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

Authors
  • Torres, Lisa M
  • Youngner, Jonathan
  • Romani, Andrea
Type
Published Article
Journal
American journal of physiology. Gastrointestinal and liver physiology
Publication Date
Feb 01, 2005
Volume
288
Issue
2
Identifiers
PMID: 15647605
Source
Medline
License
Unknown

Abstract

Alpha1- and beta-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 alpha1 (phenylephrine)- or beta (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 approximately 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.

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