Introduction: The epidemics of nonalcoholic steatohepatitis (NASH) and obesity continue to increase. Since many of the deleterious effects of obesity are thought to be due to the release of inflammatory mediators by adipose tissue, NASH may be related to the release of such cytokines. Elucidation of the pathways associated with NASH may help with novel treatment options. The study investigated the hypothesis that morbidly obese patients with NASH would have increased mRNA content of obesity-related inflammatory mediators from omental adipose tissue compared to morbidly obese patients without NASH.
Methods: Patients who were undergoing laparoscopic bariatric surgery and liver biopsy were included in this study. During each procedure, omental adipose tissue was harvested from the abdomen and mRNA content of select obesity-related inflammatory mediators (IL-6, Vaspin, MAP4k4, 11β HSD-1, visfatin, PPARγ, CIDEA, leptin, GPX-3, adiponectin, and CIDEC) was measured. Patients with NASH were matched for ethnicity, gender, body mass index, and waist to patients with no NASH. Values are presented as change from cyclophillin Cp values.
Results: There were 16 patients in this study. As the table demonstrates, there were no statistically significant changes between obesity-related inflammatory mediators from omental adipose tissue between patients who had NASH and those that did not have NASH.
Conclusions: Of the obesity-related inflammatory mediators we tested, none were related to NASH. Either other obesity-relatted mediators or mechanisms are involved with the pathogenesis of NASH.

	NASH	No NASH
IL-6	-6.2 ± 0.9	-7.7 ± 1.3
Vaspin	-1.7 ± 0.7	-1.8 ± 1.3
MAP4k4	-2.0± 2.8	-2.3 ± 0.3
11β HSD-1	0.4 ± 0.3	0.3 ± 0.3
Visfatin	2.3 ± 0.5	2.4 ± 1.3
PPARγ	1.5 ± 0.2	1.4 ± 0.1
CIDEA	1.0 ± 0.1	1.0 ± 0.3
Leptin	2.9 ± 0.2	2.0 ± 0.5
GPX-3	3.9 ± 0.3	4.0 ± 0.3
Adiponectin	4.2 ± 0.2	3.8 ± 0.7
CIDEC	3.5 ± 0.1	3.3 ± 0.2

p = NS for all comparisons between NASH and no NASH