A5072350896- Pancreatic function and diabetes
- Diabetes and associated disorders
- Adipose Tissue and Metabolism
- Metabolism, Diabetes, and Cancer
- Receptor Mechanisms and Signaling
- Ion channel regulation and function
- Cellular transport and secretion
- Adenosine and Purinergic Signaling
- Epigenetics and DNA Methylation
- Diabetes Treatment and Management
- Ion Transport and Channel Regulation
- Cannabis and Cannabinoid Research
- Pancreatic and Hepatic Oncology Research
- Endoplasmic Reticulum Stress and Disease
- Calcium signaling and nucleotide metabolism
- Ovarian function and disorders
- Ginseng Biological Effects and Applications
- RNA Interference and Gene Delivery
- Immune Cell Function and Interaction
- Erythrocyte Function and Pathophysiology
- Retinoids in leukemia and cellular processes
- Genetics and Neurodevelopmental Disorders
- MicroRNA in disease regulation
- Cancer, Lipids, and Metabolism
- SARS-CoV-2 and COVID-19 Research
Changchun University of Chinese Medicine
2025
Lund University
2013-2024
Northeastern University
2024
Type 2 diabetes (T2D) develops after years of prediabetes during which high glucose (glucotoxicity) impairs insulin secretion. We report that the ATP-conducting mitochondrial outer membrane voltage-dependent anion channel-1 (VDAC1) is upregulated in islets from T2D and non-diabetic organ donors under glucotoxic conditions. This caused by a glucotoxicity-induced transcriptional program, triggered with suboptimal blood control. Metformin counteracts VDAC1 induction. overexpression causes its...
Glucose-induced insulin secretion depends on β-cell electrical activity. Inhibition of ATP-regulated potassium (KATP) channels is a key event in this process. However, KATP channel closure alone not sufficient to induce activity; activation depolarizing membrane current also required. Here we examine the role mechanosensor ion PIEZO1 Yoda1, specific agonist, activates small and thereby triggers activity with resultant stimulation Ca2+-influx secretion. Conversely, antagonist GsMTx4 reduces...
Type 2 diabetes (T2D) is caused by insufficient insulin secretion from pancreatic β cells. To identify candidate genes contributing to T2D pathophysiology, we studied human islets approximately 300 individuals. We found 395 differentially expressed (DEGs) in individuals with T2D, including, our knowledge, novel (OPRD1, PAX5, TET1) and previously identified (CHL1, GLRA1, IAPP) candidates. A third of the expression changes may predispose diabetes, as these associated HbA1c not diagnosed T2D....
Abstract The hepatokine follistatin is elevated in patients with type 2 diabetes (T2D) and promotes hyperglycemia mice. Here we explore the relationship of plasma levels incident T2D mechanisms involved. Adjusted hazard ratio (HR) per standard deviation (SD) increase for 1.24 (CI: 1.04–1.47, p < 0.05) during 19-year follow-up ( n = 4060, Sweden); 1.31 1.09–1.58, 0.01) 4-year 883, Finland). High circulating associates adipose tissue insulin resistance non-alcoholic fatty liver disease 210,...
The relationship of ozone (O3), particularly the long-term exposure, with impacting metabolic homeostasis in population was understudied and under-recognised. Here, we used data from ChinaHEART, a nationwide, population-based cohort study, combined O3 PM2.5 concentration high spatiotemporal resolution, to explore independent association exposure prevalence insulin resistance (IR). Among 271 540 participants included, crude IR 39.1%, while age sex standardized stood at 33.0%. Higher observed...
The amplification of glucose-stimulated insulin secretion (GSIS) through incretin signaling is critical for maintaining physiological glucose levels. Incretins, like glucagon-like peptide 1 (GLP1), are a target type 2 diabetes drugs aiming to enhance secretion.Here we show that the protein phosphatase inhibitor 1A (PPP1R1A), expressed in β-cells and its expression reduced dysfunctional lacking MafA upon acute knock down. central regulator GSIS β-cell function. We observed strong correlation...
Increased PDGFRA signaling is an essential pathogenic factor in many subtypes of gliomas. In this context the cell surface expression important determinant ligand sensing glioma microenvironment. However, regulation spatial distribution cells remains poorly characterized. Here, we report that gliomas negatively regulated by ERK-dependent mechanism, resulting reduced proliferation cells. Glioma tumor tissues and their corresponding lines were isolated from 14 patients analyzed single-cell...
Highlights•MAFA controls autonomic-nervous-system-mediated insulin secretion•MAFA activates nicotinic receptor expression in mouse and human β cells•Nicotinic signaling is required for acetylcholine-mediated secretion•Polymorphisms genes affect islet diabetesSummaryMonoamine acetylcholine neurotransmitters from the autonomic nervous system (ANS) regulate secretion pancreatic islets. The molecular mechanisms controlling neurotransmitter cells their impact on diabetes development are only...
Reduced expression of exocytotic genes is associated with functional defects in insulin exocytosis contributing to impaired secretion and type 2 diabetes (T2D) development. MAFA MAFB transcription factors regulate β-cell physiology, their gene reduced T2D β cells. We investigate if loss human cells contributes progression by regulating required for exocytosis.Three approaches were performed: (1) RNAseq analysis the focus on exocytosis-related MafA-/- mouse islets, (2) correlational between...
Objective To investigate the impact of “Xinshuixiao” drug-containing serum on dDAVP-induced AQP2 expression in IMCD3 cells and to preliminarily explore its underlying mechanisms. Methods Rats were orally administered with “Xinshuixiao granules” containing medicinal compounds. The CCK-8 assay was employed determine appropriate drug concentration effect cell viability. Additionally, we assessed influence activity following dDAVP intervention. Cells divided into blank, model, low, medium,...
Abstract Voltage-gated Ca 2+ (Ca V ) channels trigger glucose-induced insulin secretion in pancreatic beta-cell and their dysfunction increases diabetes risk. These heteromeric complexes include the main subunit alpha1, accessory ones, including gamma that remains unexplored. Here, we demonstrate 4 γ4) is downregulated islets from human donors with diabetes, diabetic Goto-Kakizaki (GK) rats, as well under conditions of gluco-/lipotoxic stress. Reduction γ4 expression results decreased L-type...
Inappropriate surface expression of voltage-gated Ca2+channels (CaV) in pancreatic ß-cells may contribute to the development type 2 diabetes. First, failure increase intracellular Ca2+ concentrations at sites exocytosis impedes insulin release. Furthermore, excessive influx trigger cytotoxic effects. The regulation CaV channels β-cells remains unknown. Here, we used real-time 3D confocal and TIRFM imaging, immunocytochemistry, cellular fractionation, immunoprecipitation electrophysiology...
MicroRNAs (miRNAs) regulate β-cell function, and mitochondria insulin secretion are perturbed in diabetes. We aimed to identify key miRNAs regulating mitochondrial metabolism novel miRNA-mitochondrial pathways.
There is emerging evidence of an association between epigenetic modifications, glycemic control and atherosclerosis risk. In this study, we mapped genome-wide changes in patients with type 2 diabetes (T2D) advanced atherosclerotic disease. We performed chromatin immunoprecipitation sequencing (ChIP-seq) using a histone 3 lysine 9 acetylation (H3K9ac) mark peripheral blood mononuclear cells from T2D (n = 8) or without (ND, n 10). epigenome identified 23,394 13,133 peaks ND individuals,...
Type 1 (T1D) and type 2 (T2D) diabetes are triggered by a combination of environmental and/or genetic factors. Maf transcription factors regulate pancreatic beta (β)-cell function, have also been implicated in the regulation immunomodulatory cytokines like interferon-β (IFNβ1). In this study, we assessed MAFA MAFB co-expression with pro-inflammatory cytokine signaling genes RNA-seq data from human islets. Interestingly, expression was strongly negatively correlated cytokine-induced (such as...
Impaired fasting glucose (IFG) and impaired tolerance (IGT) are high-risk factors of diabetes development may be caused by defective insulin secretion in pancreatic beta-cells. Glucose-stimulated is mediated voltage-gated Ca2+ (CaV) channels which the gamma-4 subunit (CaVγ4) required for beta-cell to maintain its differentiated state. We here aim explore involvement CaVγ4 controlling homeostasis employing CaVγ4−/− mice study vivo glucose-metabolism-related phenotypes glucose-stimulated...
Voltage-gated Ca2+ (CaV) channel dysfunction leads to impaired glucose-stimulated insulin secretion in pancreatic β-cells and contributes the development of type-2 diabetes (T2D). The role low-voltage gated T-type CaV channels remains obscure. Here we have measured global expression CaV3.2 human islets found that gene CACNA1H, encoding CaV3.2, is negatively correlated with HbA1c donors, positively islet as well capacity isolated islets. Silencing or pharmacological blockade attenuates...
Nuclear receptor interacting protein 1 (NRIP1) is an important energy regulator, but few studies have addressed its role in humans. This study investigated adipose tissue and skeletal muscle NRIP1 gene expression serum levels response to weight loss exercise humans.NRIP1 was measured by microarray ELISA Western blotting. Skeletal transcriptomes were analyzed from Gene Expression Omnibus databases. Network-based proximity analysis performed on the of genes human interactome.In patients with...