title: Decreased STAMP2 expression in association with visceral adipose tissue dysfunction.
abstract: BACKGROUND
  Six-transmembrane protein of prostate 2 (STAMP2) is a counter-regulator of inflammation and insulin resistance according to findings in mice. However, there have been contradictory reports in humans.
  
  
  OBJECTIVE
  We aimed to explore STAMP2 in association with inflammatory and metabolic status of human obesity.
  
  
  METHODS
  STAMP2 gene expression was analyzed in adipose tissue samples (171 visceral and 67 sc depots) and during human preadipocyte differentiation. Human adipocytes were treated with macrophage-conditioned medium, TNF-α, and rosiglitazone.
  
  
  RESULTS
  In visceral adipose tissue, STAMP2 gene expression was significantly decreased in obese subjects, mainly in obese subjects with type 2 diabetes. STAMP2 gene expression and protein were significantly and inversely associated with obesity phenotype measures (body mass index, waist, hip, and fat mass) and obesity-associated metabolic disturbances (systolic blood pressure and fasting glucose). In addition, STAMP2 gene expression was positively associated with lipogenic (FASN, ACC1, SREBP1, THRSP14, TRα, and TRα1), CAV1, IRS1, GLUT4, and CD206 gene expression. In sc adipose tissue, STAMP2 gene expression was not associated with metabolic parameters. In both fat depots, STAMP2 gene expression in stromovascular cells was significantly higher than in mature adipocytes. STAMP2 gene expression was significantly increased during the differentiation process in parallel to adipogenic genes, being increased in preadipocytes derived from lean subjects. Macrophage-conditioned medium (25%) and TNF-α (100 ng/ml) administration increased whereas rosiglitazone (2 μM) decreased significantly STAMP2 gene expression in human differentiated adipocytes.
  
  
  CONCLUSIONS
  Decreased STAMP2 expression (mRNA and protein) might reflect visceral adipose dysfunction in subjects with obesity and type 2 diabetes.
authors.affiliation: Service of Diabetes, Endocrinology, and Nutrition, Institut d'Investigació Biomèdica de Girona, CIBEROBN and Instituto de Salud Carlos III, 17007 Girona, Spain.
authors.forename: José María
authors.initials: JM
authors.lastname: Moreno-Navarrete
authors.forename: Francisco
authors.initials: F
authors.lastname: Ortega
authors.forename: Marta
authors.initials: M
authors.lastname: Serrano
authors.forename: Rafael
authors.initials: R
authors.lastname: Pérez-Pérez
authors.forename: Mònica
authors.initials: M
authors.lastname: Sabater
authors.forename: Wifredo
authors.initials: W
authors.lastname: Ricart
authors.forename: Francisco
authors.initials: F
authors.lastname: Tinahones
authors.forename: Belén
authors.initials: B
authors.lastname: Peral
authors.forename: José Manuel
authors.initials: JM
authors.lastname: Fernández-Real
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D000328:Adult; D000368:Aged; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D050152:Intra-Abdominal Fat / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D009765:Obesity / Q000235:genetics / Q000378:metabolism*; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism*; D000077154:Rosiglitazone; D050151:Subcutaneous Fat / Q000187:drug effects / Q000378:metabolism; D045162:Thiazolidinediones / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D007004:Hypoglycemic Agents; D008565:Membrane Proteins; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D000077154:Rosiglitazone; D010088:Oxidoreductases; C503310:STEAP4 protein, human