title: The Metabolic Risk in Patients Newly Diagnosed with Acromegaly Is Related to Fat Distribution and Circulating Adipokines and Improves after Treatment.
abstract: Adipose tissue (AT) distribution is closely related to metabolic disease risk. Growth hormone (GH) reduces visceral and total body fat mass and induces whole-body insulin resistance. Our aim was to assess the effects of total and visceral AT (VAT) distribution and derived adipokines on systemic insulin resistance and lipid metabolism in acromegaly.
  
  
  
  Seventy adult patients with active acromegaly (43 males, age 49 ± 14 years) were evaluated before treatment, and a subset (n = 30, 20 males) was evaluated after treatment for acromegaly. Body composition and VAT, glucose metabolism parameters, lipids, C-reactive protein, and selected adipokines (vaspin, omentin, adiponectin, and leptin) were measured.
  
  
  
  At baseline, VAT was positively associated with glucose metabolism parameters and with lipids. GH, but not IGF-I, was negatively associated with all AT depots (visceral, trunk, limbs, and total; 0.41 ≤ r ≤ 0.61, p < 0.001 for all) and positively associated with vaspin (r = 0.31, p = 0.013). The fat deposition after treatment was predominantly located on trunk and visceral depots. The lipid profile partially improved, with increases in HDL and apolipoprotein A-I and a decrease in lipoprotein(a). Vaspin decreased and omentin increased. Adiponectin and leptin did not change significantly. The improvement in homeostasis model assessment for insulin resistance (HOMA-IR) was best predicted by the decreases in IGF-I and vaspin and the lack of an increase in trunk fat (R2 = 0.59, p = 0.001).
  
  
  
  (1) VAT is a metabolic risk factor for patients with active acromegaly; (2) vaspin and omentin levels are influenced by the disease activity but are not associated with VAT mass; (3) fat deposition after treatment occurs predominantly on the trunk and in visceral depots, and (4) insulin resistance decreases and the lipid profile partially improves with treatment.
authors.affiliation: Section of Specialized Endocrinology, Department of Endocrinology, Rikshospitalet, Oslo University Hospital, Oslo, Norway.
authors.forename: Nicoleta C
authors.initials: NC
authors.lastname: Olarescu
authors.forename: Ansgar
authors.initials: A
authors.lastname: Heck
authors.forename: Kristin
authors.initials: K
authors.lastname: Godang
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Jens
authors.initials: J
authors.lastname: Bollerslev
mesh_terms: D000172:Acromegaly / Q000097:blood / Q000473:pathology / Q000628:therapy; D054392:Adipokines / Q000097:blood*; D000328:Adult; D000368:Aged; D001823:Body Composition / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D058851:GPI-Linked Proteins / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000473:pathology*; D037102:Lectins / Q000378:metabolism; D008297:Male; D008659:Metabolic Diseases / Q000209:etiology*; D008875:Middle Aged; D015843:Serpins / Q000378:metabolism; D013004:Somatostatin / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D054392:Adipokines; D016207:Cytokines; D058851:GPI-Linked Proteins; C432397:ITLN1 protein, human; D036341:Intercellular Signaling Peptides and Proteins; D037102:Lectins; C507339:SERPINA12 protein, human; D015843:Serpins; D013004:Somatostatin; D007334:Insulin-Like Growth Factor I; D002097:C-Reactive Protein; D005947:Glucose