared to the diabetic db/db mice administered placebo. Fasting blood glucose levels increased continuously in diabetic db/db mice administered placebo (DMCtrl) but decreased gradually in selenate-supplemented diabetic db/db mice (DMSe) and approached normal values when the experiment ended. The size of pancreatic islets increased, causing the plasma insulin concentration to double in DMSe mice compared with that in DMCtrl mice.

2014-03-07 | GSE55636 | GEO

Expression analysis in pancreatic and liver tissues of diabetic db/db mice in response to dietary supplementation with selenate

2014-03-07 | E-GEOD-55636 | biostudies-arrayexpress

β-cell Jagged1 is sufficient but not necessary for islet Notch activity and insulin secretory defects.

Project description:Objective Notch signaling is re-activated in β cells from obese mice, and is causal to β cell dysfunction. Notch activity is determined in part by expression of transmembrane ligand availability in a neighboring cell. We hypothesized that β cell expression of Jagged1 determines the maladaptive Notch response and resultant β cell dysfunction in obese mice. Methods We assessed expression of Notch pathway components in diet-induced obese (DIO) or leptin receptor-deficient (db/db) mice, and performed single cell RNA sequencing (scRNAseq) in islets from patients with and without type 2 diabetes (T2D). We generated and performed glucose tolerance testing in inducible, β cell-specific Jagged1 gain-of- and loss-of-function mice. We also tested effects of monoclonal neutralizing antibodies to Jagged1 in glucose-stimulated insulin secretion (GSIS) assays in isolated islets. Results Jag1 was the only Notch ligand that tracked with increased Notch activity in DIO and db/db mice. Consistently, JAG1 tracked with Notch activity in metabolically inflexible β cells enriched in patients with T2D. Neutralizing antibodies to block Jagged1 in islets isolated from DIO and db/db mice potentiated GSIS ex vivo. To demonstrate if β cell Jagged1 is sufficient to cause glucose tolerance in vivo, we generated inducible β cell-specific Jag1 transgenic mice (β-Jag1TG), which showed impaired glucose intolerance due to reduced GSIS. However, β cell-specific Jagged1 loss-of-function (β-Jag1KO) did not protect against HFD-induced insulin secretory defects or glucose intolerance. Conclusions Jagged1 is increased in islets from obese mice and in patients with T2D, and neutralizing Jagged1 antibodies lead to improved GSIS, suggesting that inhibition of Jagged1-Notch signaling may have therapeutic benefit. However, genetic loss-of-function experiments suggest that β cells are not a likely source of the Jagged1 signal.

2024-02-23 | GSE249170 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Diabetic db/db Mice Islets Transcriptomes

Project description:Circular RNAs constitute an extensive fraction of the mammalian transcriptome.In this study, circular RNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. More than 5000 circRNAs were detected using RNA sequencing, indicating that circular transcripts were abundant in islets. Among them, we found that circ-Tulp4 showed significant downregulation in diabetic mouse islet cells. Further experiments indicated that modulating the expression of circ-Tulp4 in β cell lines desensitized β-cells to lipotoxicity.

2020-10-28 | GSE138096 | GEO

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