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Department of Anatomy and Physiology, Faculty of Medicine, Laval University, Quebec, Canada G1K 7P4
Submitted 6 February 2003 ; accepted in final form 2 May 2003
Norepinephrine stimulates lipolysis and concurrently inhibits
insulin-stimulated leptin secretion from white adipocytes. To assess whether
there is a cause-effect relationship between these two metabolic events, the
effects of fatty acids were investigated in isolated rat adipocytes incubated
in buffer containing low (0.1%) and high (4%) albumin concentrations. Palmitic
acid (1 mM) mimicked the inhibitory effects of norepinephrine (1 µM) on
insulin (10 nM)-stimulated leptin secretion, but only at low albumin
concentrations. Studies investigating the effects of the chain length of
saturated fatty acids [from butyric (C4) to stearic (C18) acids] revealed that
only fatty acids with a chain length superior or equal to eight carbons
effectively inhibited insulin-stimulated leptin secretion. Long-chain mono-
and polyunsaturated fatty acids constitutively present in adipocyte
triglyceride stores (oleic, linoleic, 
-linolenic, palmitoleic,
eicosapentanoic, and docosahexanoic acids) also completely suppressed leptin
secretion. Saturated and unsaturated fatty acids inhibited insulin-stimulated
leptin secretion with the same potency and without any significant effect on
basal secretion. On the other hand, inhibitors of mitochondrial fatty acid
oxidation (palmoxirate, 2-bromopalmitate, 2-bromocaproate) attenuated the
stimulatory effects of insulin on leptin release without reversing the effects
of fatty acids or norepinephrine, suggesting that fatty acids do not need to
be oxidized by the mitochondria to inhibit leptin release. These results
demonstrate that long-chain fatty acids mimic the effects of norepinephrine on
leptin secretion and suggest that they may play a regulatory role as
messengers between stimulation of lipolysis by norepinephrine and inhibition
of leptin secretion.
insulin; albumin; saturated and unsaturated fatty acids; 
-oxidation
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