HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kawaji, N. Articles by Ueki, H. Search for Related Content PubMed PubMed Citation Articles by Kawaji, N. Articles by Ueki, H. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 42, 1671-1677, October 2001
Copyright © 2001 by Lipid Research, Inc.

Original Article

Anti-leptin receptor antibody mimics the stimulation of lipolysis induced by leptin in isolated mouse fat pads

Correspondence to: Hiroshi Ueki, To whom correspondence should be addressed., ueki{at}fupharm.fukuyama-u.ac.jp (E-mail)

An anti-leptin receptor polyclonal antibody (receptor antibody), as well as leptin, stimulated the release of free fatty acids from isolated mouse fat pads in a time-dependent manner. Following a 90-min incubation, maximal lipolysis was observed at 6 µg/ml receptor antibody and 0.1 nM leptin. The receptor antibody did not show any additive effect to the stimulation of lipolysis induced by leptin, suggesting that they exert their actions through a similar mechanism involving the leptin receptor. N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), quin 2-AM, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), and neomycin sulfate (neomycin) all potently inhibited the stimulation of lipolysis by the receptor antibody and leptin. Short-term incubation of the fat pads with the receptor antibody or leptin showed a transient increase in the cellular content of cAMP and myo-inositol 1,4,5-trisphosphate (IP₃) in similar concentrations to the free fatty acid release. Quin 2-AM and W-7 also inhibited the increase in cAMP content, suggesting that a Ca²⁺/calmodulin-dependent process may be involved in a part of the mechanism in which the receptor antibody and leptin exert their effects.

The increase in cellular IP₃ content via phosphoinositide-specific phospholipase C (PLC) sensitive to neomycin appears to be a primary step to initiate intracellular events. Both the receptor antibody and leptin may stimulate the lipolysis through mechanisms involving a transient increase in the cellular IP₃ content followed by cAMP production, which leads to the activation of cAMP-dependent protein kinase. — Kawaji, N., A. Yoshida, T. Motoyashiki, T. Morita, and H. Ueki. Anti-leptin receptor antibody mimics the stimulation of lipolysis induced by leptin in isolated mouse fat pads. J. Lipid Res. 2001. 42: 1671–1677.

Supplementary key words: Ca²⁺, myo-inositol 1,4,5-trisphosphate, cAMP

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				N. Mehebik, A.-M. Jaubert, D. Sabourault, Y. Giudicelli, and C. Ribiere Leptin-induced nitric oxide production in white adipocytes is mediated through PKA and MAP kinase activation Am J Physiol Cell Physiol, August 1, 2005; 289(2): C379 - C387. [Abstract] [Full Text] [PDF]

				C. Bjorbaek and B. B. Kahn Leptin Signaling in the Central Nervous System and the Periphery Recent Prog. Horm. Res., January 1, 2004; 59(1): 305 - 331. [Abstract] [Full Text]