**5.3. Adiponectin**

228 Thyroid Hormone

**5.1. Leptin** 

expenditure [83].

**5. Thyroid hormone effects on adipokines in weight loss** 

important than the overall weight loss [179, 183].

typically accompany weight loss [184].

leptin and thyroid hormones.

**5.2. Resistin** 

After weight loss, leptin levels decrease [178-180], as well TSH and T3 reduces to normal levels [92, 93, 112]. In starvation conditions, serum leptin levels decrease and thyroid hormones levels are quickly supressed, leading to a consequent reduction in energy

Varady et al. [181] studying severely obese women have suggested that a minimum weigh loss of 5% is required to improve adipokines profile, including the reduction of leptin levels. Not only a minimal weight loss is required but a maximal weigh loss beyond which further improvements in circulating adipokine levels are no longer observed has been suggested [179, 182]. The method or diet content by which weigh loss is achieved seems to be less

As mentioned before, studies investigating the correlation between thyroid hormones and leptin levels present conflicting results. Luvizotto et al. showed that administration of physiologic levels of T3 increases leptin mRNA expression with no influence on body weight in calorie-restricted obese rats [108], while administration of supraphysiological T3 dose promotes weight loss and diminishes serum levels and gene expression of leptin [108] (Figure 3). Again, as Syed et al. [106] reported, the effects of thyroid hormones in leptin concentrations might be indirect trough the regulation of fat mass (Figure 4). The decline of TSH release and T3 concentrations associated with decrease in leptin levels after weight loss may contribute to the compensatory reductions of energy expenditure and catabolism that

As both thyroid hormones and leptin have major roles in energy balance and regulation of body weight, an interaction between these hormones could not be discarded to achieve or maintain weight loss but further studies are necessary to elucidate the relationship between

Since obesity is considered a global epidemic and one of majors public health problem, affecting developed and developing countries [185, 186], and obese subjects may presente increased resistin levels [46], which can worse insulin resistance and inflammation [119], one of the most used strategies is the weight loss by reduction of caloric intake [187]. Caloric restriction affects the regulation of adipose tissue gene expression, normalizing the adipokines changes caused by obesity [10], while thyroid hormones play a central role in regulating adipose tissue metabolism [83], being related to body weight changes, thyroid hormones may therefore play a key role in the normalization of resistin in weight loss.

Nogueiras et al. [130] show a decrease in resistin mRNA expression in epididymal adipose tissue of pregnant and nonpregnant rats that were subjected to food restriction. Kim et al. [188] showed that resistin mRNA levels were decreased during fasting, but increased considerably Negative correlation between obesity and circulanting adiponectin has been well accept, and adiponectin concentration increases concomitantly to weight loss [190].

Experimental study on caloric restriction showed increased levels of circulating adiponectin [191]. Accordingly, Zhu et al. [194] showed that calorically restricted animals exhibited a significant increase in plasma adiponectin levels accompanied by significant decline in triglyceride levels, showing that adiponectin levels are inversely proportional to the degree of adiposity [192, 193].

Thyroid hormones perform a central role in adipose tissue metabolism regulation [83], which produces the biologically active substances adipocytokines, or adipokines, that include adiponectin [127, 194], indeed thyroid hormones share some physiological actions with adiponectin, such as reduction of body fat by increased thermogenesis and lipid oxidation [194].

The interaction between thyroid hormones and adiponectin concentration remains unclear. In humans, hyperthyroidism has been associated with both similar [128, 195] and elevated adiponectin concentrations [196], while experimental study with hyperthyroid rats found an increase in adiponectin serum concentration [133]. In agreement, some data shown that therapy to normalize hyperthyroidism significantly reduced circulating adiponectin levels [197]. In contrast Luvizotto et al. [189] show that thyroid hormone, at the doses of 5 and 25 μg T3 / 100 g BW, diminishes adiponectin gene expression, suggesting that thyroid hormone modulates negatively adiponectin expression in calorie-restricted obese rats (Figure 4).
