Multisystem effects of obesity: dysregulation of leptin, thyroid hormones, autoantibodies, immune and neurological responses.

Abstract

Many changes occur in the levels of hormones, thyroid autoantibody, and some immune and neurological factors in people with obesity. It appears that these changes are a result, not a causes, of obesity. This research aimed to know the effect of obesity on the levels of leptin, leptin receptor, immunological marker, thyroid hormones, thyroid autoantibody and neurological marker. This study involved 80 participants aged 20-60 years. Of these, 40 were obese with BMI ≥30 and 40 with normal weight. Serum samples were collected for the analysis Leptin, soluble leptin receptor (SLEP-R), interleukin (IL-6), tumor necrosis factor (TNF)-α, Thyroid-Stimulating Hormone (TSH), free Triiodothyronine (FT3), free Thyroxine (FT4), thyroid autoantibody (TG-ab and TPO-ab) and neurological markers [Brain derived neurotrophic factor (BDNF), nerve growth factor (NGF), and noradrenalin (NA)]. There was a notable significant increase in leptin, but the level of SLEP-R decreased. While there was a significant increase in the level of IL-6, TNF-α, TSH, FT3, TG-ab, TPO-ab and NGF in obese patients. Also, there was significant decrease in FT4, BDNF and NA levels in obese patients compared to the control group. In conclusion, obesity is not just excess fat storage. It is associated with impaired leptin signaling, and an inflammation condition that affect the immune system, which cause changes in thyroid hormones and an increased risk of autoimmunity disorders.