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Condition: Diabetes

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Total 1499 results found since Jan 2013.

Exogenous Hydrogen Sulfide Attenuates Cardiac Fibrosis Through Reactive Oxygen Species Signal Pathways in Experimental Diabetes Mellitus Models
Conclusion: The present study shows that enhanced NOX4 expression results in cardiac fibrosis through ROS-ERK1/2-MAPkinase-dependent mechanisms in diabetic cardiomyopathy. NOX4 could be an important target for H2S to regulate redox homeostasis in cardiac fibrosis of diabetic cardiomyopathy.Cell Physiol Biochem 2015;36:917-929
Source: Cellular Physiology and Biochemistry - June 16, 2015 Category: Cytology Source Type: research

Fatty Acid-Binding Protein 4 mediates apoptosis via endoplasmic reticulum stress in mesangial cells of diabetic nephropathy
Publication date: 15 August 2015 Source:Molecular and Cellular Endocrinology, Volume 411 Author(s): Fang Yao , Zhen Li , Takashi Ehara , Lin Yang , Dandan Wang , Lulu Feng , Yiming Zhang , Kun Wang , Yonghong Shi , Huijun Duan , Lianshan Zhang Type 2 diabetes is characterized by hyperglycemia and deregulated lipid metabolism with increased plasma non-esterified fatty acids (NEFA). Apoptosis of glomerular cells is a hallmark in diabetic glomerulosclerosis. Fatty acid-binding protein 4 (FABP4), a carrier protein for fatty acids, has been linked to diabetes and diabetic nephropathy (DN). Here we aimed to investigate the lin...
Source: Molecular and Cellular Endocrinology - June 26, 2015 Category: Endocrinology Source Type: research

RNAi in murine hepatocytes: the agony of choice-a study of the influence of lipid-based transfection reagents on hepatocyte metabolism.
In conclusion, these findings demonstrate that the choice of non-viral siRNA delivery agent is critical in hepatocytes. This should be remembered, especially if RNA silencing is used for studying hepatic lipid homeostasis and its regulation. PMID: 26233687 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - August 2, 2015 Category: Toxicology Authors: Böttger J, Arnold K, Thiel C, Rennert C, Aleithe S, Hofmann U, Vlaic S, Sales S, Shevchenko A, Matz-Soja M Tags: Arch Toxicol Source Type: research

Autophagy protects Human Brain Microvascular Endothelial Cells against Methylglyoxal‐induced Injuries: in parallel with Cerebral Ischemic Model in Diabetic Rats
This article is protected by copyright. All rights reserved.
Source: Journal of Neurochemistry - August 1, 2015 Category: Neurology Authors: Lili Fang, Xue Li, Yinbo Zhong, Jing Yu, Lina Yu, Haibin Dai, Min Yan Tags: Original Article Source Type: research

Sirtuin‐6 deficiency exacerbates diabetes‐induced impairment of wound healing
Abstract Delayed wound healing is one of the major complications in diabetes and is characterized by chronic proinflammatory response, and abnormalities in angiogenesis and collagen deposition. Sirtuin family proteins regulate numerous pathophysiological processes, including those involved in promotion of longevity, DNA repair, glycolysis and inflammation. However, the role of sirtuin 6 (SIRT6), a NAD+‐dependent nuclear deacetylase, in wound healing specifically under diabetic condition remains unclear. To analyse the role of SIRT6 in cutaneous wound healing, paired 6‐mm stented wound was created in diabetic db/db mice...
Source: Experimental Dermatology - August 18, 2015 Category: Dermatology Authors: Rajarajan A. Thandavarayan, Venkata Naga Srikanth Garikipati, Darukeshwara Joladarashi, Sahana Suresh Babu, Prince Jeyabal, Suresh K. Verma, Alexander R. Mackie, Mohsin Khan, Somasundaram Arumugam, Kenichi Watanabe, Raj Kishore, Prasanna Krishnamurthy Tags: Original Article Source Type: research

Small interfering RNA Knock-down of Cannabinoid-1 Receptor (CB1R) for the Treatment or Prevention of Type-2 Diabetes
Endocannabinoids (EC) are lipid signaling molecules that act on the same cannabinoid receptors that recognize and mediate the effects of marijuana. Activation of the EC receptor CB1R has been shown to play a key role in the development of obesity and its metabolic consequences, including insulin resistance and type 2 diabetes. Researchers at NIH have now demonstrated in the Zucker diabetic fatty (ZDF) rat model of type-2 diabetes that beta-cell loss is caused by the CB1R-mediated activation of a macrophage-mediated inflammatory response. They have further demonstrated that treatment of ZDF rats with a peripheral CB1R antag...
Source: NIH OTT Licensing Opportunities - September 19, 2013 Category: Research Authors: admin Source Type: research

Increased Sphingosine 1-phosphate mediates inflammation and fibrosis in tubular injury in diabetic nephropathy.
This article is protected by copyright. All rights reserved. PMID: 26414003 [PubMed - as supplied by publisher]
Source: Clinical and Experimental Pharmacology and Physiology - September 28, 2015 Category: Drugs & Pharmacology Authors: Yaghobian D, Don AS, Yaghobian S, Chen X, Saad S, Pollock C Tags: Clin Exp Pharmacol Physiol Source Type: research

HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy.
CONCLUSIONS As a therapeutic target, HMGB-1 can inhibit inflammation and promote RGCs survival to delay DR progress through the HMGB-1-TLR4-NF-κB signaling pathway. PMID: 26454330 [PubMed - as supplied by publisher]
Source: Medical Science Monitor - October 14, 2015 Category: Research Tags: Med Sci Monit Source Type: research

TNF‐α stimulates System A amino acid transport in primary human trophoblast cells mediated by p38 MAPK signaling
In conclusion, TNF‐α regulates System A activity through increased SNAT1 and SNAT2 transporter protein expression in PHTs. These findings suggest that p38 MAPK may represent a critical mechanistic link between elevated proinflammatory cytokines and increased placental amino acid transport in obese and GDM pregnancies associated with fetal overgrowth. Altered placental amino acid transport is a common pathway which leads to pathological fetal growth. This study demonstrates that TNF‐α regulates amino acid transport activity in primary placental trophoblast cells via p38 MAPK‐dependent mechanism.
Source: Physiological Reports - October 27, 2015 Category: Physiology Authors: Irving L. M. H. Aye, Thomas Jansson, Theresa L. Powell Tags: Original Research Source Type: research

Ampelopsin protects endothelial cells from hyperglycemia‐induced oxidative damage by inducing autophagy via the AMPK signaling pathway
This study focused on the effect of ampelopsin on hyperglycemia‐induced oxidative damage and the underlying mechanism of this effect in human umbilical vein endothelial cells (HUVECs). We found that hyperglycemia impaired autophagy in HUVECs through the inhibition of AMP‐activated protein kinase (AMPK), which directly led to endothelial cell damage. Ampelopsin significantly attenuated the detrimental effect of hyperglycemia‐induced cell dysfunction in a concentration‐dependent manner in HUVECs. Ampelopsin significantly upregulated LC3‐II, Beclin1, and Atg5 protein levels but downregulated p62 protein levels in HU...
Source: BioFactors - September 10, 2015 Category: Biochemistry Authors: Xinyu Liang, Ting Zhang, Linying Shi, Chao Kang, Jing Wan, Yong Zhou, Jundong Zhu, Mantian Mi Tags: Original Article Source Type: research

Involvement of hypoxia-inducible factor-1α in the oxidative stress induced by advanced glycation end products in murine Leydig cells.
Abstract Hyperglycemia increases the formation of advanced glycation end products (AGEs), triggers oxidative impairments and influences inducible factor (HIF)-1α protein levels and transactivation function. Compromised HIF-1α in testis leads to male infertility. The aim of the study was to investigate the role of HIF-1α in oxidative stress induced by AGEs in murine Leydig TM3 cells. TM3 cells were treated with 50μg/ml of AGEs, or HIF-1α siRNA or 500μM of DMOG (dimethyloxalylglycine) respectively. The cells were also pretreated with HIF-1α siRNA or 500μM of DMOG and then were treated with 50μg/ml of AGEs. ...
Source: Toxicology in Vitro - December 29, 2015 Category: Toxicology Authors: Chen Y, Zhang Y, Ji H, Ji Y, Yang J, Huang J, Sun D Tags: Toxicol In Vitro Source Type: research

MEK/ERK pathway activation by insulin receptor isoform alteration is associated with the abnormal proliferation and differentiation of intestinal epithelial cells in diabetic mice.
Abstract In previous studies, we have reported the abnormal proliferation and differentiation of intestinal epithelial cells (IECs) in diabetes mellitus (DM) mice. The insulin receptor (IR) and its downstream mitogen-activated protein kinase kinase (MAPKK also known as MEK)/extracellular-regulated protein kinase (ERK) pathway is a classic pathway associated with cell proliferation and differentiation. The purpose of the present study is to investigate the role of the MEK/ERK pathway in abnormal proliferation and differentiation of IECs in DM mice. DM mouse models were induced by intraperitoneal injection of strept...
Source: Molecular and Cellular Biochemistry - January 2, 2016 Category: Biochemistry Authors: Ouyang H, Yang HS, Yu T, Shan TD, Li JY, Huang CZ, Zhong W, Xia ZS, Chen QK Tags: Mol Cell Biochem Source Type: research

High glucose-induced hyperosmolarity contributes to COX-2 expression and angiogenesis: implications for diabetic retinopathy
Conclusions: Glucose-related hyperosmolarity seems to be able to promote angiogenesis and retinopathy through activation of TonEBP and possibly increasing expression of AQP1 and COX-2. Osmolarity signaling may be a target for therapy.
Source: Cardiovascular Diabetology - January 29, 2016 Category: Cardiology Authors: Rosalinda MadonnaGaia GiovannelliPamela ConfaloneFrancesca RennaYong-Jian GengRaffaele De Caterina Source Type: research

Metformin inhibits growth of human non-small cell lung cancer cells via liver kinase B-1-independent activation of adenosine monophosphate-activated protein kinase.
Authors: Guo Q, Liu Z, Jiang L, Liu M, Ma J, Yang C, Han L, Nan K, Liang X Abstract Metformin, the most widely administered oral anti‑diabetic therapeutic agent, exerts its glucose-lowering effect predominantly via liver kinase B1 (LKB1)-dependent activation of adenosine monophosphate-activated protein kinase (AMPK). Accumulating evidence has demonstrated that metformin possesses potential antitumor effects. However, whether the antitumor effect of metformin is via the LKB1/AMPK signaling pathway remains to be determined. In the current study, the effects of metformin on proliferation, cell cycle progression, and...
Source: Molecular Medicine Reports - February 9, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

High-density lipoprotein of patients with breast cancer complicated with type 2 diabetes mellitus promotes cancer cells adhesion to vascular endothelium via ICAM-1 and VCAM-1 upregulation
Abstract Adhesion of disseminating tumor cells to vascular endothelium is a pivotal starting point in the metastasis cascade. We have shown previously that diabetic high-density lipoprotein (HDL) has the capability of promoting breast cancer metastasis, and this report summarizes our more recent work studying the role of abnormal HDL in facilitating the adhesion of the circulating tumor cells to the endothelium. This is an initiating step in breast cancer metastasis, and this work assesses the role of ICAM-1 and VCAM-1 in this process. MDA-MB-231, MCF 7, and human umbilical vein endothelial cells (HUVECs) were tre...
Source: Breast Cancer Research and Treatment - February 12, 2016 Category: Cancer & Oncology Source Type: research