Expression of ectonucleotide pyrophosphate phosphodiesterase and peroxisome proliferator activated receptor gamma in morbidly obese patients.
Mots clés
Abstrait
BACKGROUND
Recently, two genes, peroxisome proliferator activated receptor gamma (PPARgamma) and ectonucleotide pyrophosphate phosphodiesterase (ENPP1), have been localized and associated with diabetes and obesity. This report hypothesizes that there is a correlation between the genetic expression of ENPP1 and PPARgamma from gastrointestinal tissue and body mass index (BMI).
METHODS
Preoperative demographic data were collected from 16 severely morbidly obese patients. Extraneous gastrointestinal tissue was obtained during laparoscopic gastric bypass and gastric banding procedures. The tissue was snap frozen in liquid nitrogen. Initially, RNA extraction was performed on the tissue, followed by reverse transcription using appropriate primers and controls. Subsequently, the samples were subjected to quantitative polymerase chain reaction (PCR). Preoperative demographic data were analyzed for their influence on ENPP1 and PPARgamma expression using multivariate analysis and logistic regression models.
RESULTS
Expression of PPARgamma and ENPP1 was found in all samples. There was a higher level of PPARgamma expression in omental tissue than in enteric tissue. There was no significant difference in the expression of ENPP1 among the different tissue types. The relative level of PPARgamma expression in small bowel and gastric tissue was found to be inversely proportional to body mass index (BMI) using linear regression analysis (p = 0.01; r (2) = 0.586). Similarly, PPARgamma expression from omental tissue showed an inverse relationship with BMI (p = 0.04; r (2 )= 0.576). The levels of ENPP1 expression did not show a correlation with BMI (p = 0.25).
CONCLUSIONS
The results suggest that increasing obesity correlates with a decrease in PPARgamma expression. This decrease may induce dysfunctional adipocyte differentiation, maturation, and function, leading to diabetes and the metabolic syndrome. Similarly, the increased volume of adipose tissue may lead to a downregulation of PPARgamma. The lack of correlation between ENPP1 and BMI may suggest that glucose metabolism is more complex than lipid metabolism. Further evaluation is warranted to establish metabolic pathways for glucose and lipid biomarkers.
