title: Low fat adiponectin expression is associated with oxidative stress in nondiabetic humans with chronic kidney disease--impact on plasma adiponectin concentration.
abstract: In spite of association between high plasma adiponectin and high metabolic and cardiovascular (CV) risk, highest adiponectin increments retain CV and metabolic protective effects in advanced chronic kidney disease (CKD). Passive accumulation can favor CKD-associated hyperadiponectinemia but potential additional regulation by adipose tissue remains undefined. Oxidative stress (OS) is associated with metabolic and CV disease and with CKD [increasing from conservative treatment (CT) to maintenance hemodialysis (MHD)], and OS can reduce adiponectin expression in experimental models. OS (in the form of plasma thiobarbituric acid-reactive substances: TBARS), subcutaneous adipose adiponectin mRNA, and plasma adiponectin were studied in CKD patients (stages 4 and 5) on CT (n = 7) or MHD (n = 11). Compared with CT and controls (C: n = 6) MHD had highest TBARS and lowest adiponectin mRNA (P < 0.05) with lower adipose adiponectin protein (P < 0.05 vs. CT). MHD also had lower plasma adiponectin than CT, although both had higher adiponectin than C (P < 0.05). In renal transplant recipients (RT: CKD stage 3; n = 5) normal TBARS were, in turn, associated with normal adiponectin mRNA (P < 0.05 vs. MHD). In all CKD (n = 23), adiponectin mRNA was associated positively with adiponectin plasma concentration (P < 0.01). In all subjects (n = 29), adiponectin mRNA was related (P < 0.05) negatively with TBARS after adjusting for plasma C-reactive protein (CRP) or CRP and creatinine. Thus altered OS, adiponectin expression, and plasma concentration represent a novel cluster of metabolic and CV risk factors in MHD that are normalized in RT. The data suggest novel roles of 1) MHD-associated OS in modulating adiponectin expression and 2) adipose tissue in contributing to circulating adiponectin in advanced CKD.
authors.affiliation: Clinica Medica, Dipartimento di Scienze Cliniche, Morfologiche e Technologiche, University of Trieste, Ospedale Cattinara, Strada di Fiume 443, 34100 Trieste, Italy. barazzon@units.it
authors.forename: Rocco
authors.initials: R
authors.lastname: Barazzoni
authors.forename: Annamaria
authors.initials: A
authors.lastname: Bernardi
authors.forename: Franco
authors.initials: F
authors.lastname: Biasia
authors.forename: Annamaria
authors.initials: A
authors.lastname: Semolic
authors.forename: Alessandra
authors.initials: A
authors.lastname: Bosutti
authors.forename: Mariapia
authors.initials: M
authors.lastname: Mucci
authors.forename: Franca
authors.initials: F
authors.lastname: Dore
authors.forename: Michela
authors.initials: M
authors.lastname: Zanetti
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Guarnieri
mesh_terms: D052242:Adiponectin / Q000096:biosynthesis* / Q000097:blood*; D000273:Adipose Tissue / Q000378:metabolism*; D050154:Adiposity / Q000502:physiology; D000368:Aged; D000369:Aged, 80 and over; D000886:Anthropometry; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D016030:Kidney Transplantation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D052242:Adiponectin; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; D002097:C-Reactive Protein; D003404:Creatinine