Rg. Vernon et al., EFFECTS OF LACTATION ON THE SIGNAL-TRANSDUCTION SYSTEMS REGULATING LIPOLYSIS IN SHEEP SUBCUTANEOUS AND OMENTAL ADIPOSE-TISSUE, Biochemical journal, 308, 1995, pp. 291-296
The effect of lactation on the regulation of lipolysis by beta- and al
pha(2) adrenergic agents and by adenosine has been investigated, When
changes in adipocyte mean cell volume (which decreases with lactation)
are allowed for, lactation increased the maximum response both to bet
a-adrenergic agents and to the adenosine analogue N-6-phenylisopropyla
denosine, but had no apparent effect on the responsiveness of the alph
a(2)-adrenergic system in both subcutaneous and omental adipocytes. Fo
r subcutaneous adipocytes, there was no significant change in the numb
er of beta-adrenergic or alpha(2)-adrenergic receptors, but the amount
of G(s) and the maximum (forskolin-stimulaled) adenylate cyclase acti
vity were increased by lactation. In contrast, in omental adipocytes,
the number of beta- (but not alpha(2)-) adrenergic receptors and the a
mount of G(s) were increased, whereas forskolin-stimulated adenylate c
yclase activity was unchanged by lactation. In both types of adipocyte
, cyclic AMP phosphodiesterase and total protein kinase A activities w
ere unchanged. Lactation had no effect on the number of adenosine rece
ptors but increased the amounts of the G(i) isoforms expressed in both
types of adipocyte. These various adaptations differ markedly in a nu
mber of respects from those described previously in the rat. Lactation
, then, while having a similar overall effect on the response to beta-
adrenergic agonists of adipocytes, achieves this by depot-specific mec
hanisms. In contrast, changes in response to adenosine appear to invol
ve the same mechanism in the two depots investigated.