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Condition: Diabetes

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Total 1499 results found since Jan 2013.

Inhibition of Src Kinase Blocks High Glucose-Induced EGFR Transactivation and Collagen Synthesis in Mesangial Cells and Prevents Diabetic Nephropathy in Mice.
Abstract Chronic exposure to high glucose (HG) leads to diabetic nephropathy characterized by increased mesangial matrix protein, e.g. collagen, accumulation. Altered cell signaling and gene expression accompanied by oxidative stress has been documented. The contribution of the tyrosine kinase, c-Src (Src), which is sensitive to oxidative stress was examined.Cultured rat mesangial cells (MC) were exposed to HG (25 mM) in the presence and absence of Src inhibitors (PP2, SU6656), Src siRNA and the TNF-α converting enzyme (TACE) inhibitor, TAPI-2. Src was investigated in vivo by administration of PP2 to streptozotoc...
Source: Diabetes - August 13, 2013 Category: Endocrinology Authors: Taniguchi K, Xia L, Goldberg HJ, Lee KW, Shah A, Stavar L, A Y Masson E, Momen A, Shikatani EA, John R, Husain M, Fantus IG Tags: Diabetes Source Type: research

Effects of small interfering RNA-mediated hepatic glucagon receptor inhibition on lipid metabolism in db/db mice Research Articles
Hepatic glucose overproduction is a major characteristic of type 2 diabetes. Because glucagon is a key regulator for glucose homeostasis, antagonizing the glucagon receptor (GCGR) is a possible therapeutic strategy for the treatment of diabetes mellitus. To study the effect of hepatic GCGR inhibition on the regulation of lipid metabolism, we generated siRNA-mediated GCGR knockdown (si-GCGR) in the db/db mouse. The hepatic knockdown of GCGR markedly reduced plasma glucose levels; however, total plasma cholesterol was increased. The detailed lipid analysis showed an increase in the LDL fraction, and no change in VLDL HDL fra...
Source: The Journal of Lipid Research - September 11, 2013 Category: Lipidology Authors: Han, S., Akiyama, T. E., Previs, S. F., Herath, K., Roddy, T. P., Jensen, K. K., Guan, H.-P., Murphy, B. A., McNamara, L. A., Shen, X., Strapps, W., Hubbard, B. K., Pinto, S., Li, C., Li, J. Tags: Research Articles Source Type: research

Antioxidant effects of diallyl trisulfide on high glucose-induced apoptosis are mediated by the PI3K/Akt-dependent activation of Nrf2 in cardiomyocytes
Conclusions: Our findings indicate that DATS protects against hyperglycemia-induced ROS-mediated apoptosis by upregulating the PI3K/Akt/Nrf2 pathway, which further activates Nrf2-regulated antioxidant enzymes in cardiomyocytes exposed to HG.
Source: International Journal of Cardiology - March 1, 2013 Category: Cardiology Authors: Cheng-Yen Tsai, Chien-Chung Wang, Tung-Yuan Lai, Han-Nien Tsu, Chung-Hsing Wang, Hsin-Yueh Liang, Wei-Wen Kuo Tags: Original Articles Source Type: research

Sestrin 3 Regulation in Type 2 Diabetic Patients and its Influence on Metabolism and Differentiation in Skeletal Muscle.
Abstract In mammals, the sestrin family is composed of 3 stress responsive genes. Ablation of sestrin in Drosophila attenuates longevity, which is accompanied by increased S6K phosphorylation and decreased AMPK phosphorylation. Nevertheless, the metabolic role of sestrins in mammals is not comprehensively understood. We characterized the expression of individual sestrin family members and determined their role in vastus lateralis muscle biopsies from participants with normal glucose tolerance (NGT) or type 2 diabetes (T2D). Expression of sestrin 1 or sestrin 2 mRNA was unaltered between the NGT and T2D participant...
Source: American Journal of Physiology. Endocrinology and Metabolism - October 15, 2013 Category: Physiology Authors: Nascimento EB, Osler ME, Zierath JR Tags: Am J Physiol Endocrinol Metab Source Type: research

PPAR{gamma} Regulation by HAUSP Molecular Bases of Disease
In this study, herpesvirus-associated ubiquitin-specific protease (HAUSP) was isolated as a binding partner of PPARγ. Both endogenous and exogenous PPARγ associated with HAUSP in co-immunoprecipitation analysis. HAUSP, but not the catalytically inactive HAUSP C223S mutant, increased the stability of both endogenous and exogenous PPARγ through its deubiquitinating activity. Site-directed mutagenesis experiments showed that the Lys462 residue of PPARγ is critical for ubiquitination. HBX 41,108, a specific inhibitor of HAUSP, abolished the increase in PPARγ stability induced by HAUSP. In addition, knockdown of endogenous...
Source: Journal of Biological Chemistry - November 15, 2013 Category: Chemistry Authors: Lee, K. W., Cho, J. G., Kim, C. M., Kang, A. Y., Kim, M., Ahn, B. Y., Chung, S. S., Lim, K.-H., Baek, K.-H., Sung, J.-H., Park, K. S., Park, S. G. Tags: Metabolism Source Type: research

Sestrin 3 regulation in type 2 diabetic patients and its influence on metabolism and differentiation in skeletal muscle
In mammals, the sestrin family is composed of three stress-responsive genes. Ablation of sestrin in Drosophila attenuates longevity, which is accompanied by increased S6K phosphorylation and decreased AMPK phosphorylation. Nevertheless, the metabolic role of sestrins in mammals is not comprehensively understood. We characterized the expression of individual sestrin family members and determined their role in vastus lateralis muscle biopsies from participants with normal glucose tolerance (NGT) or type 2 diabetes (T2D). Expression of sestrin 1 or sestrin 2 mRNA was unaltered between the NGT and T2D participants. Conversely,...
Source: AJP: Endocrinology and Metabolism - December 1, 2013 Category: Endocrinology Authors: Nascimento, E. B., Osler, M. E., Zierath, J. R. Tags: Articles Source Type: research

O-GlcNAcylation under hypoxic conditions and its effects on the blood-retinal barrier in diabetic retinopathy.
In conclusion, the current study demonstrates the relationship between O-GlcNAc glycosylation and hypoxia during diabetic retinopathy and that hyperglycemia induced O2 consumption activates HIF1α and O-GlcNAc modification protein in the same retinal layer. The reduced protein BRVEC O-GlcNAcylation levels exert protective effects on the blood-retinal barrier and thus represent a potential therapeutic target for the treatment of diabetic retinopathy. PMID: 24366041 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - December 20, 2013 Category: Molecular Biology Authors: Xu C, Liu G, Liu X, Wang F Tags: Int J Mol Med Source Type: research

Overexpression of STAMP2 suppresses atherosclerosis and stabilizes plaques in diabetic mice
Abstract Our research aims to evaluate the function of the STAMP2 gene, an important trigger in insulin resistance (IR), and explore its role in macrophage apoptosis in diabetic atherosclerotic vulnerable plaques. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. The level of STAMP2 was measured by RT‐PCR and Western blot. The plaque area, lipid and collagen content of brachiocephalic artery plaques were measured by histopathological analyses, and the macrophage apoptosis was measured by TUNEL. Correlation of STAMP2/Akt signaling pathway and macrophage apoptosis was validated by...
Source: Journal of Cellular and Molecular Medicine - January 22, 2014 Category: Molecular Biology Authors: Jia Wang, Lu Han, Zhi‐hao Wang, Wen‐yuan Ding, Yuan‐yuan Shang, Meng‐xiong Tang, Wen‐bo Li, Yun Zhang, Wei Zhang, Ming Zhong Tags: Original Article Source Type: research

Enhanced p22phox expression Impairs Vascular Function through p38 and ERK1/2 MAP-Kinases-Dependent Mechanisms in Type 2 Diabetic mice.
Abstract Type 2 diabetes (T2D) is associated with vascular complication. We hypothesized that increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22(phox) expression impairs vascular endothelium-dependent relaxation in T2D. Type 2 diabetic (db(-)/db(-)) and control (db(-)/db(+)) mice were treated with reactive oxygen species (ROS) scavenger, polyethylene glycol superoxide dismutase, (PEG-SOD, 1000 units/kg daily intra-peritoneal injection) or siRNA p22(phox) (p22(phox)-lentivirus-siRNA, 100 µg, intra-venal injection twice per week) for one month. Endothelium-dependent relaxation (EDR) w...
Source: American Journal of Physiology. Heart and Circulatory Physiology - January 31, 2014 Category: Physiology Authors: Kassan M, Choi SK, Galan M, Lee YH, Trebak M, Matrougui K Tags: Am J Physiol Heart Circ Physiol Source Type: research

Insulin stimulates glucose transport via protein kinase G type I alpha-dependent pathway in podocytes.
Abstract Podocyte resistance to the actions of insulin on glucose transport could contribute to the pathogenesis of diabetic podocytopathy (DP) via disturbances in cyclic-dependent protein kinase signaling. To determine whether cGMP-dependent protein kinase (PKG) is involved in the insulin regulation of glucose transport, we measured insulin-dependent glucose uptake into cultured rat podocytes under conditions of modified PKG activity using pharmacological (PKG activator or inhibitor) and biochemical (siRNA PKGIα, siRNA insulin receptor β) means. Our findings indicate the participation of PKG in insulin-stimulat...
Source: Biochemical and Biophysical Research communications - March 3, 2014 Category: Biochemistry Authors: Piwkowska A, Rogacka D, Angielski S, Jankowski M Tags: Biochem Biophys Res Commun Source Type: research

Ezrin Is Down-Regulated in Diabetic Kidney Glomeruli and Regulates Actin Reorganization and Glucose Uptake via GLUT1 in Cultured Podocytes.
Abstract Diabetic nephropathy is a complication of diabetes and a major cause of end-stage renal disease. To characterize the early pathophysiological mechanisms leading to glomerular podocyte injury in diabetic nephropathy, we performed quantitative proteomic profiling of glomeruli isolated from rats with streptozotocin-induced diabetes and controls. Fluorescence-based two-dimensional difference gel electrophoresis, coupled with mass spectrometry, identified 29 differentially expressed spots, including actin-binding protein ezrin and its interaction partner, NHERF2, which were down-regulated in the streptozotocin...
Source: The American Journal of Pathology - April 8, 2014 Category: Pathology Authors: Wasik AA, Koskelainen S, Hyvönen ME, Musante L, Lehtonen E, Koskenniemi K, Tienari J, Vaheri A, Kerjaschki D, Szalay C, Révész C, Varmanen P, Nyman TA, Hamar P, Holthöfer H, Lehtonen S Tags: Am J Pathol Source Type: research

Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes.
Abstract As part of the filtration barrier, podocytes play an important role in the development of diabetic nephropathy. Disturbances in insulin signaling accompanied by insulin resistance can lead to various intracellular events. We hypothesized that high glucose concentrations would lead to disturbances in interactions between AMPK and PTEN proteins in podocytes. Experiments were performed in primary rat podocytes cultured with normal (5.6mM) or high (30mM) glucose concentrations for 5 d. Immunodetection methods were used to detect AMPK, PTEN, insulin receptor, and Akt proteins, and their phosphorylated forms. I...
Source: The International Journal of Biochemistry and Cell Biology - April 15, 2014 Category: Biochemistry Authors: Rogacka D, Piwkowska A, Audzeyenka I, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol Source Type: research

Advanced Glycation End Product 3 (AGE3) Suppresses the Mineralization of Mouse Stromal ST2 Cells and Human Mesenchymal Stem Cells by Increasing TGF-β Expression and Secretion.
Abstract In diabetic patients, advanced glycation end products (AGEs) cause bone fragility because of deterioration of bone quality. We previously showed that AGEs suppressed the mineralization of mouse stromal ST2 cells. Transforming growth factor (TGF)-β is abundant in bone, and enhancement of its signal causes bone quality deterioration. However, whether TGF-β signaling is involved in the AGE-induced suppression of mineralization during the osteoblast lineage remains unknown. We therefore examined the roles of TGF-β in the AGE-induced suppression of mineralization of ST2 cells and human mesenchymal stem cell...
Source: Endocrinology - April 23, 2014 Category: Endocrinology Authors: Notsu M, Yamaguchi T, Okazaki K, Tanaka KI, Ogawa N, Kanazawa I, Sugimoto T Tags: Endocrinology Source Type: research

Differential Requirements of Arrestin-3 and Clathrin for Ligand-dependent and -independent Internalization of Human G Protein-coupled Receptor 40.
Abstract G protein-coupled receptor 40 (GPR40) is believed to be an attractive target to enhance insulin secretion in patients with type 2 diabetes. GPR40 has been found to couple to Gq protein, leading to activation of phospholipase C and subsequent increases in the intracellular Ca(2+) level. However, the underlying mechanisms that regulate the internalization and desensitization of GPR40 remain to be elucidated. In the present study, a construct of GPR40 fused with enhanced green fluorescent protein (EGFP) at its C-terminus was constructed for direct imaging of the localization and internalization of GPR40 by c...
Source: Cellular Signalling - July 16, 2014 Category: Cytology Authors: Qian J, Wu C, Chen X, Li X, Ying G, Jin L, Ma Q, Li G, Shi Y, Zhang G, Zhou N Tags: Cell Signal Source Type: research

Selective inhibiton of Sphingosine kinase-1 protects adipose tissue against LPS-induced inflammatory response in Zucker diabetic fatty rats.
The objective of the present study was to evaluate whether the enzyme sphingosine kinase 1 (SPHK1) would modulate the expression of CCL5 and other inflammatory biomarkers in primary adipocytes and its potential role in lipopolysaccharide -induced AT inflammation in a rat model of diabetes. To address this, LPS-stimulated primary adipocytes and 3T3-L1 cells were treated with a sphingosine kinase inhibitor (SPHK I) and the expression of Ccl5 and other CC chemokines were studied. Moreover, the effect of Sphk-1 knockdown on cytokine production was analyzed in 3T3-L1 cells by transfection of Sphk-1-specific small interfering RN...
Source: American Journal of Physiology. Endocrinology and Metabolism - July 22, 2014 Category: Physiology Authors: Tous M, Ferrer-Lorente R, Badimon L Tags: Am J Physiol Endocrinol Metab Source Type: research