TY - JOUR
T1 - Downregulation of leptin by free fatty acids in rat adipocytes
T2 - Effects of triacsin C, palmitate, and 2-bromopalmitate
AU - Shintani, Mitsuyo
AU - Nishimura, Haruo
AU - Yonemitsu, Shin
AU - Masuzaki, Hiroaki
AU - Ogawa, Yoshihiro
AU - Hosoda, Kiminori
AU - Inoue, Gen
AU - Yoshimasa, Yasunao
AU - Nakao, Kazuwa
N1 - Funding Information:
From the Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan. Submitted March 31, 1999; accepted August 26, 1999. Supported in part by research grants from the Japanese Ministry of Education, Science, and Culture, the Japanese Ministry of Health and Welfare, and the Insulin Research Foundation. Presented in part at the 57th Annual Meeting and Scientific Session of the American Diabetes Association, Boston, MA, June 21-24, 199Z Address reprint requests to Haruo Nishimura, MD, PhD, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-850Z Japan. Copyright © 2000 by W.B. Saunders Company 0026-0495/00/4903-0008510.00/0
PY - 2000
Y1 - 2000
N2 - Free fatty acid (FFA) has been reported to decrease leptin mRNA levels in 3T3-L1 adipocytes. When using this cell line, it is difficult to determine the protein levels because a very small amount of leptin is secreted into the medium. The effect of FFA on leptin secretion from adipocytes has not yet been determined. In addition, in vivo studies have failed to demonstrate a FFA-induced decrease in plasma leptin levels. To clarify the effect of FFA on leptin production, we investigated the leptin protein level in the medium and the mRNA level in primary cultured rat adipocytes treated with triacsin C, which is a potent inhibitor of acyl-coenzyme A (CoA) synthetase, palmitate, and 2-bromopalmitate. Triacsin C (0 to 5 x 10-5 mol/L) decreased leptin concentrations in the culture medium in a close-dependent manner. Leptin mRNA levels were decreased to 10% of the control in the presence of triacsin C. The concentration of triacsin C needed to suppress leptin production was similar to the K(i) value (≃ 10-5 mol/L) for inhibition of acyl-CoA synthetase. Both palmitate and 2-bromopalmitate decreased leptin concentrations but did not affect the triacsin C-induced decrease in leptin additively. In conclusion, both protein and mRNA levels of leptin were decreased by triacsin C and FFA in primary cultured rat adipocytes. Our findings suggest that FFA is involved in the regulation of leptin production in adipocytes. (C) 2000 by W.B. Saunders Company.
AB - Free fatty acid (FFA) has been reported to decrease leptin mRNA levels in 3T3-L1 adipocytes. When using this cell line, it is difficult to determine the protein levels because a very small amount of leptin is secreted into the medium. The effect of FFA on leptin secretion from adipocytes has not yet been determined. In addition, in vivo studies have failed to demonstrate a FFA-induced decrease in plasma leptin levels. To clarify the effect of FFA on leptin production, we investigated the leptin protein level in the medium and the mRNA level in primary cultured rat adipocytes treated with triacsin C, which is a potent inhibitor of acyl-coenzyme A (CoA) synthetase, palmitate, and 2-bromopalmitate. Triacsin C (0 to 5 x 10-5 mol/L) decreased leptin concentrations in the culture medium in a close-dependent manner. Leptin mRNA levels were decreased to 10% of the control in the presence of triacsin C. The concentration of triacsin C needed to suppress leptin production was similar to the K(i) value (≃ 10-5 mol/L) for inhibition of acyl-CoA synthetase. Both palmitate and 2-bromopalmitate decreased leptin concentrations but did not affect the triacsin C-induced decrease in leptin additively. In conclusion, both protein and mRNA levels of leptin were decreased by triacsin C and FFA in primary cultured rat adipocytes. Our findings suggest that FFA is involved in the regulation of leptin production in adipocytes. (C) 2000 by W.B. Saunders Company.
UR - https://www.scopus.com/pages/publications/0034019050
UR - https://www.scopus.com/pages/publications/0034019050#tab=citedBy
U2 - 10.1016/S0026-0495(00)90154-9
DO - 10.1016/S0026-0495(00)90154-9
M3 - Article
C2 - 10726909
AN - SCOPUS:0034019050
SN - 0026-0495
VL - 49
SP - 326
EP - 330
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 3
ER -
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