Endocrine Abstracts

Obesity is defined as a state of chronic low-grade inflammation. It is associated with pro-inflammatory activity of visceral adipose tissue, regarded as a neuroendocrine organ that secretes cytotoxins and other pro-inflammatory factors, impairing metabolic pathways. The corollary of these changes is the risk of developing comorbidities. There are many similarities in the mechanisms of ageing and in obesity. The process of ageing leads to the accumulation of pro-inflammatory factors, activation of transcription factors responsible for promoting ageing (NFkB), impaired autophagy, impaired immune system function and increased senescence cells. Telomere length, levels of DNA damage and levels of inflammatory markers are considered hallmarks of ageing. Other markers of biological age are the level of cognitive function and metabolic age. The aim of this prospective cohort study was to assess the markers of premature ageing in people with extreme obesity: telomere length, DNA damage levels, IL-6 levels, cognitive function and metabolic age. All patients were recruited in 2nd Department of General Surgery in Jagiellonian University Medical College from July 2020 to May 2021. 133 patients were included and divided into two groups: SG - the extremely obese group (BMI >= 40 kg/m2 or >= 35 kg/m2 with comorbidity, n=100) and CG - the group of healthy volunteers (BMI between 18.5 and 24.9 kgm2, n=33). Blood samples were collected for serum and EDTA, DNA material was isolated for PCR telomere length assessment and enzymatic evaluation of 8-OHdG, the Wisocisin Card Sorting Test and the Colour Linkage Test were performed and body composition was analysed by bioimpedance. The SG group showed significantly shorter telomeres compared to CG (3957.4 vs 5191.53 bp) (P=0.009), higher IL-6 levels (4.57 vs 1.19) (P<0.001) and higher metabolic age (56.18+-9.85 vs 37.12+-12.8 years) (P<0.001). IL-6 levels were significantly influenced by percentage body fat (P=0.043). There were no statistically significant differences in cognitive function or levels of DNA damage in the extremely obese subjects compared to the control group. Obese patients are at a premature stage of ageing in terms of metabolic age and molecular age understood as telomere length. Elevated levels of chronic inflammation associated with body fat may be a factor in premature ageing.