In this article published in AJTR0048994, in further review of data during continuation of study, we realized certain patients didn’t meet inclusion criteria. The reanalysis of the new dataset however didn’t change our final conclusion. The data was reanalysed per IRB guidelines after removing three subjects who either had BMI > 65 or BMI < 40 (Even though they undergone bariatric surgery). One control subject was also needed to be removed from the study. We included total subjects (41 study subjects and 4 control subjects) in the study (Table 1). Biochemical profile and fatty liver grading is performed (Tables 2-4). A possible role in the underlying pathophysiology of obesity and associated co-morbidities. We examined the mRNA expression by RT-PCR and protein expression by Western blotting and immunofluorescence for TREM-1, TREM-2, DAP-12, HMGB-1, RAGE, TLR-4 and TLR-2 in omentum, subcutaneous and liver biopsy tissues of obese diabetic (n = 18) and non-diabetic subjects (n = 23) and compared with the non-obese non-diabetic controls (n = 4). There was a significantly increased expression of TREM-1, DAP-12, HMGB-1, RAGE, TLR-4 and TLR-2 and decreased expression of TREM-2 in the omentum, subcutaneous and liver biopsy of obese diabetic subjects compared to obese non-diabetics and the non-obese population (Table 4). Overall, obese diabetic subjects had high expression of TREM-1 in association with HMGB1 (100% vs 58.3%, P = 0.006), RAGE (77.3% vs 41.7%, P = 0.045), TLR4 (100% vs 58.3%, P = 0.006), and TLR2 (100% vs 50%, P = 0.002) in liver biopsy samples in comparison to obese non-diabetic subjects. Obese diabetics have significantly increased TREM-1, HMGB1, RAGE, and TLRs compared to obese non-diabetics (Table 5). Our findings suggest a potential pathophysio-logical role of TREM-1 in conjunction with HMGB1 and inflammatory cell receptors (RAGE, TLR-4 and TLR-2) in obesity-induced insulin resistance.
All Science Journal Classification (ASJC) codes
- Molecular Medicine
- Clinical Biochemistry
- Cancer Research