A role of the gastric inflammation in morbid obesity

Aybike Birerdinc, Rohini Mehta, Maria Stepanova, Arian Afendi, Z. Goodman, V. Chandhoke, Zobair M. Younossi

This is a collaborative project between

School of Systems Biology, College of Science,George Mason University, Fairfax, VA

Translational Reseach Institute, Inova Hospital, VA

Until recently, studies on obesity-related diseases have focused primarily on adipose tissue. However, adipokines and cytokines released by expanded adipose tissue into circulation exert its action upon many peripheral targets, which in turn, produce and release into circulation other bioactive molecules, thus, adding to the obesity-specific hormonal milieau that augments the development of metabolic syndrome and associated conditions. One of the neglected peripheral players in the obesity phenotype is gastric tissue. However, the discovery of ghrelin and its role in human metabolism has promoted the studies of hypothalamic control of the appetitis and its contribution to obesity and other weight-related disorders (Kojima). In 2005, iot was found that the ghrelin-encoding gene also encodes obestatin that unlike ghrelin is involved in appetite suppression (Zhang et al., 2005). In addition to ghrelin and obestatin, the stomach is the second largest source, after adipose tissue, of the appetite inhibiting peptide - leptin (S Cinti et al., 2001),(Cammisotto et al., 2010), (Cammisotto et al., 2005). While, it is known that interaction of food with the gastric tissue triggers the release of various peptides which act in an autocrine and paracrine fashion to regulate food intake (Woods et al., 1998), studies on the role of gastric tissue in obesity-related disorders are scarce.

In this study we put forth and evaluated hypothesis that gastric tissue in obese subjects is under inflammatory stress and is contributing to systemic inflammation itself, thus influencing physiological states of other organs. To investigate this, we performed comparative expression profiling for 89 genes encoding for inflammatory cytokines, their receptors and energy metabolism related molecules.

RESULTS: are to be published soon