Metabolic actions of cortisol in a macropodid marsupial Thylogale billardierii
ABSTRACT In undisturbed pademelon wallabies (Thylogale billardierii) with indwelling jugular venous catheters, an increase in the plasma cortisol concentration from 0.25±0.05 to 1.35±0.15 (s.e.m.) μmol/l in 2 h, during i.v. infusion of cortisol at 1.0 mg/kg per h, caused no significant change in the plasma glucose concentration from the control value of 4.26±0.25 mmol/l. The rates of appearance (Ra) and metabolic clearance (MCR) of glucose, measured by steady-state isotope dilution, also did not change significantly from the control values of 14.9±0.7 μmol/kg per min and 3.52±0.19 ml/kg per min respectively. Twice-daily i.m. injections of 7 mg cortisol/kg for 7 days caused increases in plasma concentrations of cortisol, from 0.26±0.02 to 0.66±0.04 μmol/l on day 7, and glucose, from 5.1±0.1 to 7.2±0.6 mmol/l by day 5. The concentration of glycogen in the liver of wallabies fasted for 24 h increased from the control level of 1.17±0.56 to 5.92±1.14 g/100 g on day 7 (P<0.01), but mean glucose Ra and MCR did not change significantly. Plasma concentrations of α-amino nitrogen rose from 2.73±0.13 to 3.22±0.12 mmol/l on day 1 and remained at this level. Plasma concentrations of urea rose from 8.59±0.62 to 9.70±0.32 mmol/l on day 1, but then declined below the control level. Food intake and urinary excretion of nitrogen did not change in undisturbed animals. However, fasting followed by liver biopsy was accompanied by urinary excretion of nitrogen in excess of food intake, persisting until day 2 of treatment. The transient effect of cortisol on the plasma concentration of urea and lack of effect on urinary excretion of nitrogen could be explained by urea recycling, as indicated by a low urinary urea nitrogen: total nitrogen ratio and failure to excrete more than a mean of 26% of infused urea. It is concluded that cortisol has no short-term effect on carbohydrate metabolism in this marsupial. In the long term it can increase hepatic carbohydrate reserves through utilization of tissue amino nitrogen, the resulting urea being conserved by recycling. J. Endocr. (1988) 116, 71–79