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Stimulation of catecholamine synthesis in cultured bovine adrenal medullary cells by leptin
Author(s) -
Utsunomiya Kensuke,
Yanagihara Nobuyuki,
Tachikawa Eiichi,
Cheah Tat Beng,
Kajiwara Koji,
Toyohira Yumiko,
Ueno Susumu,
Izumi Futoshi
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00123.x
Subject(s) - leptin , medicine , endocrinology , tyrosine hydroxylase , catecholamine , phosphorylation , chemistry , chromaffin cell , tyrosine , tyrosine 3 monooxygenase , mapk/erk pathway , adrenal medulla , tyrosine phosphorylation , biology , dopamine , biochemistry , obesity
Recently, we characterized leptin receptors in bovine adrenal medullary cells (Yanagihara et al . 2000). Here we report the stimulatory effect of leptin on catecholamine synthesis in the cells. Incubating cells with leptin (10 n m ) for 20 min increased the synthesis of 14 C‐catecholamines from [ 14 C]tyrosine, but not from l ‐3,4‐dihydroxyphenyl [3– 14 C]alanine. The stimulation of catecholamine synthesis in the cells by leptin was associated with the phosphorylation and activation of tyrosine hydroxylase, the rate‐limiting enzyme of catecholamine biosynthesis. The incubation of cells with leptin resulted in a rapid activation of the mitogen‐activated protein kinases (MAPKs). An inhibitor of MAPK kinase, U0126, nullified the stimulatory effect of leptin on the synthesis of 14 C‐catecholamines. Leptin potentiated the stimulatory effect of acetylcholine on 14 C‐catecholamine synthesis, whereas leptin failed to enhance the phosphorylation and activation of tyrosine hydroxylase induced by acetylcholine. These findings suggest that leptin stimulates catecholamine synthesis via the activation of tyrosine hydroxylase by two different mechanisms, i.e., one is dependent on tyrosine hydroxylase phosphorylation mediated through the MAPK pathway and the second is independent of enzyme phosphorylation.