Obesity is considered the most common metabolic disorder in the world21,22, being considered a public health problem that affects both developed and developing countries23. Obesity occurs when energy consumption exceeds energy expenditure21 and is mainly characterized by excessive adipose tissue (AT)24,25. The amount and distribution of adipose tissue are associated with many adverse consequences, such as hypertension, type 2 Diabetes Mellitus or cardiovascular diseases26.
Approaches used to deal with individuals with obesity include food restriction and physical exercise27. According to some authors, the determination of individualized epigenetic profiles can be used to guide clinical decision-making, in the progression of treatment to improve the health and quality of life of people with obesity28. Pharmacological therapy has been used to treat obesity, but its success is relative and sometimes it does not overcome their adverse effects29. Thus, bariatric surgery is the most effective treatment for weight loss and maintenance. Weight loss with bariatric surgery can reach 50–75% of excess body weight and can be maintained for a long period or for life depending on the patient's lifestyle30,31.
In our study, bariatric surgery proved to be efficient in controlling the obesity of the evaluated patients, since 100% of the patients had a decrease in the degree of obesity, leaving morbid obesity in the 4 groups presented. Concomitantly, there was an improvement in lipid profiles with a reduction in total cholesterol and triglyceride levels, which indicates that a smaller amount of adipose tissue combined with a reduction in caloric intake leads to metabolic improvement32. The reduced levels of blood glucose in the postoperative period also indicate the influence that adipose tissue can promote on carbohydrate metabolism, acting mainly on the insulin resistance of patients33.
Studies show improvement in metabolic parameters in the postoperative period as a result of normalization of fasting blood glucose, decrease in insulinemia and calculation of insulin resistance by the Homeostasis Assessment Model of Insulin Resistance (HOMA-IR)34, in addition to an increase in the levels of glucagon-like peptide 1 (Glucagon-like peptide-1, GLP-1) and Peptide YY, which are hormones produced by the intestines that play an anorectic role in controlling hunger and satiety35. The increase in these hormones was attributed to the faster arrival of food in the ileum without being completely digested33.
Several studies have demonstrated the relationship between thyroid function and weight status, especially in obesity. Different studies, mainly of cross-sectional design, have found an association between changes in TSH and thyroid hormone levels, even within the normal range, and a higher body mass index 13,36,37,38.
The relationship between serum TSH levels and obesity is widely studied. It is described in the literature that obese populations have increased TSH levels23; however, the pathophysiological mechanism responsible for this metabolic adjustment is still undetermined39. The present study demonstrated a significant positive relationship between the change in BMI classification due to weight loss, and the decrease in serum TSH levels. Many authors have studied the influence of adipokines in this process. Among them, leptin would play an important role in this scenario. It is believed that leptin can mediate both obesity and TSH factors. Produced by adipocytes, leptin is a substance that acts on hypothalamic cells informing the central nervous system about satiety13, as well as at the hypothalamic level, modulating the stimulation of pituitary secretion of TSH40.
At the same time, it is known that TSH has an effect on adipose tissue and directly promotes that is, without the involvement of thyroid hormones - the differentiation of preadipocytes into adipocytes41. Thus, obesity is a scenario in which the individual has high levels of leptin13 with greater stimulus for TSH secretion, which will act on adipose tissue, stimulating adipogenesis or accumulation of lipids in existing adipocytes that will secrete more leptin, who in its turn stimulates neurons in the hypothalamic supraventricular nucleus to secrete more TRH and, consequently, an even greater TSH secretion. This mechanism could be part of an adaptive response to supply the high thermogenesis resulting from the increase in the amount of body fat13.
TSH may represent a marker of altered energy, with high levels of TSH being a metabolic adjustment for adiposity, as it directly stimulates adipogenesis independent of thyroid hormones.
This alteration in the thyroid axis in obesity may represent a metabolic alert of these individuals, suggesting that obesity is the cause of this alteration and instead of initiating treatments for subclinical hypothyroidism, one should first treat the obesity status of these individuals. Studies have shown that individuals with an established diagnosis of subclinical hypothyroidism who did not receive hormone treatment had a reduction and consequent normalization of TSH within a 12 months period after bariatric surgery42. However, our study demonstrated that the treatment of obesity through bariatric surgery already results in benefits for the patient within the first six months of evolution, resulting in the reduction of TSH levels in obese euthyroid individuals.