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Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) Regulates Insulin Resistance in Morbidly Obese Population
Kalyana Nandipati*1, Saravanan Subramnian2, Pradeep Pallati1, Devendra K. Agrawal2, Poona Sharma2
1Department of Surgery, Creighton University, School of Medicine, Omaha, NE; 2Department of Biomedical sciences, Creighton University, Omaha, NE

Obesity-induced chronic inflammation is critical in the pathogenesis of insulin resistance, diabetes, and metabolic syndrome. Identification of chronic inflammatory key factors in the resolution of diabetes is essential in developing strategies to prevent the development of obesity-induced diabetes mellitus. Triggering receptor expressed on myeloid cells (TREM)-1 has recently been recognized as one of the potent amplifier of acute and chronic inflammation. However, exact role of TREM-1 in regard to insulin insensitivity is unknown. In this study, we examined the mRNA transcripts and protein expression of TREM-1, TREM-2, CD68 and CD16 in the biopsied tissues (liver, omentum and subcutaneous fat) and blood neutrophils and monocytes of obese diabetic (n=20) and non-diabetic subjects (n=21) and compared with non-obese and non-diabetic controls (n=5). RT-PCR study of the biopsy samples showed significantly increased TREM-1, CD68 and CD16 and decreased TREM-2 expression levels in obese diabetic patients compared to obese non-diabetics and non-obese subjects. Based on the findings of dual immunofluorescence studies, we found that the levels of TREM-1 were significantly (p<0.05) up-regulated and co-localized with CD68 or CD16 in the biopsy tissue samples of obese diabetic patients; however, the levels of TREM-2 were co-localized with CD68 or CD16 was significantly (p<0.05) down regulated in obese diabetic patients compared to obese non-diabetics and non-obese patients. TREM-1 was significantly over-expressed in the liver and blood neutrophils and monocytes of all obese subjects with a HOMA-IR index of >2. Overall, the obese diabetic population had shown increased infiltration of myeloid cells and TREM-1 expression in liver (100% vs 28.6%, p<0.0001), Omentum (100% vs 57.1%, P=0.001), subcutaneous (75% vs 38.1%, p=0.019) and serum (soluble-TREM-1; 100% vs 28.6%, p<0.0001) compared to obese non-diabetics. In conclusion, we found a remarkable infiltration of myeloid cells and significantly elevated TREM-1 levels in biopsied tissues and blood of obese diabetic patients. Thus, TREM-1 could serve as potential biomarker for the development of insulin resistance in obese patient.

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