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Condition: Diabetes

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Total 1499 results found since Jan 2013.

LncRNA uc.48+ is involved in the diabetic immune and inflammatory responses mediated by P2X7 receptor in RAW264.7 macrophages.
Abstract High glucose combined with high FFAs can contribute to the unfavorable development of type 2 diabetes mellitus (T2DM) and monocytes/macrophages are important in the occurrence and development of T2DM, which is regarded as a type of low‑grade inflammation. Although our previous study demonstrated that increased expression of P2X7 receptor (P2X7R) in peripheral blood monocytes may alter the innate immune system and that long non‑coding (lnc)RNA uc.48+ was involved in diabetic neuropathic pain, the involvement of uc.48+ mediated by the P2X7R in monocyte/macrophages during T2DM has not been reported. In t...
Source: International Journal of Molecular Medicine - May 9, 2018 Category: Molecular Biology Authors: Wu H, Wen F, Jiang M, Liu Q, Nie Y Tags: Int J Mol Med Source Type: research

SIRT1 suppresses high glucose and palmitate-induced osteoclast differentiation via deacetylating p66Shc
In conclusion, this study confirms the role of DM in osteoclast differentiation in vitro. SIRT1 suppresses HG- and PA-induced osteoclast differentiation via p66Shc/ROS/NF-κB signaling.
Source: Molecular and Cellular Endocrinology - July 5, 2018 Category: Endocrinology Source Type: research

Effect of celastrol on toll ‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells.
Effect of celastrol on toll‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells. Int J Mol Med. 2018 Jul 12;: Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Abstract Toll‑like receptor 4 (TLR4)‑mediated immune and inflammatory signaling serves a pivotal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study demonstrated that celastrol treatment was able to improve hepatic steatosis and inhibit the TLR4 signaling cascade pathway in type 2 diabetic rats. The present study aimed to investigate the effects of celastrol on trigly...
Source: International Journal of Molecular Medicine - July 12, 2018 Category: Molecular Biology Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Tags: Int J Mol Med Source Type: research

LAZ3 protects cardiac remodeling in diabetic cardiomyopathy via regulating miR-21/PPARa signaling
In conclusion, LAZ3 protects against cardiac remodeling in DCM by decreasing miR-21, thus regulating PPARa/NRF2 signaling.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - July 19, 2018 Category: Molecular Biology Source Type: research

SIRT1 suppresses high glucose and palmitate-induced osteoclast differentiation via deacetylating p66Shc
In conclusion, this study confirms the role of DM in osteoclast differentiation in vitro. SIRT1 suppresses HG- and PA-induced osteoclast differentiation via p66Shc/ROS/NF-κB signaling.
Source: Molecular and Cellular Endocrinology - July 21, 2018 Category: Endocrinology Source Type: research

LAZ3 protects cardiac remodeling in diabetic cardiomyopathy via regulating miR-21/PPARa signaling.
In conclusion, LAZ3 protects against cardiac remodeling in DCM by decreasing miR-21, thus regulating PPARa/NRF2 signaling. PMID: 30031228 [PubMed - as supplied by publisher]
Source: Biochimica et Biophysica Acta - July 18, 2018 Category: Biochemistry Authors: Gao L, Liu Y, Guo S, Xiao L, Wu L, Wang Z, Liang C, Yao R, Zhang Y Tags: Biochim Biophys Acta Source Type: research

The differentiation of human MSCs derived from adipose and amniotic tissues into insulin-producing cells, induced by PEI@Fe3O4 nanoparticles-mediated NRSF and SHH silencing.
Abstract Type 1 diabetes involves the immunologically mediated destruction of insulin‑producing cells (IPCs) in the pancreatic islet. Mesenchymal stem cells (MSCs) have the ability to differentiate into IPCs and have become the most promising means for diabetes therapy. The present study demonstrated that human adipose‑derived stem cells (hADSCs) and human amniotic MSCs (hAMSCs) are able to differentiate into functional IPCs by knocking down neuronal restrictive silencing factor (NRSF) and Sonic hedgehog (SHH). In the current study, PEI@Fe3O4 nanoparticles (NPs) were used to deliver NRSF small interfering (si)...
Source: International Journal of Molecular Medicine - August 14, 2018 Category: Molecular Biology Authors: Wang R, Zhang D, Zhang T, Zhao F, Lang H, Lin X, Pang X Tags: Int J Mol Med Source Type: research

Gp91 < sup > phox < /sup > (NOX < sub > 2 < /sub > ) in Activated Microglia Exacerbates Neuronal Damage Induced by Oxygen Glucose Deprivation and Hyperglycemia in an in Vitro Model
Conclusion: Knockdown of gp91phoxsiRNA significantly reduced oxidative stress and the inflammatory response, and alleviated neuronal damage after HG and OGD treatment in a rat neuronal-microglial co-culture model.Cell Physiol Biochem 2018;50:783 –797
Source: Cellular Physiology and Biochemistry - October 12, 2018 Category: Cytology Source Type: research

Activation of the Notch ‑Nox4‑reactive oxygen species signaling pathway induces cell death in high glucose‑treated human retinal endothelial cells.
Activation of the Notch‑Nox4‑reactive oxygen species signaling pathway induces cell death in high glucose‑treated human retinal endothelial cells. Mol Med Rep. 2018 Nov 09;: Authors: Jiao W, Ji J, Li F, Guo J, Zheng Y, Li S, Xu W Abstract Diabetic retinopathy (DR) occurs in almost all patients with diabetes and remains as one of the major causes of vision loss worldwide. Nevertheless, the molecular mechanisms underlying the pathogenesis of DR remain elusive. The present study aimed to investigate the role and association of Notch signaling and NADPH oxidase 4 (Nox4)‑mediated oxidative stress in...
Source: Molecular Medicine Reports - November 16, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.
Abstract Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylatio...
Source: J Cell Mol Med - February 22, 2019 Category: Molecular Biology Authors: Wu J, Liang W, Tian Y, Ma F, Huang W, Jia Y, Jiang Z, Wu H Tags: J Cell Mol Med Source Type: research

A Novel Regulator of Preadipocyte Differentiation, Transcription Factor TCF21, Functions Partially Through Promoting LPL Expression
Discussion Excessive fat deposition in chickens can result in many undesirable consequences within the poultry industry, including reduced feeding efficiency (Zhou et al., 2006) and decreased reproductive performance (Walzem and Chen, 2014). Thus, broiler breeders urgently require a more thorough understanding of the molecular mechanism governing chicken adipogenesis. We previously found that broilers from lean and fat lines exhibit clear differences in reproductive performance (Zhang et al., 2018). In addition, TCF21 was found to be related to testis growth and development in these broilers (Zhang et al., 2017). In mice ...
Source: Frontiers in Physiology - April 22, 2019 Category: Physiology Source Type: research

Silencing of GPR82 with Interference RNA Improved Metabolic Profiles in Rats with High Fructose Intake
Metabolic syndrome (MS) is a clinical condition, constituted by alterations that lead to the onset of type II diabetes and cardiovascular disease. It has been reported that orphan G-protein-coupled receptor 82 (GPR82) participates in metabolic processes. The aim of this study was to evaluate the  function of GPR82 in MS using a small interfering RNA (siRNA) against this receptor. We used Wistar rats of 10–12 weeks of age fed with a high-fructose solution (70%) for 9 weeks to induce MS. Subsequently, the rats were treated with an intrajugular dose of an siRNA against GPR82 and the effects were evaluated on day 3 and 7 af...
Source: Journal of Vascular Research - July 2, 2019 Category: Research Source Type: research

Sam68 mediates high glucose ‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.
This study sought to examine the effect of Sam68 on high glucose (HG)‑induced podocytes apoptosis, and the mechanism underlying this effect. Immortalized mouse podocytes were exposed to medium containing normal glucose, or HG and Sam68 siRNA, respectively. The expression of Sam68 in podocytes was determined by fluorescence quantitative PCR (qPCR), immunofluorescence and immunoblotting. The role of Sam68 in HG‑induced podocyte apoptosis was further evaluated by inhibiting Sam68 expression by Sam68 siRNA and performing flow cytometry. The mRNA and protein expression of pro‑apoptosis gene Bax and anti‑apoptotic gene B...
Source: Molecular Medicine Reports - September 7, 2019 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Regulation of Lnc-NTF3-5 on islet β-cell dysfunction in high glucose environment and related mechanisms.
CONCLUSIONS: Lnc-NTF3-5 expression is increased in high glucose environment. Targeting Lnc-NTF3-5 can inhibit islet cell apoptosis, oxidative stress, and promote islet cell proliferation and insulin secretion. PMID: 31841205 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - December 18, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Dysregulation of microRNA-770-5p influences pancreatic- β-cell function by targeting TP53 regulated inhibitor of apoptosis 1 in gestational diabetes mellitus.
CONCLUSIONS: The data demonstrated that miR-770-5p was a vital regulator in pancreatic β-cell proliferation, apoptosis and insulin secretion by targeting TRIAP1, and dysregulation of miR-770-5p resulted in the development of GDM via APAF1 signaling pathway. PMID: 32016984 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - February 6, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research