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Specialty: Chemistry
Condition: Diabetes
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Total 31 results found since Jan 2013.
Molecules, Vol. 26, Pages 1328: Identification of a Sesquiterpene Lactone from Arctium lappa Leaves with Antioxidant Activity in Primary Human Muscle Cells
In this study, we investigated the antioxidant properties of Arctium lappa leaves in a model of primary human muscle cells exposed to H2O2 oxidative stress. We identified using bioassay-guided purification, onopordopicrin, a sesquiterpene lactone as the main molecule responsible for the antioxidant activity of A. lappa leaf extract. According to our findings, onopordopicrin inhibited the H2O2-mediated loss of muscle cell viability, by limiting the production of free radicals and abolishing DNA cellular damages. Moreover, we showed that onopordopicrin promoted the expression of the nuclear factor-erythroid-2-related factor ...
Source: Molecules - March 2, 2021 Category: Chemistry Authors: Nour El Khatib Sylvie Morel G érald Hugon Sylvie Rapior Gilles Carnac Nathalie Saint Tags: Article Source Type: research
Molecules, Vol. 24, Pages 4208: Deficiency of Urokinase Plasminogen Activator May Impair β Cells Regeneration and Insulin Secretion in Type 2 Diabetes Mellitus
Conclusion: uPA may play a substantial role in insulin secretion, β cell regeneration, and progressive development of T2DM. Supplementation of uPA might be a novel approach for prevention and treatment of T2DM in the future.
Source: Molecules - November 19, 2019 Category: Chemistry Authors: Wu Ou Chang Lin Pei Chen Tags: Article Source Type: research
Deacetylation of S6 kinase promotes high glucose-induced glomerular mesangial cell hypertrophy and matrix protein accumulation Signal Transduction
S6 kinase acts as a driver for renal hypertrophy and matrix accumulation, two key pathologic signatures of diabetic nephropathy. As a post-translational modification, S6 kinase undergoes acetylation at the C terminus. The role of this acetylation to regulate kidney glomerular cell hypertrophy and matrix expansion is not known. In mesangial cells, high glucose decreased the acetylation and enhanced phosphorylation of S6 kinase and its substrates rps6 and eEF2 kinase that lead to dephosphorylation of eEF2. To determine the mechanism of S6 kinase deacetylation, we found that trichostatin A, a pan-histone deacetylase (HDAC) in...
Source: Journal of Biological Chemistry - June 13, 2019 Category: Chemistry Authors: Falguni Das, Soumya Maity, Nandini Ghosh-Choudhury, Balakuntalam S. Kasinath, Goutam Ghosh Choudhury Tags: Molecular Bases of Disease Source Type: research
The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages Signal Transduction
In conclusion, these findings reveal that C5aR2 contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages.
Source: Journal of Biological Chemistry - May 23, 2019 Category: Chemistry Authors: Songlin Yu, Dan Wang, Lingmin Huang, Yening Zhang, Ruiheng Luo, Dickson Adah, Yiting Tang, Kai Zhao, Ben Lu Tags: Immunology Source Type: research
Pancreatic {beta}-cells detoxify H2O2 through the peroxiredoxin/thioredoxin antioxidant system Metabolism
Oxidative stress is thought to promote pancreatic β-cell dysfunction and contribute to both type 1 and type 2 diabetes. Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, are mediators of oxidative stress that arise largely from electron leakage during oxidative phosphorylation. Reports that β-cells express low levels of antioxidant enzymes, including catalase and GSH peroxidases, have supported a model in which β-cells are ill-equipped to detoxify ROS. This hypothesis seems at odds with the essential role of β-cells in the control of metabolic homeostasis and organismal survival through exquisite...
Source: Journal of Biological Chemistry - March 28, 2019 Category: Chemistry Authors: Jennifer S. Stancill, Katarzyna A. Broniowska, Bryndon J. Oleson, Aaron Naatz, John A. Corbett Tags: Signal Transduction Source Type: research
The orphan nuclear receptor Nor1/Nr4a3 is a negative regulator of {beta}-cell mass Molecular Bases of Disease
The Nr4a subfamily of nuclear receptor comprises three members in mammalian cells: Nur77/Nr4a1, Nurr1/Nr4a2, and Nor1/Nr4a3. Nr4a proteins play key roles in the regulation of glucose homeostasis in peripheral metabolic tissues. However, their biological functions in β-cells remain relatively uncharacterized. Here we sought to investigate the potential role of Nor1 in the regulation of β-cell mass and, in particular, β-cell survival/apoptosis. We used histological analysis to examine the consequences of genetic deletion of either Nur77 and Nor1 on β-cell mass, investigated the expression patterns of Nr4as in human islet...
Source: Journal of Biological Chemistry - March 28, 2019 Category: Chemistry Authors: Anne–Francoise Close, Nidheesh Dadheech, Barbara Scoralick Villela, Claude Rouillard, Jean Buteau Tags: Molecular Bases of Disease Source Type: research
F-box protein-32 down-regulates small-conductance calcium-activated potassium channel 2 in diabetic mouse atria Molecular Bases of Disease
In conclusion, DM-induced SK2 channel down-regulation appears to be due to an FBXO-32-dependent increase in UPS-mediated SK2 protein degradation.
Source: Journal of Biological Chemistry - March 14, 2019 Category: Chemistry Authors: Tian-You Ling, Fu Yi, Tong Lu, Xiao-Li Wang, Xiaojing Sun, Monte S. Willis, Li-Qun Wu, Win-Kuang Shen, John P. Adelman, Hon-Chi Lee Tags: Molecular Bases of Disease Source Type: research
Complement 1q-like-3 protein inhibits insulin secretion from pancreatic {beta}-cells via the cell adhesion G protein-coupled receptor BAI3 Cell Biology
Secreted proteins are important metabolic regulators in both healthy and disease states. Here, we sought to investigate the mechanism by which the secreted protein complement 1q-like-3 (C1ql3) regulates insulin secretion from pancreatic β-cells, a key process affecting whole-body glucose metabolism. We found that C1ql3 predominantly inhibits exendin-4– and cAMP-stimulated insulin secretion from mouse and human islets. However, to a lesser extent, C1ql3 also reduced insulin secretion in response to KCl, the potassium channel blocker tolbutamide, and high glucose. Strikingly, C1ql3 did not affect insulin secretion stimula...
Source: Journal of Biological Chemistry - November 23, 2018 Category: Chemistry Authors: Rajesh Gupta, Dan C. Nguyen, Michael D. Schaid, Xia Lei, Appakalai N. Balamurugan, G. William Wong, Jeong-a Kim, James E. Koltes, Michelle E. Kimple, Sushant Bhatnagar Tags: Metabolism Source Type: research
Fibroblast growth factor receptor 5 (FGFR5) is a co-receptor for FGFR1 that is up-regulated in beta-cells by cytokine-induced inflammation Metabolism
Fibroblast growth factor receptor-1 (FGFR1) activity at the plasma membrane is tightly controlled by the availability of co-receptors and competing receptor isoforms. We have previously shown that FGFR1 activity in pancreatic beta-cells modulates a wide range of processes, including lipid metabolism, insulin processing, and cell survival. More recently, we have revealed that co-expression of FGFR5, a receptor isoform that lacks a tyrosine-kinase domain, influences FGFR1 responses. We therefore hypothesized that FGFR5 is a co-receptor to FGFR1 that modulates responses to ligands by forming a receptor heterocomplex with FGFR...
Source: Journal of Biological Chemistry - November 2, 2018 Category: Chemistry Authors: Romario Regeenes, Pamuditha N. Silva, Huntley H. Chang, Edith J. Arany, Andrey I. Shukalyuk, Julie Audet, Dawn M. Kilkenny, Jonathan V. Rocheleau Tags: Signal Transduction Source Type: research
TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis Signal Transduction
High-glucose (HG) levels and hyperglycemia associated with diabetes are known to cause neuronal damage. The detailed molecular mechanisms, however, remain to be elucidated. Here, we investigated the role of transient receptor potential melastatin 7 (TRPM7) channels in HG-mediated endoplasmic reticulum stress (ERS) and injury of NS20Y neuronal cells. The cells were incubated in the absence or presence of HG for 48 h. We found that mRNA and protein levels of TRPM7 and of ERS-associated proteins, such as C/EBP homologous protein (CHOP), 78-kDa glucose-regulated protein (GRP78), and inducible nitric-oxide synthase (iNOS), incr...
Source: Journal of Biological Chemistry - September 14, 2018 Category: Chemistry Authors: Yan Huang, Tian-Dong Leng, Koichi Inoue, Tao Yang, Mingli Liu, F. David Horgen, Andrea Fleig, Jun Li, Zhi-Gang Xiong Tags: Molecular Bases of Disease Source Type: research
Overexpression of sphingosine-1-phosphate lyase protects insulin-secreting cells against cytokine toxicity Metabolism
In conclusion, the relatively low endogenous Spl expression level in insulin-secreting cells contributes to their extraordinary vulnerability to proinflammatory cytokine toxicity and may therefore represent a promising target for β-cell protection in type 1 diabetes mellitus.
Source: Journal of Biological Chemistry - December 8, 2017 Category: Chemistry Authors: Claudine Hahn, Karolina Tyka, Julie D. Saba, Sigurd Lenzen, Ewa Gurgul-Convey Tags: Molecular Bases of Disease Source Type: research
Hydrogen sulfide inhibits high glucose-induced NADPH oxidase 4 expression and matrix increase by recruiting inducible nitric oxide synthase in kidney proximal tubular epithelial cells Glycobiology and Extracellular Matrices
High-glucose increases NADPH oxidase 4 (NOX4) expression, reactive oxygen species generation, and matrix protein synthesis by inhibiting AMP-activated protein kinase (AMPK) in renal cells. Because hydrogen sulfide (H2S) inhibits high glucose-induced matrix protein increase by activating AMPK in renal cells, we examined whether H2S inhibits high glucose-induced expression of NOX4 and matrix protein and whether H2S and NO pathways are integrated. High glucose increased NOX4 expression and activity at 24 h in renal proximal tubular epithelial cells, which was inhibited by sodium hydrosulfide (NaHS), a source of H2S. High gluc...
Source: Journal of Biological Chemistry - April 7, 2017 Category: Chemistry Authors: Hak Joo Lee, Doug Yoon Lee, Meenalakshmi M. Mariappan, Denis Feliers, Goutam Ghosh-Choudhury, Hanna E. Abboud, Yves Gorin, Balakuntalam S. Kasinath Tags: Glycobiology and Extracellular Matrices Source Type: research
Protein Phosphotyrosine Phosphatase 1B (PTP1B) in Calpain-dependent Feedback Regulation of Vascular Endothelial Growth Factor Receptor (VEGFR2) in Endothelial Cells Molecular Bases of Disease
In conclusion, our data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-induced angiogenesis. Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment of impaired wound healing in diabetes.
Source: Journal of Biological Chemistry - January 12, 2017 Category: Chemistry Authors: Yixuan Zhang, Qiang Li, Ji Youn Youn, Hua Cai Tags: Signal Transduction Source Type: research
Mitochondrial Activity in Human White Adipocytes Is Regulated by the Ubiquitin Carrier Protein 9/microRNA-30a Axis Cell Biology
In this study, we demonstrate that the mRNA and protein expression of Ubc9 are regulated by the microRNA miRNA-30a (miR-30a) in human subcutaneous adipocytes. Ubc9 and miR-30a exhibit inverse expression in adipose tissue, with miR-30a robustly elevated in brown fat. Depletion of Ubc9 by siRNA or enforced expression of a miR-30a mimic augments mitochondrial volume and respiration in human white adipocytes, reflecting features of brown fat cells. Furthermore, Ubc9 depletion induces a brown fat gene program in human subcutaneous adipocytes. Induction of the beige-selective gene program corresponds to stabilization of the PR d...
Source: Journal of Biological Chemistry - November 17, 2016 Category: Chemistry Authors: Eun Hee Koh, Yong Chen, David A. Bader, Mark P. Hamilton, Bin He, Brian York, Shingo Kajimura, Sean E. McGuire, Sean M. Hartig Tags: Gene Regulation Source Type: research
MIOX in Diabetic Nephropathy Molecular Bases of Disease
In conclusion, this study highlights a novel mechanism where MIOX under HG ambience exacerbates renal injury during the progression of diabetic nephropathy following the generation of excessive ROS via an unexplored G-X pathway.
Source: Journal of Biological Chemistry - March 11, 2016 Category: Chemistry Authors: Sun, L., Dutta, R. K., Xie, P., Kanwar, Y. S. Tags: Glycobiology and Extracellular Matrices Source Type: research
