Filtered By:
Condition: Diabetes

This page shows you your search results in order of relevance. This is page number 20.

Order by Relevance | Date

Total 1499 results found since Jan 2013.

SRT2104 attenuates diabetes-induced aortic endothelial dysfunction via inhibition of P53
Endothelial dysfunction contributes to diabetic macrovascular complications. Sirtuin 1 (SIRT1) protects against diabetic vasculopathy. SRT2104 is a novel SIRT1 activator and was not previously studied for its effects on diabetes-induced aortic endothelial dysfunction. Additionally, whether or to what extent deacetylation of P53, a substrate of SIRT1, is required for the effects of SIRT1 activation was unclear, given the fact that SIRT1 has multiple targets. Moreover, little was known about the pathogenic role of P53 in diabetes-induced aortic injury. To these ends, diabetes was induced by streptozotocin in C57BL/6 mice. Th...
Source: Journal of Endocrinology - February 21, 2018 Category: Endocrinology Authors: Wu, H., Wu, J., Zhou, S., Huang, W., Li, Y., Zhang, H., Wang, J., Jia, Y. Tags: Research Source Type: research

Klotho plays a protective role against glomerular hypertrophy in a cell cycle-dependent manner in diabetic nephropathy.
Abstract There are few studies on the effect of klotho on podocytes in diabetic nephropathy. Thus, we tested whether klotho exerts protective effect against glomerular injury in diabetes. Mouse podocytes were cultured in media containing 5.6mM or 30mM glucose(HG) with or without 200pM of recombinant klotho(rKL). Additionally, 32 mice were injected with either diluent(n=16, C) or with streptozotocin intraperitoneally(n=16, DM). Control and diabetic mice underwent sham operation and unilateral nephrectomy, respectively. Eight mice from each control and DM group were treated daily with 10μg/kg per day of rKL using o...
Source: American Journal of Physiology. Renal Physiology - April 11, 2018 Category: Physiology Authors: Oh HJ, Nam BY, Wu M, Kim S, Park J, Kang S, Park JT, Yoo TH, Kang SW, Han SH Tags: Am J Physiol Renal Physiol Source Type: research

TLR4/MyD88 -mediated CCL2 production by lipopolysaccharide (endotoxin): Implications for metabolic inflammation
ConclusionOverall, our data reveal that LPS induces CCL-2 in monocytes/macrophages via TLR4/MyD88 signaling which leads to the activation of NF-kB/AP-1 transcription factors.
Source: Journal of Diabetes and Metabolic Disorders - April 16, 2018 Category: Endocrinology Source Type: research

Palmitate Activates CCL4 Expression in Human Monocytic Cells via TLR4/MyD88 Dependent Activation of NF- κB/MAPK/ PI3K Signaling Systems
Conclusion: Collectively, our results show that palmitate induces CCL4 expression via activation of the TLR4-MyD88/NF-kB/MAPK/ PI3K signaling cascade. Thus, our findings suggest that the palmitate-induced CCL4 production might be an underlying mechanism of metabolic inflammation.Cell Physiol Biochem 2018;46:953 –964
Source: Cellular Physiology and Biochemistry - April 18, 2018 Category: Cytology Source Type: research

Genistein and Myd88 Activate Autophagy in High Glucose-Induced Renal Podocytes In Vitro.
CONCLUSIONS This study demonstrated that Genistein-induced autophagy could be a potential treatment strategy for glomerular diseases. PMID: 29999001 [PubMed - in process]
Source: Medical Science Monitor - July 14, 2018 Category: Research Tags: Med Sci Monit Source Type: research

MicroRNA-141 Inhibits the Proliferation of Penile Cavernous Smooth Muscle Cells Associated with Down-Regulation of the Rhoa/Rho Kinase Signaling Pathway
Conclusion: Decreased expression of miR-141 is associated with up-regulation of RhoA and ROCK2 in the RhoA/ROCK signaling pathway in rats with diabetic erectile dysfunction. miR-141 inhibits the growth of penile cavernous smooth muscle cells associated with down-regulation of the RhoA/ROCK signaling pathwayin vitro.Cell Physiol Biochem 2018;48:348 –360
Source: Cellular Physiology and Biochemistry - July 17, 2018 Category: Cytology Source Type: research

Loss of histone deacetylase 2 inhibits oxidative stress induced by high glucose via the HO-1/SIRT1 pathway in endothelial progenitor cells.
In conclusion, these findings indicate that an HDAC2 inhibitor may prevent impaired cell proliferation, tube formation, inflammation, and ROS production in high-glucose EPCs. PMID: 30063937 [PubMed - as supplied by publisher]
Source: Gene - July 28, 2018 Category: Genetics & Stem Cells Authors: Gao J, Wang Y, Li W, Zhang J, Che Y, Cui X, Sun B, Zhao G Tags: Gene Source Type: research

PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose
ConclusionsPKA requires active IGFBP-3 and SIRT1 to inhibit HMGB1 inflammatory actions in the retina vasculature. Activation of these pathways may offer new targets for therapy development.
Source: Inflammation Research - October 17, 2018 Category: Research Source Type: research

Ectopic lipid accumulation: potential role in tubular injury and inflammation in diabetic kidney disease.
Emerging studies suggest that lipid accumulates in the kidneys during diabetic kidney disease (DKD). However, the correlation between ectopic lipid accumulation with tubular damage has not been thoroughly elucidated to date. Using Oil Red staining, lipid accumulation was observed in the kidneys of type 2 DKD patients (class II-III) and db/db mice compared to the control and was predominantly located in the proximal tubular compartment. Immunohistochemistry staining showed that the intensity of adipose differentiation related protein (ADRP) and sterol-regulatory element binding protein-1 (SREBP-1) was clearly upregulated, w...
Source: Clinical Science - October 22, 2018 Category: Biomedical Science Authors: Yang, W., Luo, Y., Yang, S., Zeng, M., Zhang, S., Liu, J., Han, Y., Liu, Y., Zhu, X., Wu, H., Liu, F., Sun, L., Xiao, L. Tags: PublishAheadOfPrint Source Type: research

Hyperglycemia aggravates microenvironment hypoxia and promotes the metastatic ability of pancreatic cancer
ConclusionOur results demonstrate that the association between hyperglycemia and poor prognosis can be attributed to microenvironment hypoxia in pancreatic cancer.Graphical Abstract
Source: Computational and Structural Biotechnology Journal - October 30, 2018 Category: Biotechnology Source Type: research

Genome-wide profiling of histone H3K27 acetylation featured fatty acid signalling in pancreatic beta cells in diet-induced obesity in mice
Conclusions/interpretationThese results suggest novel roles for DNA-binding proteins and fatty acid signalling in obesity-induced epigenomic regulation of beta cell function.Data availabilityThe next-generation sequencing data in the present study were deposited at ArrayExpress.RNA-Seq:Dataset name: ERR2538129 (Control), ERR2538130 (Diet-induced obesity)Repository name and number: E-MTAB-6718 - RNA-Seq of pancreatic islets derived from mice fed a long-term high-fat diet against chow-fed controls.ChIP-Seq:Dataset name: ERR2538131 (Control), ERR2538132 (Diet-induced obesity)Repository name and number: E-MTAB-6719 - H3K27ac C...
Source: Diabetologia - November 5, 2018 Category: Endocrinology Source Type: research

Exploiting novel tailored immunotherapies of type 1 diabetes: Short interfering RNA delivered by cationic liposomes enables efficient Down-regulation of variant PTPN22 gene in T lymphocytes
Publication date: Available online 12 November 2018Source: Nanomedicine: Nanotechnology, Biology and MedicineAuthor(s): Marsha Pellegrino, Francesca Ceccacci, Stefania Petrini, Marco Cappa, Giovanna Mancini, Alessandra FierabracciAbstractIn autoimmune diseases as Type 1 diabetes, the actual treatment that provides the missing hormones is not able, however, to interrupt the underlining immunological mechanism. Importantly, novel immunotherapies are exploited to protect and rescue the remaining hormone producing cells. Among probable targets of immunotherapy, the C1858T mutation in the PTPN22 gene, which encodes for the lymp...
Source: Nanomedicine: Nanotechnology, Biology and Medicine - November 12, 2018 Category: Nanotechnology Source Type: research

Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.
This study was designed to explore the inductive effect of glycated high-density lipoprotein (gly-HDL) on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its relationship with autophagy. Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2α, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and th...
Source: J Cell Mol Med - February 12, 2019 Category: Molecular Biology Authors: Tian H, Li Y, Kang P, Wang Z, Yue F, Jiao P, Yang N, Qin S, Yao S Tags: J Cell Mol Med Source Type: research

AIM2 gene silencing attenuates diabetic cardiomyopathy in type 2 diabetic rat model
Publication date: Available online 18 February 2019Source: Life SciencesAuthor(s): Xuyang Wang, Jinyu Pan, Hui Liu, Mingjun Zhang, Dian Liu, Lu Lu, Jingjing Tian, Ming Liu, Tao Jin, Fengshuang AnAbstractAimsAbsent in melanoma 2 (AIM2) is a cytosolic DNA sensor which plays an important role in inflammasome formation and is involved in various cellular functions including pyroptosis, fibrosis, and tissue injury. Our study aimed to investigate whether AIM2 plays a role in diabetic cardiomyopathy (DCM) and to explore its potential molecular mechanism.Main methodsSprague-Dawley rats were randomly divided into 4 groups: Control,...
Source: Life Sciences - February 18, 2019 Category: Biology Source Type: research

Asprosin impairs insulin secretion in response to glucose and viability through TLR4/JNK-mediated inflammation
This report suggests asprosin as a novel therapeutic target for the treatment of type 2 diabetes through preservation of β-cell function.Graphical abstract
Source: Molecular and Cellular Endocrinology - March 8, 2019 Category: Endocrinology Source Type: research