Preliminary Report
Effects of L-Thyroxine Therapy on Circulating Leptin and Adiponectin Levels in Subclinical Hypothyroidism: A Prospective Study

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Subclinical hypothyroidism (SCH) is defined by increased thyrotropin (TSH) and normal free thyroxine (fT4) levels. Controversial data are available regarding the effects of SCH on adipose tissue. Adiponectin and leptin are two major adipokines secreted from adipose tissue. We aimed to determine the levels of adiponectin and leptin in women with SCH and potential effects of L-thyroxine therapy on those levels.

Forty three women with SCH and 53 age- and BMI-matched healthy euthyroid control women were included. Adiponectin and leptin levels, total cholesterol (TC), triglycerides (TG), HDL-, and LDL cholesterol, fat mass (FM) and fat-free mass (FFM) were determined in all participants. Patients received L-thyroxine treatment for 6 months after which all measurements were repeated.

Patients with SCH and controls had similar baseline values for adiponectin, leptin, lipids, FM and FFM. All patients reached euthyroid status after 6 months of replacement therapy. Treatment resulted in an increase in adiponectin (p <0.01) and a decrease in leptin levels (p <0.05). Lipid levels, FM and FFM did not show a significant change.

Achievement of euthyroid status by replacement therapy increases adiponectin and decreases leptin levels in women with SCH in this prospective study independent of a change in body fat mass.

Introduction

Subclinical hypothyroidism (SCH) is defined as a serum thyroid-stimulating hormone (TSH) level above the upper limit of normal despite normal levels of serum free thyroxine (1). Although studies have demonstrated some adverse effects of SCH, there is neither a consensus regarding the clinical importance of the adverse effects nor the benefits of L-thyroxine therapy especially for patients with TSH levels <10 mIU/mL (1).

Adipose tissue is a hormonally active system that produces and releases different bioactive substances. Adiponectin and leptin are two of the adipokines released from adipose tissue and modulate homeostasis, lipid and glucose metabolism. Plasma adiponectin levels are correlated negatively with adiposity, insulin resistance, type 2 diabetes and metabolic syndrome. Leptin serves as a major ‘adipostat’ by repressing food intake and promoting energy expenditure. Independent of these, leptin improves peripheral insulin sensitivity and modulates pancreatic β-cell function (2).

Hypothyroidism appears to be associated with alterations in the function of adipose tissue. Controversial data are available regarding changes in circulating adipokine levels in hypothyroid patients. Studies conducted in patients mainly with overt hypothyroidism due to various causes reported low, normal or high circulating leptin levels, whereas circulating adiponectin levels were unaltered in the majority of the studies (3). Similar discordant results have been reported with normalization of hypothyroidism by L-thyroxine treatment in that leptin levels either increased 4, 5, 6, unaltered 7, 8 or decreased 9, 10, whereas adiponectin levels did not show a significant change (11).

It is not clear whether adipose tissue function and secretion of adiponectin and leptin are altered in SCH. The aim of the current study was to determine levels of adiponectin and leptin in women with SCH and potential effects of L-thyroxine therapy on those levels.

Section snippets

Subjects

Forty three regularly menstruating premenopausal women with SCH and 53 age- and BMI-matched healthy control women were included. All participants were >18 years of age with normal body weight. SCH was defined as a TSH level >4.5 mIU/L associated with normal free thyroxine (fT4) (normal range: 12–22 pmol/l) and free triiodothyronine (fT3) (normal range 3.1–6.8 pmol/L) levels. Patients with a history of radioiodine exposure or thyroid surgery were excluded. Other exclusion criteria were

Results

Clinical, hormonal and metabolic characteristics of the patients and controls are shown in Table 1. Patients with SCH had higher TSH (p <0.001) and lower fT4 levels (p <0.001) than controls at baseline. The two groups had similar values for other clinical and laboratory parameters (Table 1). Leptin and adiponectin did not correlate with TSH or free thyroid hormones in patients and controls using Spearman’s correlation.

All patients with SCH reached euthyroid status after 6 months of L-thyroxine

Discussion

We report here that premenopausal women with SCH have similar adiponectin and leptin levels in comparison with age- and BMI-matched healthy women. Achievement of euthyroid status by replacement therapy increases adiponectin and decreases leptin levels. These alterations do not appear to be accompanied by any change in body fat amount or distribution.

Studies comparing hypothyroid patients with euthyroid controls have reported normal, decreased or increased serum leptin levels (11). Leptin

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