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Adaptive Contribution of Thyroid Hormones in Obesity

Nowadays, obesity is seriously threatening healthy life in all societies, especially in developed societies. Obesity is showing its likely effects through biologically active substances called adipokines. The most familiar of these is leptin. Leptin is synthesized in directly proportional to the amount of adipose tissue and reduced appetite by stimulating the satiety center. This status is like a protective mechanism that tries to reverse severe pathological process. Similar to this behavior of leptin, thyroid hormones are increasing in the advanced stages of obesity, increasing the resting energy expenditure (REE). The accelerating oxidative phosphorylation causes the use of energy as heat, the energy that has not transformed into ATP, together with ATP synthesis. This situation, the significant portion of energy provides to consumed instead of storing as fat. In addition, finding that T3 accelerates glucose transport and the TCA cycle without changing the rate of ATP synthesis in skeletal muscles suggests that thyroid hormones may be an effective tool in standing against obesity. In addition of that, the presence of studies indicating that thyroid hormones have an increasing tendency in the advanced stages of obesity is likely thought to be a rescuer mechanism to increase the effectiveness of suppressed thyroid hormones. On the contrary of these ideas, having been reported suppressing 5’-deiodinease enzyme activity in chronic diseases causes anxiety about the effectiveness of thyroid hormones in obesity. Based on available information, we aimed to prepare a review evaluating of this adaptive condition of thyroid hormones. DOI: 10.14302/issn.2641-9181.ijnr-18-2530 Corresponding author: Fatih Ozcelik, Department of Medical Biochemistry, University of Health Sciences, Faculty of Medicine, 34668, Istanbul, Turkey, Tel: +90 216 5422020 Fax: +90 216 5422010 Email: 68ozcelik@mynet.com


Introduction
Nowadays, obesity has become the leading health problem with its increasing prevalence day by day. Because of the effects on all systems in the advanced stages of obesity is seriously threatening healthy life. In addition, thereby obesity cause significant effects on endocrine, cardiovascular, respiratory, gastrointestinal and leukomotor systems, increasing the morbidity and mortality of the society.
With a simple definition is that obesity is an observed situation a result of taking more energy than needed.
Genetic structure, endocrine conditions affecting the metabolism (such as Cushing's disease, hypothyroidism and polycystic ovary syndrome), nutritional habits, the psycho-social and cultural factors the interaction of one or more these factors are the main causes of obesity.
Obesity, which is characterized by an abnormal increase in the amount of adipose tissue, is the most common chronic disease of our age in developed and developing countries [1,2]. According to the latest data shared by the World Health Organization (WHO), the incidence of obesity is increasing among European countries as in the USA. It was found that obesity, having become a serious public health problem in developed societies was associated with insulin resistance, diabetes, atherosclerosis, hypertension, chronic kidney disease, and increasing cardiovascular morbidity and mortality [3,4].
The main role of adipose tissue is to store energy. It fulfills this role by storing fat transported through lipoproteins or by synthesizing fatty acid from glucose [5]. In addition, physical preservation, as well as showed that white adipose tissue was also an endocrine organ [6]. Since then, white adipose tissue has been found to release many adipokines having several functions. Interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) secreted from macrophages in adipose tissue were also counted among adipokines. IL-6 has been found to have a regulating effect on other adipokines and reported that decrease adiponectin levels [7]. Likewise, TNF-α has been found to have regulatory effects on other adipokines (reducing adiponectin levels and increasing leptin levels). With reduced the development of obesity, and decreased insulin and leptin levels have been reported in animal studies in which the effect of TNF-α was blocked [8,9].
Recently, adipokines have been found to be secreted from other cells, except for adipocyte cells.  Therefore, brain tissue is considered to be the main site for the plasma T3 to be transformed by inactivation (cleaning) and plasma rT3 production [37][38][39][40][41] obesity, which is commonly seen in chronic diseases, will probably be negatively affected by the transformation of T4 to T3 since D2 is suppressed ( Figure 2). Therefore, more rT3 formation will occur. However, more conclusive evidence is needed.

Important in Energy Metabolism of Thyroid Hormones
It is known that thyroid hormones play an  Considering the effects of thyroid hormones on metabolism, the relationship between obesity and thyroid hormone will be better understood. That is, the effect of T3 on Na + /K + -ATPase is well known [66] and T3 increases the ATP consumption by accelerating the activity of Na+/K+-ATPase in almost all tissues.
Accelerating oxidative phosphorylation leads to the use of energy as heat instead of converted to ATP, as well as the synthesis of ATP. Therefore, O2 consumption and metabolic rate will increase [67]. Thus, it will be ensured that the excess energy is consumed instead of storing it as fat.
Thyroid hormones increase the sensitivity of β-adrenergic receptors to catecholamines and then stimulate respiration, heart rate and systole (Figure 3).
To achieve this, the rate of glucose metabolism through glycogenolysis and gluconeogenesis will increase. In