title: Gene expression of leptin, resistin, and adiponectin in the white adipose tissue of obese patients with non-alcoholic fatty liver disease and insulin resistance.
abstract: BACKGROUND
  Adipose tissue is an active endocrine organ that secretes a variety of metabolically important substances including adipokines. These factors affect insulin sensitivity and may represent a link between obesity, insulin resistance, type 2 diabetes (DM), and nonalcoholic fatty liver disease (NAFLD). This study uses real-time polymerase chain reaction (PCR) quantification of mRNAs encoding adiponectin, leptin, and resistin on snap-frozen samples of intra-abdominal adipose tissue of morbidly obese patients undergoing bariatric surgery.
  
  
  METHODS
  Morbidly obese patients undergoing bariatric surgery were studied. Patients were classified into two groups: Group A (with insulin resistance) (N=11; glucose 149.84 +/- 40.56 mg/dL; serum insulin 8.28 +/- 3.52 microU/mL), and Group B (without insulin resistance) (N=10; glucose 102.2 +/- 8.43 mg/dL; serum insulin 3.431 +/- 1.162 microU/mL).
  
  
  RESULTS
  Adiponectin mRNA in intra-abdominal adipose tissue and serum adiponectin levels were significantly lower in Group A compared to Group B patients (P<0.016 and P<0.03, respectively). Although serum resistin was higher in Group A than in Group B patients (P<0.005), resistin gene expression was not different between the two groups. Finally, for leptin, neither serum level nor gene expression was different between the two groups. Serum adiponectin level was the only predictor of nonalcoholic steatohepatitis (NASH) in this study (P=0.024).
  
  
  CONCLUSIONS
  Obese patients with insulin resistance have decreased serum adiponectin and increased serum resistin. Additionally, adiponectin gene expression is also decreased in the adipose tissue of these patients. This low level of adiponectin expression may predispose patients to the progressive form of NAFLD or NASH.
authors.affiliation: Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA 22042, USA.
authors.forename: Ancha
authors.initials: A
authors.lastname: Baranova
authors.forename: Shobha J
authors.initials: SJ
authors.lastname: Gowder
authors.forename: Karen
authors.initials: K
authors.lastname: Schlauch
authors.forename: Hazem
authors.initials: H
authors.lastname: Elariny
authors.forename: Rochelle
authors.initials: R
authors.lastname: Collantes
authors.forename: Arian
authors.initials: A
authors.lastname: Afendy
authors.forename: Janus P
authors.initials: JP
authors.lastname: Ong
authors.forename: Zachary
authors.initials: Z
authors.lastname: Goodman
authors.forename: Vikas
authors.initials: V
authors.lastname: Chandhoke
authors.forename: Zobair M
authors.initials: ZM
authors.lastname: Younossi
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005234:Fatty Liver / Q000150:complications / Q000378:metabolism*; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D050152:Intra-Abdominal Fat / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000150:complications / Q000378:metabolism*; D036361:Peptide Hormones / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D036361:Peptide Hormones; D012333:RNA, Messenger