title: Adiponectin, diabetes and ischemic heart failure: a challenging relationship.
abstract: BACKGROUND
  Several peptides, named adipokines, are produced by the adipose tissue. Among those, adiponectin (AD) is the most abundant. AD promotes peripheral insulin sensitivity, inhibits liver gluconeogenesis and displays anti-atherogenic and anti-inflammatory properties. Lower levels of AD are related to a higher risk of myocardial infarction and a worse prognosis in patients with coronary artery disease. However, despite a favorable clinical profile, AD increases in relation to worsening heart failure (HF); in this context, higher adiponectinemia is reliably related to poor prognosis. There is still little knowledge about how certain metabolic conditions, such as diabetes mellitus, modulate the relationship between AD and HF.We evaluated the level of adiponectin in patients with ischemic HF, with and without type 2 diabetes, to elucidate whether the metabolic syndrome was able to influence the relationship between AD and HF.
  
  
  RESULTS
  We demonstrated that AD rises in patients with advanced HF, but to a lesser extent in diabetics than in non-diabetics. Diabetic patients with reduced systolic performance orchestrated a slower rise of AD which began only in face of overt HF. The different behavior of AD in the presence of diabetes was not entirely explained by differences in body mass index. In addition, NT-proBNP, the second strongest predictor of AD, did not differ significantly between diabetic and non-diabetic patients. These data indicate that some other mechanisms are involved in the regulation of AD in patients with type 2 diabetes and coronary artery disease.
  
  
  CONCLUSIONS
  AD rises across chronic heart failure stages but this phenomenon is less evident in type 2 diabetic patients. In the presence of diabetes, the progressive increase of AD in relation to the severity of LV dysfunction is hampered and becomes evident only in overt HF.
authors.affiliation: Department of Critical Care Medicine and Surgery, Geriatric Medicine Unit, University of Florence, Florence, Italy. pesine@libero.it.
authors.forename: Samuele
authors.initials: S
authors.lastname: Baldasseroni
authors.forename: Alessandro
authors.initials: A
authors.lastname: Antenore
authors.forename: Claudia
authors.initials: C
authors.lastname: Di Serio
authors.forename: Francesco
authors.initials: F
authors.lastname: Orso
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Lonetto
authors.forename: Nadia
authors.initials: N
authors.lastname: Bartoli
authors.forename: Alice
authors.initials: A
authors.lastname: Foschini
authors.forename: Andrea
authors.initials: A
authors.lastname: Marella
authors.forename: Alessandra
authors.initials: A
authors.lastname: Pratesi
authors.forename: Salvatore
authors.initials: S
authors.lastname: Scarantino
authors.forename: Stefano
authors.initials: S
authors.lastname: Fumagalli
authors.forename: Matteo
authors.initials: M
authors.lastname: Monami
authors.forename: Edoardo
authors.initials: E
authors.lastname: Mannucci
authors.forename: Niccolò
authors.initials: N
authors.lastname: Marchionni
authors.forename: Francesca
authors.initials: F
authors.lastname: Tarantini
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000368:Aged; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications*; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000097:blood / Q000150:complications; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain