Inhibition of leptin release by atrial natriuretic peptide (ANP) in human adipocytes

The addition of atrial natriuretic peptide (ANP) to isolated human adipocytes in primary culture from very obese individuals resulted in an inhibition of leptin release after a 24- or 48-hr incubation. There was also an inhibition of leptin release by isoproterenol (ISO) that was partially reversed...

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Bibliographic Details
Published in:Biochemical pharmacology 2003-06, Vol.65 (11), p.1883-1888
Main Authors: Fain, John N., Kanu, Alie, Bahouth, Suleiman W., Cowan, George S.M., Lloyd Hiler, M.
Format: Article
Language:English
Subjects:
Adipocytes - drug effects
Adipocytes - metabolism
Adipose Tissue - cytology
Animals
ANP
Atrial Natriuretic Factor - pharmacology
Biological and medical sciences
Cyclic GMP
Cyclic GMP - metabolism
Drug Interactions
H-89
Humans
Insulin
Insulin - pharmacology
Leptin
Leptin - metabolism
Lipolysis
Lipolysis - drug effects
Medical sciences
Nitric Oxide
Pertussis Toxin - pharmacology
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Summary:The addition of atrial natriuretic peptide (ANP) to isolated human adipocytes in primary culture from very obese individuals resulted in an inhibition of leptin release after a 24- or 48-hr incubation. There was also an inhibition of leptin release by isoproterenol (ISO) that was partially reversed by insulin, whereas the inhibition due to ANP was unaffected. Similar results were seen with N-[2-( p-bromocinnamylamino)ethyl]-5-isoquinolinesulphonamide (H-89), which is a cell-permeable inhibitor of protein kinase A. H-89 markedly reduced the effects of ISO on both lipolysis and leptin release without affecting the stimulation of lipolysis or the inhibition of leptin release due to ANP. Inhibition of endogenous nitric oxide formation using N ω-nitro- l-arginine resulted in a 20% increase in leptin release over 48 hr, which suggests that the nitric oxide/cyclic GMP pathway might play a small role in the regulation of endogenous leptin release. Similarly, the addition of the nitric oxide donor ( Z)-1-[2-aminoethyl)- N-(2-aminoethyl)diazen-1-ium-1,2-diolate (DETA NONOate) at 0.1 or 1 μM to explants of human adipose tissue enhanced lipolysis by 29%. Our data demonstrate that the lipolytic effect of ANP is probably secondary to stimulation of cyclic GMP accumulation in human adipocytes, and this is accompanied by an inhibition of leptin release.
ISSN:0006-2952
1873-2968
DOI:10.1016/S0006-2952(03)00154-0