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Condition: Diabetes Type 2

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Total 421 results found since Jan 2013.

Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose.
Abstract Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix-loop-helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated the role of ChREBP in the pathogenesis of DN. The expression of ChREBP was detected in patients with type 2 diabetes mellitus (T2DM), diabetic mice and mesangial cells. ELISA was used to measure cytokine production in mesangial cells. Flow cytometry analysis was performed to detect the apoptosis of mes...
Source: Bioscience Reports - November 12, 2018 Category: Biomedical Science Authors: Chen Y, Wang YJ, Zhao Y, Wang JC Tags: Biosci Rep Source Type: research

The TRPC6-AMPK Pathway is Involved in Insulin-Dependent Cytoskeleton Reorganization and Glucose Uptake in Cultured Rat Podocytes
Conclusion: These results suggest a potentially important new mechanism that regulates glucose transport in podocytes and that could be injurious during diabetes.Cell Physiol Biochem 2018;51:393 –410
Source: Cellular Physiology and Biochemistry - November 19, 2018 Category: Cytology 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

Insulin-like growth factor-1 activates AMPK to augment mitochondrial function and correct neuronal metabolism in sensory neurons in type 1 diabetes
ConclusionsIn DRG neuron cultures IGF-1 signals via AMPK to elevate mitochondrial function and drive axonal outgrowth. We propose that this signaling axis mediates IGF-1-dependent protection from distal dying-back of fibers in diabetic neuropathy.
Source: Molecular Metabolism - November 29, 2018 Category: Endocrinology Source Type: research

Hepatic miR-181b-5p Contributes to Glycogen Synthesis Through Targeting EGR1
ConclusionWe demonstrated that miR-181b-5p contributes to glycogen synthesis by targeting EGR1, thereby regulating PTEN expression to mediate hepatic insulin resistance.
Source: Digestive Diseases and Sciences - January 9, 2019 Category: Gastroenterology Source Type: research

Anagliptin ameliorates high glucose- induced endothelial dysfunction via suppression of NLRP3 inflammasome activation mediated by SIRT1
Publication date: March 2019Source: Molecular Immunology, Volume 107Author(s): Tiechao Jiang, Dongli Jiang, Lirong Zhang, Mei Ding, Hui ZhouAbstractHigh glucose- induced endothelial dysregulation has been recognized as an initiation of vascular complications in Type 2 diabetes mellitus (T2DM). Anagliptin is a novel licensed dipeptidyl peptidase-4 (DPP-4) inhibitor for the treatment of T2DM. The effects of anagliptin in high glucose- induced endothelial dysfunction are less reported. In the current study, we found that treatment with anagliptin prevented high glucose- induced reduction of cell viability and increase in LDH ...
Source: Molecular Immunology - January 18, 2019 Category: Allergy & Immunology Source Type: research

Translocator protein 18 kDa ligand alleviates neointimal hyperplasia in the diabetic rat artery injury model via activating PKG
This study suggests that TSPO inhibition suppresses the proliferation and migration of VSMCs induced by hyperglycemia, consequently, preventing atherosclerosis and restenosis after angioplasty in diabetic conditions. TSPO may be a potential therapeutic target to reduce arterial remodeling induced by angioplasty in diabetes.
Source: Life Sciences - February 9, 2019 Category: Biology Source Type: research

Nucleophosmin/B23 contributes to hepatic insulin resistance through the modulation of NF- κB pathway.
Nucleophosmin/B23 contributes to hepatic insulin resistance through the modulation of NF-κB pathway. Biochem Biophys Res Commun. 2019 Feb 21;: Authors: Wang X, Ma H, Wang X Abstract Nucleophosmin (NPM)/B23 is an important nucleolar phosphoprotein involved in the regulation of assorted cellular signaling pathways. In the present study, we revealed a critical role of NPM in liver insulin resistance. NPM is markedly upregulated in insulin-resistant liver tissues and palmitic acid (PA)-exposed HepG2 cells both at mRNA and protein levels. Ectopic expression of NPM in hepatocytes aggravated PA-induced insu...
Source: Biochemical and Biophysical Research communications - February 21, 2019 Category: Biochemistry Authors: Wang X, Ma H, Wang X Tags: Biochem Biophys Res Commun Source Type: research

EPHA4 regulates vascular smooth muscle cell contractility and is a sex-specific hypertension risk gene in individuals with type 2 diabetes
Conclusion: EPHA4 appears to be a sex-specific hypertension risk gene in type 2 diabetic patients. Forward EPHA4 signalling reduces VSMC contractility, and estrogen is a modifier of this effect. The effect of EPHA4 on VSMCs contractility explains the association of EPHA4 gene with hypertension risks in female patients.
Source: Journal of Hypertension - March 1, 2019 Category: Cardiology Tags: ORIGINAL PAPERS: Heart and vessels 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

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

NF κB and Kidney Injury
Conclusion As a critical regulator of inflammation and cell survival, the NFκB pathway is a promising target for diagnosing and treating kidney diseases. For modulation of the NFκB pathway in the clinic, a number of molecules can effectively inhibit NFκB signaling by targeting the receptors, associated adaptors, IKKs, IκBs and transcriptional regulators (144). There is further clinical evidence on small-molecule inhibitors of IKKα and NIK from recent trials on anti-cancer therapies (145). These clinical trials showed that the cancer-selective pharmacodynamic response of DTP3, the co...
Source: Frontiers in Immunology - April 15, 2019 Category: Allergy & Immunology Source Type: research

Systems Biology Approaches and Precision Oral Health: A Circadian Clock Perspective
Conclusion Most head and neck pathologies show a broad cellular heterogeneity making it difficult to achieve an accurate diagnosis and efficient treatment (Graf and Zavodszky, 2017; Lo Nigro et al., 2017). Single cell analysis of circadian omics (Lande-Diner et al., 2015; Abraham et al., 2018), may be a crucial tool needed in the future to fully understand the circadian control of head and neck diseases. It becomes more obvious that there is only a small genetic component but a largely unknown epigenetics and/or environmental component for most of the head and neck pathologies (Moosavi and Motevalizadeh Ardekani, 2016; He...
Source: Frontiers in Physiology - April 15, 2019 Category: Physiology Source Type: research

FGF21 as Modulator of Metabolism in Health and Disease
In conclusion, FGF21 belongs to a promising class of cytokines that are induced in response to stress and that can be used as a drug, drug target, or through a biomarker, depending on the physio-pathological context. All these findings will become clear when FGF21 will be used as a therapeutic molecule, exploiting the beneficial effects of FGF21 for treating metabolic disease or when it will be blocked to ameliorate disease progression and the onset of disease. Author Contributions CT and MS wrote the manuscript. VR contributed to the discussion. Funding This work was supported from the AFM-Telethon (19524), Italian Mi...
Source: Frontiers in Physiology - April 16, 2019 Category: Physiology Source Type: research