title: CIDE--A gene expression in patients with abdominal obesity and LDL hyperlipoproteinemia qualified for surgical revascularization in chronic limb ischemia.
abstract: According to the latest data, CIDE -A gene plays a key role in the regulation of body weight in both humans and mice, and therefore it is regarded a potential candidate gene for human obesity. The aim of the study was to define the role of CIDEA gene in patients with dyslipidemia and symptomatic limb ischemia.
  
  
  METHODS
  The study group contained 28 patients, including 17 men and 11 women. Patients were enrolled in the study group, depending on the value of body mass index (BMI); there was BMI>30 for obese patients. The group included untreated patients (n=14) and patients (n=14) receiving atorvastatin 20 mg/day for at least three months prior to the initiation of the study. The control group (n=16) contained patients with no lipid disorders. A one-step isolation of RNA from lymphocytes and adipose tissue cells was carried out using the TRI method modified by Chomczyński and Sacchi. Next, gene expression was tested using real-time PCR.
  
  
  RESULTS
  The highest mean relative expression of CIDE -A gene occurred in patients with normal body weight. The lowest mean relative expression of CIDE-A gene was observed in obese patients with lipid disorders. A high negative correlation (r=-0.7919) of CIDE -A gene expression, depending on BMI, was reported in the group of obese patients with lipid disorders.
  
  
  CONCLUSIONS
  Due to an important role of Cide-A protein demonstrated in the development of metabolic diseases such as obesity, metabolic syndrome, type 2 diabetes and their vascular complications, CIDE -A gene and protein are potential therapeutic targets in the case of these diseases.
authors.forename: Marcin
authors.initials: M
authors.lastname: Feldo
authors.forename: Janusz
authors.initials: J
authors.lastname: Kocki
authors.forename: Sylwia
authors.initials: S
authors.lastname: Lukasik
authors.forename: Jacek
authors.initials: J
authors.lastname: Bogucki
authors.forename: Jan
authors.initials: J
authors.lastname: Feldo
authors.forename: Piotr
authors.initials: P
authors.lastname: Terlecki
authors.forename: Jan
authors.initials: J
authors.lastname: Kęsik
authors.forename: Jacek
authors.initials: J
authors.lastname: Wroński
authors.forename: Tomasz
authors.initials: T
authors.lastname: Zubilewicz
mesh_terms: D000368:Aged; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D000069059:Atorvastatin / Q000627:therapeutic use*; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D006951:Hyperlipoproteinemias / Q000150:complications / Q000188:drug therapy* / Q000235:genetics*; D007511:Ischemia / Q000150:complications / Q000235:genetics / Q000601:surgery; D007866:Leg / Q000098:blood supply; D008077:Lipoproteins, LDL / Q000235:genetics*; D008297:Male; D024821:Metabolic Syndrome / Q000235:genetics; D008875:Middle Aged; D056128:Obesity, Abdominal / Q000150:complications / Q000235:genetics*
chemical_list: D051017:Apoptosis Regulatory Proteins; C502539:CIDEA protein, human; D008077:Lipoproteins, LDL; D000069059:Atorvastatin