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Condition: Diabetes Mellitus

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Total 263 results found since Jan 2013.

A Critical Role for Thioredoxin Interacting Protein in Diabetes-Related Impairment of Angiogenesis.
Abstract Impaired angiogenesis in ischemic tissue is a hallmark of diabetes mellitus. Thioredoxin interacting protein (TXNIP) is an exquisitely glucose-sensitive gene that is overexpressed in diabetes. Since TXNIP modulates the activity of the key angiogenic cytokine vascular endothelial growth factor (VEGF), we hypothesized that hyperglycemia-induced dysregulation of TXNIP may play a role in the pathogenesis of impaired angiogenesis in diabetes. In the current study, we report that high glucose-mediated overexpression of TXNIP induces a widespread impairment in endothelial cell function and survival by reducing V...
Source: Diabetes - November 5, 2013 Category: Endocrinology Authors: Dunn LL, Simpson PJ, Prosser HG, Lecce L, Yuen GS, Buckle A, Sieveking DP, Vanags LZ, Lim PR, Chow RW, Lam YT, Clayton Z, Bao S, Davies MJ, Stadler N, Celermajer DS, Stocker R, Bursill CA, Cooke JP, Ng MK Tags: Diabetes 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

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

Gestational diabetes impairs Nrf2-mediated adaptive antioxidant defenses and redox signaling in fetal endothelial cells in utero.
We examined the effects of GDM on the proteome, redox status and nuclear factor erythroid 2-related factor 2 (Nrf2) mediated antioxidant gene expression in human fetal endothelial cells. Proteomic analysis revealed that proteins involved in redox homeostasis were significantly altered in GDM and associated with increased mitochondrial superoxide generation, protein oxidation, DNA damage and diminished glutathione synthesis. In GDM cells, the lipid peroxidation product 4-hydroxynonenal (HNE) failed to induce nuclear Nrf2 accumulation and mRNA and/or protein expression of Nrf2 and its target genes NAD(P)H:quinone oxidoreduct...
Source: Diabetes - August 23, 2013 Category: Endocrinology Authors: Cheng X, Chapple SJ, Patel B, Puszyk W, Sudgen D, Yin X, Mayr M, Siow RC, Mann GE Tags: Diabetes Source Type: research

Advanced glycation end products suppress osteoblastic differentiation of stromal cells by activating endoplasmic reticulum stress.
In conclusion, AGEs inhibited the osteoblastic differentiation of stromal cells by suppressing ER stress sensors and accumulating abnormal proteins in the cells. This process might accelerate AGEs-induced suppression of bone formation found in diabetes mellitus. PMID: 23933252 [PubMed - as supplied by publisher]
Source: Biochemical and Biophysical Research communications - August 7, 2013 Category: Biochemistry Authors: Tanaka KI, Yamaguchi T, Kaji H, Kanazawa I, Sugimoto T Tags: Biochem Biophys Res Commun Source Type: research

Marine natural product des-O-methyllasiodiplodin effectively lowers the blood glucose level in db/db mice via ameliorating inflammation.
Conclusion:DML effectively lowers the blood glucose level in db/db mice possibly via ameliorating the expression of obesity-related pro-inflammatory cytokines, highlighting the potential of the marine natural product as a drug lead for the treatment of metabolic disorders. PMID: 23852084 [PubMed - as supplied by publisher]
Source: Acta Pharmacologica Sinica - July 15, 2013 Category: Drugs & Pharmacology Authors: Zhou R, Lin ZH, Jiang CS, Gong JX, Chen LL, Guo YW, Shen X Tags: Acta Pharmacol Sin Source Type: research

The role of toll-like receptor proteins (tlr) 2 and 4 in mediating inflammation in proximal tubules.
THE ROLE OF TOLL-LIKE RECEPTOR PROTEINS (TLR) 2 AND 4 IN MEDIATING INFLAMMATION IN PROXIMAL TUBULES. Am J Physiol Renal Physiol. 2013 Apr 10; Authors: Mudaliar H, Pollock CA, Komala MG, Chadban SJ, Wu H, Panchapakesan U Abstract Inflammatory responses are central to the pathogenesis of diabetic nephropathy. Toll-like receptors (TLRs) are ligand activated membrane-bound receptors which induce inflammatory responses predominantly through the activation of nuclear factor-kappa B (NF-ĸB). TLR2 and 4 are present in proximal tubular cells and are activated by endogenous ligands upregulated in diabetic nephropat...
Source: American Journal of Physiology. Renal Physiology - April 10, 2013 Category: Physiology Authors: Mudaliar H, Pollock CA, Komala MG, Chadban SJ, Wu H, Panchapakesan U Tags: Am J Physiol Renal Physiol Source Type: research

Ginkgo biloba Extract Reduces High-Glucose-Induced Endothelial Reactive Oxygen Species Generation and Cell Adhesion Molecule Expression by Enhancing HO-1 Expression via Akt/eNOS and P38 MAP Kinase Pathways.
CONCLUSION: GBE could reduce high glucose-induced endothelial adhesion via enhancing HO-1 expression through the Akt/eNOS and P38/MAPK pathways. Our findings suggest a potential strategy targeting on HO-1 induction by GBE for endothelial protection in the presence of high glucose such as that in diabetes mellitus. PMID: 23357604 [PubMed - as supplied by publisher]
Source: European Journal of Pharmaceutical Sciences - January 25, 2013 Category: Drugs & Pharmacology Authors: Tsai HY, Huang PH, Lin FY, Chen JS, Lin SJ, Chen JW Tags: Eur J Pharm Sci Source Type: research