Thyrotropin decreses leptin production in rat adipocytes

• Published in: Metabolism, clinical and experimental clinical and experimental, 1999-12, Vol.48 (12), p.1570-1574
• Main Authors: Shintani, Mitsuyo, Nishimura, Haruo, Akamizu, Takashi, Yonemitsu, Shin, Masuzaki, Hiroaki, Ogawa, Yoshihiro, Hosoda, Kiminori, Inoue, Gen, Yoshimasa, Yasunao, Nakao, Kazuwa
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/S0026-0495(99)90247-0

Leptin, which is secreted from adipocytes, has a role in the regulation of appetite and energy expenditure. The thyrotropin receptor (TSH-R) was recently found in adipocytes. We examined the effects of TSH on leptin production and lipolysis in rat epididymal adipocytes. TSH decreased the concentration of leptin in the medium time (∼24 hours)- and dose (∼10 −7 mol/L)-dependently (half-maximal inhibition [IC 50] ≈ 10 −9 mol/L). TSH also decreased the ob mRNA level approximately 55% in adipocytes. We confirmed the presence of TSH-R mRNA in the adipocytes by reverse transcription-polymerase chain reaction (RT-PCR). TSH stimulated glycerol release dose-dependently (IC 50 ≈ 10 −8 mol/L) in adipocytes. This TSH-induced glycerol release was further enhanced by adenosine deaminase (ADA). In summary, TSH reduced leptin production and stimulated lipolysis in rat epididymal adipocytes. Although the pathophysiological relevance of the regulation of leptin production and lipolysis by TSH is unknown, we speculate that TSH may affect the regulation of appetite and energy expenditure in pathophysiological states.