Filtered By:
Specialty: Biomedical Science
Condition: Diabetes

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

Order by Relevance | Date

Total 31 results found since Jan 2013.

Upregulation of Unc-51-Like Kinase 1 by Nitric Oxide Stabilizes SIRT1, Independent of Autophagy
by Junhui Xing, Hongtao Liu, Huabing Yang, Rui Chen, Yuguo Chen, Jian Xu SIRT1 is central to the lifespan and vascular health, but undergoes degradation that contributes to several medical conditions, including diabetes. How SIRT1 turnover is regulated remains unclear. However, emerging evidence suggests that endothelial nitric oxide synthase (eNOS) positively regulates SIRT1 protein expression. We recently identified NO as an endogenous inhibitor of 26S proteasome functionality with a cellular reporter system. Here we extended this finding to a novel pathway that regulates SIRT1 protein breakdown. In cycloheximide (CHX)-...
Source: PLoS One - December 26, 2014 Category: Biomedical Science Authors: Junhui Xing et al. Source Type: research

Ampelopsin Improves Insulin Resistance by Activating PPARγ and Subsequently Up-Regulating FGF21-AMPK Signaling Pathway
by Yong Zhou, Ying Wu, Yu Qin, Lei Liu, Jing Wan, Lingyun Zou, Qianyong Zhang, Jundong Zhu, Mantian Mi Ampelopsin (APL), a major bioactive constituent of Ampelopsis grossedentata, exerts a number of biological effects. Here, we explored the anti-diabetic activity of APL and elucidate the underlying mechanism of this action. In palmitate-induced insulin resistance of L6 myotubes, APL treatment markedly up- regulated phosphorylated insulin receptor substrate-1 and protein kinase B, along with a corresponding increase of glucose uptake capacity. APL treatment also increased expressions of fibroblast growth factor (FGF21) and...
Source: PLoS One - July 7, 2016 Category: Biomedical Science Authors: Yong Zhou Source Type: research

Effects of microRNA-211 on proliferation and apoptosis of lens epithelial cells by targeting SIRT1 gene in diabetic cataract mice.
Abstract Our study aimed at exploring the effects of microRNA-211 (miR-211) on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targeting NAD + -dependent histone deacetylase sirtulin 1 (SIRT1). Healthy male mice were assigned to normal and diabetic cataract groups. Blood glucose, lens turbidity and apoptosis were measured. Lens epithelial cells were classified into the normal, blank, negative control (NC), miR-211 mimics, miR-211 inhibitors, siRNA-SIRT1, and miR-211 inhibitors + siRNA-SIRT1 groups. MiR-211, Bcl-2, Bax, p53, and SIRT1 expressions of each group were detected. Ce...
Source: Bioscience Reports - July 5, 2017 Category: Biomedical Science Authors: Zeng K, Feng QG, Lin BT, Ma DH, Liu CM Tags: Biosci Rep Source Type: research

HSPB8 Promotes the Fusion of Autophagosome and Lysosome during Autophagy in Diabetic Neurons.
Authors: Li XC, Hu QK, Chen L, Liu SY, Su S, Tao H, Zhang LN, Sun T, He LJ Abstract Although autophagy has been proposed to play an emerging role in diabetic neuropathy, autophagy and its possible role remains unclear. Moreover, only few studies about diabetes have explored the autophagy mediated by heat shock protein beta-8 (HSPB8) and Bcl-2 associated athanogene 3 (BAG3). In the present study, we examined the autophagy induced by high glucose levels in an in vivo rat model of diabetes induced by streptozotocin (STZ) and an in vitro model of retinal ganglion cell-5 (RGC5) cells under high glucose conditions. In th...
Source: International Journal of Medical Sciences - December 6, 2017 Category: Biomedical Science Tags: Int J Med Sci 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

Inhibition of acid sphingomyelinase activity ameliorates endothelial dysfunction in db/db mice.
Abstract Acid sphingomyelinase (aSMase) plays an important role in endothelial dysfunction. Here, we show that elevated aSMase activity and ceramide content were reduced by desipramine treatment in diabetic animals. The inhibitor of aSMase, desipramine, improved vascular dysfunction in db/db mice. High glucose-induced upregulation of aSMase activity and ceramide levels were restored by treatment with aSMase siRNA or desipramine in endothelial cells. In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mou...
Source: Bioscience Reports - March 24, 2019 Category: Biomedical Science Authors: Jiang M, Huang S, Duan W, Liu Q, Lei M Tags: Biosci Rep Source Type: research

High Glucose Provokes Microvesicles Generation from Glomerular Podocytes via NOX4/ROS Pathway.
Abstract Microvesicles (MVs) were involved in the pathogenesis of many diseases, such as cardiovascular diseases and diabetes. Oxidative stress played a key role in the development and progression of diabetic nephropathy. Our aim of this study was to investigate whether high glucose could provoke microvesicles generation from podocytes and its potential mechanism. Mouse podocyte clone 5 (MPC-5) were stimulated by high glucose. The intracellular reactive oxygen species (ROS) of podocytes were measured by fluorescence microscopy with the probe of CM-H2DCFDA and MitoSOXTM. Antioxidants N-Acetyl-L-cysteine (NAC) and ...
Source: Bioscience Reports - October 29, 2019 Category: Biomedical Science Authors: Li M, Zhang T, Wu X, Chen Y, Sun L Tags: Biosci Rep Source Type: research

Calcium/calmodulin-dependent serine protein kinase is involved in exendin-4-induced insulin secretion in INS-1 cells
Conclusion: Our study suggests that the stimulation of β-cell insulin secretion by Ex-4 is mediated, at least in part, by CASK via a novel signaling mechanism.
Source: Metabolism - Clinical and Experimental - October 21, 2013 Category: Biomedical Science Authors: Zheng-Qiu Zhu, Dong Wang, Dan Xiang, Yue-Xing Yuan, Yao Wang Tags: Basic Science Source Type: research

TRIB3 alters endoplasmic reticulum stress-induced β-cell apoptosis via the NF-κB pathway
Conclusion: TRIB3 mediated ER stress-induced β-cell apoptosis via the NF-κB pathway.
Source: Metabolism - Clinical and Experimental - March 12, 2014 Category: Biomedical Science Authors: Ni Fang, Wenjian Zhang, Shiqing Xu, Hua Lin, Zai Wang, Honglin Liu, Qing Fang, Chenghui Li, Liang Peng, Jinning Lou Tags: Basic Science Source Type: research

Imatinib mesylate stimulates low-density lipoprotein receptor-related protein 1-mediated ERK phosphorylation in insulin producing cells
LRP1 is an endocytic and multifunctional type I cell surface membrane protein, which is known to be phosphorylated by the activated PDGF receptor (PDGFR). The tyrosine kinase inhibitor imatinib, which inhibits PDGFR and c-Abl, and which has previously been reported to counteract beta-cell death and diabetes, has been suggested to ameliorate atherosclerosis by inhibiting PDGFR-induced LRP1 phosphorylation. The aim of this investigation was to study LRP1 function in beta-cells and to what extent imatinib modulates LRP1 activity. LRP1 and c-Abl gene knockdown was performed by RNAi using rat INS-1 832/13 and human EndoC1-bH1 c...
Source: Clinical Science - May 28, 2014 Category: Biomedical Science Authors: R Göran Fred, S Kumar Boddeti, M Lundberg, N Welsh Source Type: research

Inhibition of PKC{beta}2 Overexpression Ameliorates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats via Restoring Caveolin-3/Akt Signaling
Activation of Protein Kinase Cβ (PKCβ) plays a critical role in myocardial ischemia/reperfusion (I/R) injury in non-diabetic rodents. In the myocardium of diabetes, PKCβ2 is overexpressed that is associated with increased vulnerability to post-ischemic I/R injury with concomitantly impaired cardiomyocyte caveolin (Cav)-3 and Akt signaling as compared with non- diabetic rats. We hypothesized that myocardial PKCβ overexpression in diabetes exacerbates myocardial I/R injury through impairing Cav-3/Akt signaling. Streptozotocin-induced diabetic rats were treated with the selective PKCβ inhibi...
Source: Clinical Science - April 7, 2015 Category: Biomedical Science Authors: Y Liu, J Jin, S Qiao, S Lei, S Liao, Z Ge, H Li, G Tin-chun Wong, M G Irwin, Z Xia Source Type: research

Human umbilical cord matrix-derived stem cells exert trophic effects on {beta}-cell survival in diabetic rats and isolated islets RESEARCH ARTICLE
ABSTRACT Human umbilical cord matrix-derived stem cells (uMSCs), owing to their cellular and procurement advantages compared with mesenchymal stem cells derived from other tissue sources, are in clinical trials to treat type 1 (T1D) and type 2 diabetes (T2D). However, the therapeutic basis remains to be fully understood. The immunomodulatory property of uMSCs could explain the use in treating T1D; however, the mere immune modulation might not be sufficient to support the use in T2D. We thus tested whether uMSCs could exert direct trophic effects on β-cells. Infusion of uMSCs into chemically induced diabetic rats preve...
Source: DMM Disease Models and Mechanisms - December 4, 2015 Category: Biomedical Science Authors: Zhou, Y., Hu, Q., Chen, F., Zhang, J., Guo, J., Wang, H., Gu, J., Ma, L., Ho, G. Tags: RESEARCH ARTICLE Source Type: research

The AMPK-related kinase SNARK regulates muscle mass and myocyte survival
The maintenance of skeletal muscle mass is critical for sustaining health; however, the mechanisms responsible for muscle loss with aging and chronic diseases, such as diabetes and obesity, are poorly understood. We found that expression of a member of the AMPK-related kinase family, the SNF1-AMPK-related kinase (SNARK, also known as NUAK2), increased with muscle cell differentiation. SNARK expression increased in skeletal muscles from young mice exposed to metabolic stress and in muscles from healthy older human subjects. The regulation of SNARK expression in muscle with differentiation and physiological stress suggests t...
Source: Journal of Clinical Investigation - December 22, 2015 Category: Biomedical Science Authors: Sarah J. Lessard, Donato A. Rivas, Kawai So, Ho-Jin Koh, André Lima Queiroz, Michael F. Hirshman, Roger A. Fielding, Laurie J. Goodyear Source Type: research

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts
Abnormal fibroblast function underlies poor wound healing in patients with diabetes; however, the mechanisms that impair wound healing are poorly defined. Here, we evaluated fibroblasts from individuals who had type 1 diabetes (T1D) for 50 years or more (Medalists, n = 26) and from age-matched controls (n = 7). Compared with those from controls, Medalist fibroblasts demonstrated a reduced migration response to insulin, lower VEGF expression, and less phosphorylated AKT (p-AKT), but not p-ERK, activation. Medalist fibroblasts were also functionally less effective at wound closure in nude mice. Activation of the δ isoform o...
Source: Journal of Clinical Investigation - January 26, 2016 Category: Biomedical Science Authors: Mogher Khamaisi, Sayaka Katagiri, Hillary Keenan, Kyoungmin Park, Yasutaka Maeda, Qian Li, Weier Qi, Thomas Thomou, Danielle Eschuk, Ana Tellechea, Aris Veves, Chenyu Huang, Dennis Paul Orgill, Amy Wagers, George L. King Source Type: research

Atorvastatin Alleviates Experimental Diabetic Cardiomyopathy by Regulating the GSK-3 β-PP2Ac-NF-κB Signaling Axis
by Xiao-min Ren, Guang-feng Zuo, Wen Wu, Jie Luo, Peng Ye, Shao-liang Chen, Zuo-ying Hu Recent studies reported that atorvastatin (ATOR) alleviated progression of experimental diabetic cardiomyopathy (DCM), possibly by protecting against apoptosis. However, the underlying mechanisms of this protective effect remain unclear. Therefore, our study investigated the role of the glycogen s ynthase kinase (GSK)-3β-protein phosphatase 2A(PP2A)-NF-κB signaling pathway in the anti-apoptotic and cardioprotective effects of ATOR on cardiomyocytes cultured in high glucose (HG) and in DCM. Our results showed that, in HG-cultured card...
Source: PLoS One - November 15, 2016 Category: Biomedical Science Authors: Xiao-min Ren Source Type: research