Sympathetic stimulation has long been recognized to mobilise fatty acids fr
om white adipose tissue. However, it is now apparent that adipose tissue is
not only concerned with energy storage as fat, but is a major endocrine an
d secretory organ. This change has resulted from the identification of lept
in as a hormone of energy balance secreted by white adipose tissue. The sym
pathetic system is a key regulator of leptin production in white fat. Sympa
thomimetic amines, cold exposure or fasting (which lead to sympathetic stim
ulation of white fat), decrease ob gone expression in the tissue and leptin
production. On the other hand, sympathetic blockade often increases circul
ating leptin and ob gene expression, and it is postulated that the sympathe
tic system has a tonic inhibitory action on leptin synthesis. In rodents th
is action is through stimulation of beta (3)-adrenoceptors. The adrenal med
ulla (as opposed to the direct sympathetic innervation) has been thought to
play only a minor role in the catecholaminergic regulation of white adipos
e tissue. However, in rodents responses of the leptin system to adrenergic
blockade vary with the method used. Changes in leptin and ob gene expressio
n are considerably less using methods of blockade that only effect the term
inal adrenergic innervation, rather than medullary secretions as well. Stim
ulation of the leptin system increases sympathetic activity and hence metab
olic activity in many tissues. As well as leptin, other (but not all) secre
tions from white adipose tissue are subject to sympathetic regulation. In o
besity the sympathetic sensitivity of adipose tissue is reduced and this fa
ctor may underlie the dysregulation of leptin production and other adipose
tissue secretions.