Abstract
Thermogenesis is the production of heat that occurs in all warm-blooded animals. During cold exposure, there is obligatory thermogenesis derived from body metabolism as well as adaptive thermogenesis through shivering and non-shivering mechanisms. The latter mainly occurs in brown adipose tissue (BAT) and muscle; however, white adipose tissue (WAT) also can undergo browning via adrenergic stimulation to acquire thermogenic potential. Thyroid hormone (TH) also exerts profound effects on thermoregulation, as decreased body temperature and increased body temperature occur during hypothyroidism and hyperthyroidism, respectively. We have termed the TH-mediated thermogenesis under thermoneutral conditions “activated” thermogenesis. TH acts on the brown and/or white adipose tissues to induce uncoupled respiration through the induction of the uncoupling protein (Ucp1) to generate heat. TH acts centrally to activate the BAT and browning through the sympathetic nervous system. However, recent studies also show that TH acts peripherally on the BAT to directly stimulate Ucp1 expression and thermogenesis through an autophagy-dependent mechanism. Additionally, THs can exert Ucp1-independent effects on thermogenesis, most likely through activation of exothermic metabolic pathways. This review summarizes thermogenic effects of THs on adipose tissues.
Highlights
These findings show that exogenous levothyroxine can increase glucose uptake in the brown adipose tissue (BAT) during cold exposure [60], and higher levels of thyroid hormones are associated with higher amounts of cold-induced BAT activity
thyroid hormone (TH) induced TRβ-mediated browning in the inguinal white adipose tissue (WAT), the induction of browning did not increase glucose or triglyceride-rich protein uptake at thermoneutrality [104]. These data suggesting TRβ-selective GC-1-activated browning of the WAT and thermogenesis are difficult to reconcile with the TRα KO data showing that lack of functional TRα impaired thermogenesis during cold exposure
Sympathetic activation appears to be the main driver for thermogenic activation; the induction of deiodinase 2 (Dio2) in the BAT and WAT during cold exposure strongly implicates an indispensable role of intracellular T3 in adipose tissues during thermogenesis
Summary
Thermogenesis is an essential survival mechanism for homeotherms. Obligatory thermogenesis is sufficient to maintain body temperature and normal body function when the ambient temperature is at thermoneutrality, which is about 23 ◦C for an adult man [1]. Chronic cold exposure causes metabolic changes in the BAT to maximize β-oxidation of fatty acids, electron transport activity, and Ucp expression to generate heat [6,13,14]. SNS stimulation in response to cold induces competent white adipocytes to express Ucp and various BAT-associated genes such as Cidea and Cox7a1 in a process known as browning/beiging. These beige adipocytes increase their mitochondria levels and, in conjunction with the induction of Ucp expression, acquire the thermogenic capability [10].
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