102
deficiency or autoimmune thyroiditis induced subclinical hypothyroidism, leptin
derived disturbance in hypothalamic-pituitary functions, partially disturbed negative feedback mechanism due to partial bio-inactivation of TSH proteins in obese
individuals, hormone resistance owing to increased TSH levels in obesity, increase
in TSH levels as a consequence of adaptation to increased resting energy expenditure (REE) to cope up with increased energy expenditure are postulated to be
important ones [15].
It has been reported that increased TSH level may not necessarily increase total
and free T4 levels in obese subjects. However, several studies have suggested a
moderate increase in the level of free and total T3 in obese individuals. Change in
Fig. 6.2 Release of leptin
under the influence of
adipocytes. The leptin
released as a result of
expanding adipocytes
causes the secretion of
thyrotropin-releasing
hormone (TRH) and
thyrotropin (TSH), via its
action on Janus activating
kinase (JAK)-2/signal
transducer and activator of
transcription (STAT)-3
factor, which in turn
sustains the secretion of
leptin. The circulating
leptin also stimulates the
suppressor of cytokine
signaling-3 (SOCS-3),
with ultimate inhibition of
leptin signalling (autoregulation) T4, thyroxine;
T3, tri-iodothyronine
Y. H. Khan et al.