Short-term hyperthyroidism has no effect on leptin levels in man.

Leptin, a 16-kDa adipocyte-derived protein whose circulating levels reflect energy stores, increases the resting metabolic rate and thermogenesis in rodents. Thyroid hormones also increase the basal metabolic rate, but nothing is known about possible interactions between leptin and thyroid hormone. Activation of beta-adrenergic receptors decreases leptin levels in rodents. To test the hypothesis that thyroid hormones, by causing a "functional hyperadrenergic" state, result in decreased leptin concentrations in humans, we studied 22 normal healthy men before and after the administration of T3 for 1 week to induce moderate hyperthyroidism. Short term thyroid hormone excess does not alter circulating leptin concentrations despite a demonstrated effect on heart rate, systolic blood pressure, cholesterol levels, and metabolic indexes of bone turnover. Elucidation of the apparently separate pathways by which thyroid hormones, beta-agonists, and leptin regulate energy expenditure and food intake may have important implications for our understanding of the mechanisms for regulating energy homeostasis in health and disease.

[1]  C. Mantzoros,et al.  Activation of β3 Adrenergic Receptors Suppresses Leptin Expression and Mediates a Leptin-Independent Inhibition of Food Intake in Mice , 1996, Diabetes.

[2]  L. Slieker,et al.  Regulation of Expression of ob mRNA and Protein by Glucocorticoids and cAMP (*) , 1996, The Journal of Biological Chemistry.

[3]  J. Friedman,et al.  Abnormal splicing of the leptin receptor in diabetic mice , 1996, Nature.

[4]  R. Considine,et al.  Serum immunoreactive-leptin concentrations in normal-weight and obese humans. , 1996, The New England journal of medicine.

[5]  Rene Devos,et al.  Identification and expression cloning of a leptin receptor, OB-R , 1995, Cell.

[6]  E. Ravussin,et al.  Leptin levels in human and rodent: Measurement of plasma leptin and ob RNA in obese and weight-reduced subjects , 1995, Nature Medicine.

[7]  Janet,et al.  Recombinant ob protein reduces feeding and body weight in the ob/ob mouse. , 1995, The Journal of clinical investigation.

[8]  J. Weissenbach,et al.  The human obese (OB) gene: RNA expression pattern and mapping on the physical, cytogenetic, and genetic maps of chromosome 7. , 1995, Genome research.

[9]  R. Devos,et al.  Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks. , 1995, Science.

[10]  M. Pelleymounter,et al.  Effects of the obese gene product on body weight regulation in ob/ob mice. , 1995, Science.

[11]  Steven L. Cohen,et al.  Weight-reducing effects of the plasma protein encoded by the obese gene. , 1995, Science.

[12]  M. Maffei,et al.  Positional cloning of the mouse obese gene and its human homologue , 1994, Nature.

[13]  T. Rink.  In search of a satiety factor , 1994, Nature.

[14]  M. Holick,et al.  Therapy with parenteral pamidronate prevents thyroid hormone-induced bone turnover in humans. , 1993, The Journal of clinical endocrinology and metabolism.

[15]  E. Danforth,et al.  The role of thyroid hormones in the control of energy expenditure. , 1984, Clinics in endocrinology and metabolism.

[16]  J. Lian,et al.  Osteocalcin: isolation, characterization, and detection. , 1984, Methods in enzymology.

[17]  E. Danforth.  The role of thyroid hormones and insulin in the regulation of energy metabolism. , 1983, The American journal of clinical nutrition.

[18]  J. Cook,et al.  Factors Influencing the Assay of Creatinine , 1975, Annals of clinical biochemistry.