Role of glucose in modulating Mg2+ homeostasis in liver cells from starved rats (original) (raw)

and ␤-Adrenoceptor stimulation elicits Mg 2ϩ extrusion from liver cells in conjunction with hepatic glucose output (T. Fagan and A. Romani. Am J Physiol Gastrointest Liver Physiol 279: G943-G950, 2000.). To characterize the role of intrahepatic glucose on Mg 2ϩ transport, male Sprague-Dawley rats were starved overnight before being anesthetized and used as organ donors. Perfused livers or collagenase-dispersed hepatocytes were stimulated by ␣ 1 (phenylephrine)-or ␤ (isoproterenol)adrenergic agonists. Mg 2ϩ extrusion was assessed by atomic absorbance spectrophotometry. In both experimental models, the administration of pharmacological doses of adrenergic agonists did not elicit Mg 2ϩ extrusion. The determination of cellular Mg 2ϩ indicated an ϳ9% decrease in total hepatic Mg 2ϩ content in liver cells after overnight fasting, whereas the ATP level was unchanged. Hepatocytes from starved rats accumulated approximately four times more Mg 2ϩ than liver cells from fed animals. This enlarged Mg 2ϩ accumulation depended in part on extracellular glucose, since it was markedly reduced in the absence of extracellular glucose or in the presence of the glucose transport inhibitor phloretin. The residual Mg 2ϩ accumulation observed in the absence of extracellular glucose was completely abolished by imipramine or removal of extracellular Na ϩ . Taken together, these data indicate 1) that hepatic glucose mobilization is essential for Mg 2ϩ extrusion by adrenergic agonist and 2) that starved hepatocytes accumulate Mg 2ϩ via two distinct pathways, one of which is associated with glucose transport, whereas the second can be tentatively identified as an imipramine-inhibited Na ϩ -dependent pathway.