Endocrine Abstracts

Introduction: DNA methylation is one of the epigenetic mechanisms existing to regulate gene expression. It is believed that methylation of DNA is susceptible of change by environmental and nutritional factors. Thus, epigenetics provides a mechanism which may explain the etiology of some metabolic disorders and obesity.

Aim: The aim of this study is to analyze the DNA methylation level of several lipoprotein lipase (LPL)-promoter-CpG island in human visceral adipose tissue (VAT), as well as the gene and protein expression of this gene.

Material and methods: A total of 90 VAT samples were obtained during bariatric or hiatal hernia surgeries. Biochemical parameters from these patients were measured, and samples were assigned to two groups attending their BMI (BMI<30, BMI>30). We also assigned the samples according to glucose status in pre-diabetic/diabetic subjects (NG<100 mg/dl, P/D>100 mg/dl). Methylation level was measured through pyrosequentation, using the Pyromark technology and predesigned CpG methylation assays (Qiagen). The results were analyzed using the CpG methylation software (Qiagen) and the statistical package SPSS.

Results: We found higher levels of DNA methylation in P/D respect to NG subjects, while the gene expression was inverse. There was also a significant difference between subjects with BMI<30 and subjects with BMI>30, being lower the DNA methylation and higher the gene expression respectively. There was the same tendency in protein expression, with lower levels in PD subjects and lower levels in subjects with BMI>30. Furthermore, LPL methylation and LPL gene expression correlated negatively. LPL methylation correlated positively with insulin, glucose, triglycerides, and HOMA-IR. There was a negative correlation between LPL gene expression with BMI and glucose.

Conclusion: LPL gene expression is related to the methylation level in its promoter. LPL methylation and LPL gene expression is associated to metabolic profile and BMI.