Abstract
The net catabolic effect of glucocorticoids on protein metabolism is well documented but the acute and chronic effect of glucocorticoids on protein breakdown remains controversial. In the present studies protein breakdown was measured by the release of tyrosine from the isolated soleus and extensor digitorum longus (EDL) muscles of control rats and rats treated with corticosterone (10 mg/100 g body weight/day) for 5 days.
The effect of corticosterone in arresting growth was confirmed since corticosterone-treated rats weighed significantly less than control rats after 2, 3, 4 and 5 days of treatment (P<0·001). Furthermore, the weights of soleus and EDL muscles from corticosterone-treated rats were significantly reduced (P<0·001, at least P<0·05 respectively) compared with muscles from control rats on days 3–5.
In the EDL muscle tyrosine release was significantly elevated after corticosterone treatment for 2 days (257 ± 21 nmol/g tissue/h, P<0·05), 3 days (205 ± 9 nmol/g tissue/h, P<0·01), 4 days (255 ± 20 nmol/g tissue/h, P<0·005) and 5 days (218 ± 8 nmol/g tissue/h, P<0·05) compared with EDL from control rats (192 ± 13, 171 ± 7, 187 ± 7, 180 ± 12 nmol/g tissue/h respectively). In the soleus muscle, tyrosine release was significantly elevated after corticosterone treatment for 2 days (226 ± 14 nmol/g tissue/h, P<0·001), 3 days (223 ± 16 nmol/g tissue/h, P<0·001) and 4 days (199 ± 10 nmol/g tissue/h, P<0·001) compared with control rats (158 ± 7, 132 ± 6 and 153 ± 7 nmol/g tissue/h respectively). After 5 days there was no significant difference in tyrosine release from soleus muscle between corticosterone-treated (176 ± 15 nmol/g tissue/h) and control rats (157 ± 6 nmol/g tissue/h). Plasma glucose concentrations were not significantly different in rats treated with corticosterone and control rats whilst insulin levels were significantly raised in the corticosterone-treated rats on all days compared with control rats (P<0·05 on day 1; P<0·001 on days 2, 3, 4 and 5). It is suggested that insulin may have prevented hyperglycaemia developing in the corticosterone-treated rats. Results from these studies indicate that the acute effect of glucocorticoids is to increase muscle proteolysis but this is not maintained with longer-term treatment.
Journal of Endocrinology (1996) 148, 501–507