AGER-1 Long Non-Coding RNA Levels Correlate with the Expression of the Advanced Glycosylation End-Product Receptor, a Regulator of the Inflammatory Response in Visceral Adipose Tissue of Women with Obesity and Type 2 Diabetes Mellitus

The advanced glycosylation end-product receptor (AGER) is involved in the development of metabolic inflammation and related complications in type 2 diabetes mellitus (T2DM). Tissue expression of the AGER gene ( ) is regulated by epigenetic mediators, including a long non-coding RNA AGER-1 (lncAGER-1). This study aimed to investigate whether human obesity and T2DM are associated with an altered expression of and lncAGER-1 in adipose tissue and, if so, whether these changes affect the local inflammatory milieu. The expression of genes encoding AGER, selected adipokines, and lncAGER-1 was assessed using real-time PCR in visceral (VAT) and subcutaneous (SAT) adipose tissue. VAT and SAT samples were obtained from 62 obese (BMI > 40 kg/m ; = 24 diabetic) and 20 normal weight (BMI = 20-24.9 kg/m ) women, while a further 15 SAT samples were obtained from patients who were 18 to 24 months post-bariatric surgery. Tissue concentrations of adipokines were measured at the protein level using an ELISA-based method. Obesity was associated with increased mRNA levels in SAT compared to normal weight status ( = 0.04) and surgical weight loss led to their significant decrease compared to pre-surgery levels ( = 0.01). Stratification by diabetic status revealed that mRNA levels in VAT were higher in diabetic compared to non-diabetic women ( = 0.018). Elevated mRNA levels in VAT of obese diabetic patients correlated with lncAGER-1 ( = 0.04, r = 0.487) and with interleukin 1β ( = 0.008, r = 0.525) and resistin ( = 0.004, r = 0.6) mRNA concentrations. In conclusion, obesity in women is associated with increased expression of in SAT, while T2DM is associated with increased mRNA levels and pro-inflammatory adipokines in VAT.