Adrenergic regulation of gluconeogenesis: possible involvement of two mechanisms of signal transduction in alpha 1-adrenergic action.
We have previously suggested that the effects of alpha 1-adrenergic agents on hepatocyte metabolism involve two mechanisms: (i) a calcium-independent insulin-sensitive process that is modulated by glucocorticoids and (ii) a calcium-dependent insulin-insensitive process that is modulated by thyroid hormones. We have studied the effect of epinephrine (plus propranolol) on gluconeogenesis from lactate and dihydroxyacetone. It was observed that the adrenergic stimulation of gluconeogenesis from lactate seemed to occur through both mechanisms, whereas when the substrate was dihydroxyacetone the action took place exclusively through the calcium-independent insulin-sensitive process. This effect was absent in hepatocytes from adrenalectomized rats, suggesting that it is modulated by glucocorticoids.
D000315:Adrenalectomy; D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D004098:Dihydroxyacetone / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology*; D005260:Female; D005943:Gluconeogenesis / Q000187:drug effects*; D007037:Hypothyroidism; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology; D007700:Kinetics; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D007328:Insulin; D007773:Lactates; D011942:Receptors, Adrenergic, alpha; D003513:Cycloheximide; D011433:Propranolol; D004098:Dihydroxyacetone; D004837:Epinephrine