ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P740

Serum ghrelin levels are increased in hypothyroid patient and become normalized after L-thyroxin treatment

Signe Gjedde1, Esben Thyssen Vestergaard1, Lars Christian Gormsen2, Anne Lene Riis1, Jorgen Rungby3, Niels Moller1, Jorgen Weeke1 & Jens Otto Jorgensen1

1Medical Department M (Endocrinology and Diabetes), Aarhus University Hospital, Aarhus, Denmark; 2Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital, Aarhus, Denmark; 3Medical Department C and Department of Pharmacology, Aarhus University Hospital, Aarhus, Denmark.

Context: An interaction between gut-derived ghrelin, which is implicated in the regulation of short- and long-term energy balance, and thyroid function has previously been reported in patients with hyperthyroidism, in whom ghrelin levels are reversibly suppressed. In the present study, we measured total serum ghrelin levels and pertinent metabolic indices in hypothyroid patients before end after L-thyroxin replacement.

Patients and methods: Eleven patients were examined twice: 1) in the hypothyroid state, and 2) after at least 2 months of euthyroidism. Ten healthy subjects served as a control group. Ghrelin was measured in conjunction with indirect calorimetry and a hyperinsulinemic euglycemic clamp.

Results: Serum ghrelin levels were increased by 32% under basal conditions in the hypothyroid state (PRE) as compared to post treatment (POST) (pg/ml): 976.4±80.8 vs 736.8±67.1 (P<0.001). This difference prevailed during the clamp but a decline was observed in both states: 641.4±82.2 vs 444.3±66.8 μg/ml (P=0.005). The hypothyroid state was associated with decreased resting energy expenditure, increased respiratory quotient and insulin resistance. Serum ghrelin levels as well as the metabolic aberrations became normalised after L-thyroxin replacement as compared to the control subjects.

Conclusion: Serum ghrelin levels are reversibly increased in hypothyroid patients. It remains to be investigated whether this represents a direct effect of iodothyronines or a compensatory response to the abnormal energy metabolism in hypothyroid patients.

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