Regulation of expression of leptin mRNA and secretion of leptin by thyroid hormone in 3T3-L1 adipocytes

Tadashi Yoshida, Toshiaki Monkawa, Matsuhiko Hayashi, Takao Saruta

Research output: Contribution to journalArticle

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Abstract

Leptin, the obese gene product, is secreted exclusively by adipocytes and regulates energy balance. We examined the effects of thyroid hormones on the regulation of leptin in 3T3-L1 adipocytes. Fully differentiated adipocytes were incubated with thyroid hormones, and the expression of leptin mRNA was measured by quantitative reverse transcription-polymerase chain reaction. After a 24-h incubation, triiodothyronine (T3) at 10-1000 nmol/l significantly increased the expression of leptin mRNA (237-337%). These stimulatory effects were not observed in preadipocytes. By contrast, thyroxine (T4) at 1-1000 nmol/l did not affect leptin mRNA expression in adipocytes. We also measured the levels of secreted leptin in conditioned media using radioimmunoassay. T3 at 10 and 1000 nmol/l significantly increased the levels of secreted leptin (132% and 126%, respectively) after a 24 h incubation. Our present data suggest that thyroid hormone is a novel regulator of leptin mRNA expression and protein secretion in 3T3-L1 adipocytes.

Original languageEnglish
Pages (from-to)822-826
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume232
Issue number3
DOIs
Publication statusPublished - 1997 Mar 27

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Leptin
Thyroid Hormones
Adipocytes
Messenger RNA
Polymerase chain reaction
Triiodothyronine
Transcription
Conditioned Culture Medium
Energy balance
Thyroxine
Reverse Transcription
Radioimmunoassay
Polymerase Chain Reaction

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Regulation of expression of leptin mRNA and secretion of leptin by thyroid hormone in 3T3-L1 adipocytes. / Yoshida, Tadashi; Monkawa, Toshiaki; Hayashi, Matsuhiko; Saruta, Takao.

In: Biochemical and Biophysical Research Communications, Vol. 232, No. 3, 27.03.1997, p. 822-826.

Research output: Contribution to journalArticle

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