Abstract
A lack of glucocorticoids causes fasting hypoglycemia. This is usually ascribed to impaired gluconeogenesis from protein. We examined the metabolic response of adrenalectomized (adrenx)rats to fasting.
Adrenx rats (n=32; confirmed by corticosterone assay), after restabilization, were fasted for 48 hours. They exhibited lower levels of glucose (55.2± 3.3 vs. 66.5± 3.5 mg/dl, mean ± SEM; p < 0.025), free fatty acids (FFA) (781± 38 vs. 1010± 44μEq/l; p <0.001) and ketones (2.4± 0.24 vs. 5.56± 0.33 mM; p<0.001)than sham-operated controls (n=27).
Intramuscular cortisone acetate (0.5 mg/day) raised the fasting levels of FFA (830± 85), ketones (3.46± 0.65) and glucose (69.7± 4.0).The urinary excretion of urea nitrogen in the adrenx rats exceeded that of controls (263.2± 14.3 vs. 166.7± 14.0 mg/48 hours; p< 0.001), and was not increased by the glucocorticoid therapy (253.3± 14.7).
Clearly, glucocorticoids did not raise the glucose in the adrenx rats by enhancing gluconeogenesis from protein.
FFA and ketones are major fuels of fasting. A lack would increase glucose oxidation and predispose to hypoglycemia.
We conclude that glucocorticoids do not sustain fasting levels of glucose by enhancing gluconeogenesis from protein but by reducing the consumption of glucose through greater availability and utilization of fuels derived from fat.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Wolfsdorf, J., Senior, B. 905 FAT-CARBOHYDRATE INTERRELATIONSHIPS: THE ROLE OF GLUCOCORTICOIDS. Pediatr Res 12 (Suppl 4), 514 (1978). https://doi.org/10.1203/00006450-197804001-00910
Issue Date:
DOI: https://doi.org/10.1203/00006450-197804001-00910