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Review
. 2021 Sep 7;18(18):9434.
doi: 10.3390/ijerph18189434.

Obesity and Thyroid Axis

Krzysztof Walczak  1 , Lucyna Sieminska  2
Affiliations
Review

Obesity and Thyroid Axis

Krzysztof Walczak et al. Int J Environ Res Public Health. .

Abstract

Development of obesity is primarily the result of imbalance between energy intake and energy expenditure. Thyroid hormones influence energy expenditure by regulating cellular respiration and thermogenesis and by determining resting metabolic rate. Triiodothyronine influences lipid turnover in adipocytes and impacts appetite regulation through the central nervous system, mainly the hypothalamus. Thyroid-stimulating hormone may also influence thermogenesis, suppress appetite and regulate lipid storage through lipolysis and lipogenesis control. Subclinical hypothyroidism may induce changes in basal metabolic rate with subsequent increase in BMI, but obesity can also affect thyroid function via several mechanisms such as lipotoxicity and changes in adipokines and inflammatory cytokine secretion. The present study investigated the complex and mutual relationships between the thyroid axis and adiposity.

Keywords: TSH; adipokines; adipose tissue; obesity; thyroid.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The size of adipocytes is the result of the balance between lipogenesis, lipolysis and fatty acid oxidation; these processes are regulated by THs and TSH.
Figure 2
Figure 2
Adipose tissue grows by two mechanisms: hyperplasia (increased number of fat cells) and hypertrophy (increased adipocyte volume). The differentiation of progenitor cells through preadipocytes into adipocytes, as well as the proliferation of adipocytes, is also under TSH/THs control.
Figure 3
Figure 3
In conditions of excessive caloric supply, leptin activates TRH expression and then synthesis of TSH and THs. It suppresses appetite and promotes energy expenditure by increasing lipolysis and thermogenesis. In obese people, leptin can activate DIO expression and can increase conversion of T4 to T3. THs play a role in the browning of adipose tissue.
Figure 4
Figure 4
Adipose tissue dysfunction through insulin resistance, altered secretion of adipocytokines and inflammatory state are involved in the development of diabetes mellitus and vascular diseases. The excess of adipose tissue may initiate the lipotoxicity and inflammatory process within the thyroid gland. That leads to the dysfunction of the thyroid gland and results in an energy imbalance. FGF21 is produced mainly by the liver, under T3 control. In the liver, FGF21 increases β-oxidation of fatty acids and downregulates lipogenesis. In WAT, FGF21 stimulates lipolysis and the browning process.
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