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LIVER AND BILIARY TRACT

Role of glucose in modulating Mg²⁺ homeostasis in liver cells from starved rats

Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio

Submitted 19 November 2003 ; accepted in final form 7 September 2004

₁- and -Adrenoceptor stimulation elicits Mg²⁺ 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 Mg²⁺ 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. Mg²⁺ extrusion was assessed by atomic absorbance spectrophotometry. In both experimental models, the administration of pharmacological doses of adrenergic agonists did not elicit Mg²⁺ extrusion. The determination of cellular Mg²⁺ indicated an 9% decrease in total hepatic Mg²⁺ content in liver cells after overnight fasting, whereas the ATP level was unchanged. Hepatocytes from starved rats accumulated approximately four times more Mg²⁺ than liver cells from fed animals. This enlarged Mg²⁺ 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 Mg²⁺ accumulation observed in the absence of extracellular glucose was completely abolished by imipramine or removal of extracellular Na⁺. Taken together, these data indicate 1) that hepatic glucose mobilization is essential for Mg²⁺ extrusion by adrenergic agonist and 2) that starved hepatocytes accumulate Mg²⁺ via two distinct pathways, one of which is associated with glucose transport, whereas the second can be tentatively identified as an imipramine-inhibited Na⁺-dependent pathway.

magnesium; adrenergic stimulation; amiloride; magnesium transport