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2
3.53; P 0.06): hypothyroidism was overt in seven
obese andnocontrol (
2
5.39; P0.05) andsubclinical
in 10 obese and 5 controls. Thyroid autoantibodies were
found in 39 obese and 15 controls (23.6 vs. 12.7%;
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J Clin Endocrinol Metab, August 2010, 95(8):39653972 jcem.endojournals.org 3969
vated TSH (28); and no association links BMI to TPOAb
(9). The prevalence of AITDin obesity spans from12.4%
inchildrento1016%inadults (25, 26), a figure that does
not seemto vary significantly fromour results. In fact, the
rate of AITD herein observed in obesity doubled that of
lean subjects, and nearly 60%of obese patients with high
TSHtested positive for AITD, therefore suggesting an un-
derlying autoimmune thyroid disorder. A recent study
(26) found a lower prevalence of AITD-associated hypo-
thyroidismcomparedwithhypothyroidismwithout AITD
(17 vs. 31 cases, respectively), a surprising circumstance
that questions the diagnostic value of abnormal TSH el-
evation in obesity. At variance with our study, however,
this latter investigation included patients with a wide age
range regardless of menopausal status and previous treat-
ment with T
4
. Importantly, we failed to document asso-
ciations between AITDand body composition, glucolipid
homeostasis, proinflammatory state, or any variable re-
lated to weight accrual and the development of obesity.
Although bio-impedance analysis-derived body composi-
tion cannot reflect body composition as well as dual x-ray
absorptiometry, our results appear toparallel those seenin
the general population (7, 9).
Althoughgenetic andenvironmental factors are known
contributors of AITD, the link between obesity and thy-
roid autoimmunity remains primarily undefined. It is
known that obesity enhances susceptibility to infections
(29), promotes a low-grade chronic proinflammatory
TABLE 3. Spearmans correlation analysis on pooled data obtained from both study groups
Sex BMI Obesity %FM REE AITD Leptin TSH FT
3
FT
4
HOMA-IR
Age
0.02 0.02 0.01 0.03 0.03 0.1 0.02 0.09 0.1 0.16 0.15
P 0.01 0.02
Sex
0.17 0.08 0.31 0.58 0.25 0.39 0.15 0.08 0.07 0.20
P 0.01 0.0001 0.0001 0.0001 0.0001 0.02 0.001
BMI
0.83 0.79 0.68 0.04 0.68 0.21 0.21 0.21 0.56
P 0.0001 0.0001 0.0001 0.0001 0.001 0.001 0.001 0.0001
Obesity
0.82 0.57 0.08 0.73 0.07 0.21 0.22 0.44
P 0.0001 0.0001 0.0001 0.001 0.001 0.0001
FM (%)
0.33 0.13 0.87 0.13 0.15 0.20 0.41
P 0.0001 0.03 0.0001 0.03 0.02 0.001 0.0001
REE
0.05 0.21 0.04 0.13 0.13 0.50
P 0.001 0.05 0.05 0.0001
AITD
0.20 0.23 0.04 0.21 0.02
P 0.001 0.0001 0.001
Leptin
0.12 0.1 0.31 0.36
P 0.05 0.0001 0.0001
TSH
0.04 0.08 0.02
P
FT
3
0.16 0.03
P 0.01
FT
4
0.13
P 0.03
Any P 0.05 or 0.0001 are not detailed. For categorical variables: male 0 and female 1; non-obese 0 and obese 1; AITD-negative 0
and AITD-positive 1. FM, Fat body mass.
FIG. 3. Cumulative leptin data obtained in obese (gray boxes) and
control (white boxes) subjects after exclusion of TSH-RAb-positive
subjects. Data are expressed as means SD). NS, Not significant.
3970 Marzullo et al. Thyroid Autoimmunity and Leptin in Obesity J Clin Endocrinol Metab, August 2010, 95(8):39653972
state that favors metabolic complications (30), and acti-
vates inflammatory pathways ensuing a greater cancers
risk (31). The adipocytokines IL-6 and leptin inhibit reg-
ulatory T cells (32), and obesity alters cell-mediated Th-1
immune response thereby generating defects in CD3
and
CD4
T-suppressor/cytotoxic cells
(3335). Leptin acts to regulate the Th-1 response (13, 36,
37) and has been shown recently to control T-cell energy
and, importantly, to regulate the proliferation of
CD4
CD25