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Department of Cardiovascular Disease Research, Novo Nordisk, Måløv, Denmark
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( Briet & Burns 2012 ). The initial phase of kidney disease or injury involves changes in the renal vasculature including loss of capillaries ( Choi et al. 2000 , Horbelt et al. 2007 ). Ischaemia and resulting activation of inflammatory pathways
Department of Nephrology, The Second Hospital of Jilin University, Changchun, Jilin, People’s Republic of China
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Department of Acupuncture and Tuina, Changchun University of Chinese Medicine, Changchun, Jilin, People’s Republic of China
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Introduction As one of the long-term complications of diabetes, diabetic nephropathy (DN) is the main cause of end-stage renal disease ( Dronavalli et al . 2008 ). Thus, end-stage renal disease cannot be effectively prevented or treated
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recognized as important contributors to cardiovascular pathology. Growing evidence supports the presence of MR in many extra-renal tissues, including vascular and immune cells, fibroblasts, adipocytes, and myocytes. In these tissues, the MR exerts functions
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inhibits mineralization and renal phosphate uptake ( Lajeunesse et al. 1996 , Nesbitt et al. 1999 , Xiao et al. 1998 ). MEPE, a matrix extracellular phosphoglycoprotein was recently cloned from a tumor resected from a patient with TIO ( Rowe et al
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significance of DPP4 activity in insulin-dependent diabetes, dyslipidaemia and diabetic renal dysfunction. In the present study, the changes in DPP4 expressions of plasma and several tissues (kidney, liver, pancreas and adipose tissue) were determined in a
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Introduction The population with type 2 diabetes mellitus and metabolic syndrome has been increasing worldwide and diabetic nephropathy is a leading cause in many countries, requiring renal replacement therapy. Obesity and insulin
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Bioscience Metabolism, Research and Early Development, Cardiovascular, Renal and Metabolism, Biopharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
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Here we have investigated the role of the protein caveolin 1 (Cav1) and caveolae in the secretion of the white adipocyte hormone adiponectin. Using mouse primary subcutaneous adipocytes genetically depleted of Cav1, we show that the adiponectin secretion, stimulated either adrenergically or by insulin, is abrogated while basal (unstimulated) release of adiponectin is elevated. Adiponectin secretion is similarly affected in wildtype mouse and human adipocytes where the caveolae structure was chemically disrupted. The altered ex vivo secretion in adipocytes isolated from Cav1 null mice is accompanied by lowered serum levels of the high-molecular weight (HMW) form of adiponectin, whereas the total concentration of adiponectin is unaltered. Interestingly, levels of HMW adiponectin are maintained in adipose tissue from Cav1-depleted mice, signifying that a secretory defect is present. The gene expression of key regulatory proteins known to be involved in cAMP/adrenergically triggered adiponectin exocytosis (the beta-3-adrenergic receptor and exchange protein directly activated by cAMP) remains intact in Cav1 null adipocytes. Microscopy and fractionation studies indicate that adiponectin vesicles do not co-localise with Cav1 but that some vesicles are associated with a specific fraction of caveolae. Our studies propose that Cav1 has an important role in secretion of HMW adiponectin, even though adiponectin-containing vesicles are not obviously associated with this protein. We suggest that Cav1, and/or the caveolae domain, is essential for the organisation of signalling pathways involved in the regulation of HMW adiponectin exocytosis, a function that is disrupted in Cav1/caveolae-depleted adipocytes.
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)-induced early-diabetic rats, with associated renal hypertrophy, and that insulin replacement by insulin treatment or islet transplantation reversed the inhibition of autophagy (Barbosa et al . 1992, Han et al . 1997 ). Impaired autophagy evidenced by renal
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pressure after UNX, suggesting a renal mechanism for this type of hypertension. Interestingly, Mimran et al . (1993) reported a decline in plasma renin activity in individuals with an increase in blood pressure after UNX, a finding tentatively explained
Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Korea
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Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Korea
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Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, Korea
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Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Korea
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patients include mesangial expansion, glomerulosclerosis, tubular atrophy and interstitial fibrosis ( Kambham et al. 2001 ). These structural changes are followed by a progressive decrease in renal function, including increased proteinuria and decreased