GEO accession GSE213919 is currently private and is scheduled to be released on Dec 31, 2025.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA883182 | ENA |
REPOSITORIES: ENA
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Project description:Genome-wide association studies (GWAS) have so far identified a large number of genetic loci associated with metabolic diseases. SEC16B, an endoplasmic reticulum (ER) export factor, has emerged as a strong candidate associated with obesity in multiple GWAS yet its physiological function on metabolism has not been characterized. Here, by using global Sec16b knockout mice, we show that loss of Sec16b gene causes glucose intolerance without an effect on body weight. At the cellular level, Sec16b loss damages the morphology of the ER and mitochondria in pancreatic β cells. Mechanistically, Sec16b loss impairs insulin secretion via blocking intracellular Ca2+ influx via down-regulating cholinergic synapse signaling in β cells. Moreover, dSec16 loss disrupts glucose homeostasis in Drosophila melanogaster, highlighting a core and evolutionarily conserved role of dSec16 in glucose homeostasis. Taken together, our study has for the first time established SEC16B as a conserved key regulator of metabolic heath across phyla.
2025-12-31 | GSE213919 | GEO
Project description:Illuminating the mechanisms controlling glucose homeostasis may deepen our understanding of the pathogenesis of T2DM and provide new therapeutic strategies for T2DM in future. As reported, Dyrk1b is a pleiotropic protein and its genetic mutations associate with blood glucose levels. Yet, the role of Dyrk1b in glucose metabolism is not well understood. Herein, we find that hepatic Dyrk1b overexpression in mice impairs the glucose tolerance and insulin resistance, whereas global Dyrk1b deficiency improves glucose metabolism of mcie. Dyrk1b overexpression in vitro blunts insulin signalling and glucose uptake. Collectively, our study uncovers a novel link between hepatic Dyrk1b and whole body glucose homeostasis.
2025-05-29 | GSE234405 | GEO
Project description:Illuminating the mechanisms controlling glucose homeostasis may deepen our understanding of the pathogenesis of T2DM and provide new therapeutic strategies for T2DM in future. As reported, Dyrk1b is a pleiotropic protein and its genetic mutations associate with blood glucose levels. Yet, its role in glucose metabolism remains to be established. Herein, we invetigate the role of Dyrk1b in glucose metabolism and the underlying mechanisms. We find that hepatic Dyrk1b overexpression in mice impairs the glucose tolerance and insulin resistance, whereas global Dyrk1b deficiency improves glucose metabolism of mcie. Dyrk1b overexpression in vitro blunts insulin signalling and glucose uptake. Quantitative proteomic analyses further reveal that Wbp2 is a putative target of Dyrk1b. Importantly, hepatic Wbp2 restoration rescues the glucose homeostasis in Dyrk1b overexpression mice. Additionally, ATAC-seq analyses indicate Dyrk1b’s role in remodelling hepatic chromatin landscape. Collectively, our study uncovers a novel link between hepatic Dyrk1b and whole body glucose homeostasis via modulation of hepatic Wbp2 expression.
2025-05-29 | GSE234275 | GEO
Project description:Elucidation of the mechanisms controlling glucose homeostasis may deepen our understanding of the pathogenesis of T2DM and provide new therapeutic strategies for T2DM in the future. As reported, Dyrk1b is a pleiotropic protein and its genetic mutations are associated with blood glucose levels. However, the role of Dyrk1b in glucose metabolism is not well understood. Herein, we find that hepatic Dyrk1b overexpression in mice impairs the glucose tolerance and insulin resistance, whereas global Dyrk1b deficiency improves glucose metabolism of mcie. Dyrk1b overexpression in vitro blunts insulin signalling and glucose uptake. Collectively, our study uncovers a novel link between hepatic Dyrk1b and whole body glucose homeostasis.
2025-08-01 | GSE237672 | GEO
Project description:Exercise training improves whole body glucose homeostasis through effects largely attributed to adaptations in skeletal muscle; however, training also affects other tissues including adipose tissue. To determine if exercise-induced adaptations to adipose tissue contribute to training-induced improvements in glucose homeostasis, subcutaneous white adipose tissue (scWAT) from trained or sedentary donor mice was transplanted into the visceral cavity of sedentary recipients. Remarkably, nine days post-transplantation, mice receiving trained scWAT had improved glucose tolerance and enhanced insulin sensitivity compared to mice transplanted with sedentary scWAT or sham-treated mice. Mice transplanted with trained scWAT had increased insulin-stimulated glucose uptake in tibialis anterior and soleus muscles and brown adipose tissue, suggesting that the transplanted scWAT exerted endocrine effects. Furthermore, the deleterious effects of high-fat feeding on glucose tolerance and insulin sensitivity were completely reversed if high-fat fed recipient mice were transplanted with trained scWAT. In additional experiments, voluntary exercise training by wheel running for only 11 days resulted in profound changes in scWAT including increased expression of ∼1550 genes involved in numerous cellular functions, including metabolism. Exercise training causes adaptations to scWAT that elicit metabolic improvements in other tissues, demonstrating a previously unrecognized role for adipose tissue in the beneficial effects of exercise on systemic glucose homeostasis. Microarray analysis of scWAT obtained from a cohort of mice that were housed in wheel cages for 11 days compared to sedentary control mice.
2015-04-22 | E-GEOD-68161 | biostudies-arrayexpress
Project description:GRAMD1B is a novel regulator of lipid homeostasis, autophagic flux, and phosphorylated tau.
| PRJNA1168106 | ENA
Project description:Adjudin improves beta cell maturation, hepatic glucose uptake and glucose homeostasis
| PRJNA985789 | ENA
Project description:Hepatic Dyrk1b regulates whole body glucose homeostasis
| PRJNA981190 | ENA
Project description:THE SSBP3 CO-REGULATOR IS REQUIRED FOR GLUCOSE HOMEOSTASIS, PANCREATIC ISLET ARCHITECTURE, AND BETA-CELL IDENTITY
| PRJNA973693 | ENA
Project description:Objective: Transcriptional complex activity drives the development and function of pancreatic islet cells to allow for proper glucose regulation. Our prior work highlighted that the LIM-homeodomain transcription factor (TF), Islet-1 (Isl1), and its interacting co-regulator, Ldb1, are vital effectors of developing and adult β-cells. We further found that a member of the Single Stranded DNA-Binding Protein (SSBP) co-regulator family, SSBP3, interacts with Isl1 and Ldb1 in β-cells and primary islets (mouse and human) to impact β-cell target genes MafA and Glp1R. Members of the SSBP family stabilize TF complexes by binding directly to Ldb1 and protecting the complex from ubiquitin-mediated turnover. In this study, we hypothesized that SSBP3 would have critical roles in pancreatic islet cell development and function in vivo, similar to the Isl1::Ldb1 complex. Methods: We first generated a novel SSBP3 LoxP allele mouse line, where Cre-mediated recombination imparts a predicted early protein termination. We bred this mouse to constitutive Cre lines (Pdx1- and Pax6-driven) to recombine of SSBP3 in the developing pancreas and islet (SSBP3DeltaPanc and SSBP3DeltaIslet), respectively. We assessed glucose tolerance and used immunofluorescence to detect changes in islet cell abundance and markers of β-cell identity and function. Using an inducible Cre system we also deleted SSBP3 in the adult β-cell, a model termed SSBP3Deltaβ-cell. We measured glucose tolerance as well as glucose-stimulated insulin secretion (GSIS), both in vivo and in isolated islets in vitro. Using islets from control and SSBP3Deltaβ-cell we conducted RNA-Seq and compared our results to published datasets for similar β-cell specific Ldb1 and Isl1 knockouts to identify commonly regulated target genes. Results: SSBP3DeltaPanc and SSBP3DeltaIslet neonates present with hyperglycemia. SSBP3DeltaIslet mice are glucose intolerant by P21 and exhibit a reduction of β-cell maturity markers MafA, Pdx1, and UCN3. We observe disruptions in islet cell architecture with an increase in glucagon+ α-cells and ghrelin+ ε-cells at P10. Inducible loss of β-cell SSBP3 in SSBP3Deltaβ-cell causes hyperglycemia, glucose intolerance, and reduced GSIS. Transcriptomic analysis of 14-week SSBP3Deltaβ-cell islets revealed a decrease in β-cell function gene expression (Ins, MafA, Ucn3), increased stress and dedifferentiation markers (Neurogenin-3, Aldh1a3, Gastrin), and shared differentially expressed genes between SSBP3, Ldb1, and Isl1 in adult β-cells. Conclusions: SSBP3 drives proper islet development and identity, where its loss causes altered islet-cell abundance and glucose regulatory function. β-cell SSBP3 is required for GSIS and glucose homeostasis, at least partially through shared regulation of Ldb1 and Isl1 target genes.
2023-08-16 | GSE232750 | GEO