F. Tebar et al., Epidermal growth factor secreted from submandibular salivary glands interferes with the lipolytic effect of adrenaline in mice, ENDOCRINOL, 141(3), 2000, pp. 876-882
We had described that epidermal growth factor (EGF) interfered with the lip
olytic effect of catecholamines in isolated adipocytes. Since catecholamine
s stimulate the release of EGF hom submandibular salivary glands to blood p
lasma in male mice, we studied whether EGF affected also the lipolytic resp
onse to adrenaline in whole animals. We studied the effect of adrenaline in
sialoadenectomized and sham-operated mice receiving or not a high dose of
EGF following adrenaline injection. There was no difference in plasma EGF c
oncentration between sham-operated and sialoadenectomized animals receiving
saline. After adrenaline administration plasma EGF increased by 20-fold in
sham-operated but did not increase in sialoadenectomized mice. Indeed, the
increase was much higher (more than 100-fold) in mice receiving exogenous
EGF. The effect of adrenaline on plasma concentration of both glycerol and
nonesterified fatty acids was higher as lower was plasma EGF concentration.
Isolated adipocytes obtained from sham-operated or sialoadenectomized mice
had identical lipolytic response to adrenaline. The lipolytic response of
adipocytes to isoproterenol was decreased by addition of EGF. To study whet
her the interference with the in vivo lipolytic effect of adrenaline had fu
rther metabolic consequences, we measured plasma beta-hydroxybutyrate conce
ntration in plasma. There was no difference in the response to adrenaline b
etween sham-operated and sialoadenectomized mice in spite of the difference
in plasma nonsterified fatty acid concentration. Studies in isolated hepat
ocytes indicated that ketogenesis run at near maximal rate in this range of
substrate concentration. These results suggest that EGF in the physiologic
al range decreases the Lipolytic effect of adrenaline but does not compromi
se further metabolic events like the enhancement of ketogenesis.