Horm Metab Res 2007; 39(12): 867-870
DOI: 10.1055/s-2007-992131
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Chronic Leptin Treatment Inhibits Liver Mitochondrial α-Glycerol-β-phosphate Dehydrogenase in Euthyroid Rats

E. Oliveira 1 , A. T. S. Fagundes 1 , S. B. Alves 1 , C. C. Pazos-Moura 2 , E. G. Moura 1 , M. C. F. Passos 3 , P. C. Lisboa 1
  • 1Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Brazil
  • 2Laboratório de Endocrinologia Molecular, Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil
  • 3Departamento de Nutrição Aplicada, Instituto de Nutrição, Universidade do Estado do Rio de Janeiro, Brazil
Further Information

Publication History

received 05.03.2007

accepted 19.04.2007

Publication Date:
31 October 2007 (online)

Abstract

Leptin modulates the hypothalamus-pituitary-thyroid axis and peripheral metabolism of thyroid hormones (THs). We have studied the effect of acute and chronic leptin treatment upon liver mitochondrial glycerol phosphate dehydrogenase activity (mGPD), whose expression and activity are TH dependent. We performed 2 experiments: 1) acute leptin treatment - LepA: adult rats received a single leptin injection (8 μg/100 g BW); 2) chronic leptin treatment - LepC: adult rats received leptin (8 μg/100 g BW) daily, for 6 days. In both experiments, control groups were saline-treated. All rats were sacrificed 2 hours after the last dose. Liver mGPD activity was determined by colorimetric method. Liver D1 activity was measured by the release of 125I from 125I-rT3. Serum hormones were measured by RIA. LepA rats showed higher serum thyroid stimulating hormone (TSH) (+ 64%, p<0.05), free T4 (+ 34%, p<0.05), free T3 (+ 64%, p<0.05), and liver D1 activity (+ 85%, p<0.05), but no change in mGPD activity. Since THs increase mGPD activity, the unchanged level in the acute experiment is suggestive of an inhibitory role of leptin. LepC rats presented lower mGPD activity (-1.7-fold, p<0.05) and higher liver D1 activity (+ 32%, p<0.05), but no alteration in serum TSH and free THs. Our results show that leptin downregulates mGPD activity, mainly when hyperleptinemia is chronic.

References

Correspondence

Dr. P. C. Lisboa

Departamento de Ciências Fisiológicas - 5° andar

Instituto de Biologia

Universidade do Estado do Rio de Janeiro

Av. 28 de setembro, 87

20551-030 Rio de Janeiro

Brazil

Phone: +55/021/2587 61 34

Fax: +55/021/2587 61 29

Email: [email protected]

Email: [email protected]