Purchase this article with an account.
Michele Crisp, Kerry Jo Starkey, Carol Lane, Jack Ham, Marian Ludgate; Adipogenesis in Thyroid Eye Disease. Invest. Ophthalmol. Vis. Sci. 2000;41(11):3249-3255.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. Adipogenesis contributes to the pathogenesis of thyroid eye disease
(TED). Thyrotropin receptor (TSHR) transcripts are present in orbital
fat. This study was conducted to determine whether they are expressed
as functional protein, and if so, whether this is restricted to TED
orbits or to a particular stage in adipocyte differentiation.
methods. Samples of fat were obtained from 18 TED-affected orbits and 4 normal
orbits, and 9 were obtained from nonorbital locations. Frozen sections
were examined by immunocytochemistry using monoclonal antibodies
specific for the human TSHR. Samples were disaggregated and the
preadipocytes separated from the mature by differential centrifugation
and cultured in serum-free or DM and examined for morphologic changes,
oil red O and TSHR staining, and TSH-induced cyclic adenosine
monophosphate (cAMP) production.
results. Marked immunoreactivity was observed in frozen sections from all three
TED samples and faint staining in both normal orbital fat samples. In
vitro, 1% to 5% of preadipocytes displayed TSHR immunoreactivity in
five of six TED and two of three normal orbital samples and in three of
five nonorbital samples. Differentiation, was induced in all 14 orbital
samples. Three of four nonorbital samples contained occasional
differentiated cells. Fifty percent to 70% of differentiating cells
demonstrated receptor immunoreactivity. Two of three TED and four of
four nonorbital preadipocytes in DM and/or mature adipocytes displayed
a TSH-mediated increase in cAMP.
conclusions. The results indicate that orbital fat TSHR transcripts are expressed as
protein, which can be functional. This is not aberrant in TED orbits,
although expression may be upregulated. The majority of preadipocytes
undergoing differentiation express the receptor, indicating a key role
for this population in one mechanism for increasing orbital
This PDF is available to Subscribers Only