title: Adipose tissue cytokines, insulin sensitivity, inflammation, and cardiovascular outcomes in end-stage renal disease patients.
abstract: From an evolutionary perspective, Darwinian selection has favored insulin-resistant individuals, ie, those with a trait ensuring brain functioning in situations of extreme fuel deprivation. The ability to mount a powerful inflammatory response to infection was another survival advantage in our ancestors, and we now have solid evidence showing that these 2 traits, insulin resistance and inflammation (as measured by serum C-reactive protein [CRP]), are associated in modern human beings. In an analysis of 192 nondiabetic hemodialysis patients, leptin and adiponectin were related in an opposite fashion with insulin sensitivity in end-stage renal disease (ESRD) and interacted in determining insulin resistance in these patients. The risk of insulin resistance was about 6 times higher in ESRD patients with an unfavorable combination of the 2 adipokines (high leptin and low adiponectin) than in those with a favorable combination (low leptin and high adiponectin). Low adiponectin but not high leptin predicted incident cardiovascular events in this cohort. Neither leptin nor adiponectin were associated with CRP in a cross-sectional analysis, but they were linked in an opposite fashion to CRP in a longitudinal study in 21 patients with acute inflammation secondary to infection. High sympathetic activity predicts adverse cardiovascular outcomes in ESRD. Of note, we found that the risk for cardiovascular events is more than 3 times higher in patients with high sympathetic activity and low adiponectin than in those with high adiponectin and low sympathetic activity. The adipocyte hormones leptin and adiponectin are associated in an opposite fashion to insulin sensitivity and inflammation in ESRD patients. Relatively lower plasma adiponectin levels are associated with a higher rate of incident cardiovascular events. Finally, low adiponectin and high norepinephrine seem to be interacting factors in the dismal cardiovascular outcomes with ESRD.
authors.affiliation: Consiglio Nazionale Ricerche-Istituto BIo Medicina Epidemiologia Clinica e Fisiopatologia delle Malattie Renali e dell'Ipertensione Arteriosa, Reggio Calabria, Italy. carmine.zoccali@tin.it
authors.forename: Carmine
authors.initials: C
authors.lastname: Zoccali
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.forename: Francesco
authors.initials: F
authors.lastname: Cambareri
authors.forename: Francesco
authors.initials: F
authors.lastname: Catalano
authors.forename: Pietro
authors.initials: P
authors.lastname: Finocchiaro
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Cutrupi
authors.forename: Patrizia
authors.initials: P
authors.lastname: Pizzini
authors.forename: Alessandra
authors.initials: A
authors.lastname: Testa
authors.forename: Belinda
authors.initials: B
authors.lastname: Spoto
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Panuccio
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Enia
authors.forename: Francesca
authors.initials: F
authors.lastname: Mallamaci
mesh_terms: D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism*; D001823:Body Composition; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000453:epidemiology*; D016207:Cytokines / Q000378:metabolism*; D004734:Energy Metabolism; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000378:metabolism; D007333:Insulin Resistance; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000628:therapy; D020738:Leptin / Q000097:blood; D006435:Renal Dialysis; D012307:Risk Factors
chemical_list: D052242:Adiponectin; D016207:Cytokines; D020738:Leptin; D002097:C-Reactive Protein