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Streptozotocin-induced diabetes impairs Mg²⁺ homeostasis and uptake in rat liver cells

Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106

Submitted 2 May 2003 ; accepted in final form 6 October 2003

Male Sprague-Dawley rats rendered diabetic by streptozotocin injection presented 10 and 20% decreases in total hepatic Mg²⁺ content at 4 and 8 wk, respectively, following diabetes onset. This decrease was associated with a parallel decrease in K⁺ and ATP content and an increase in Na⁺ level. In diabetic liver cells, the Mg²⁺ extrusion elicited by ₁-adrenoceptor stimulation was markedly reduced compared with nondiabetic livers, whereas that induced by -adrenoceptor stimulation was unaffected. In addition, diabetic hepatocytes did not accumulate Mg²⁺ following stimulation of protein kinase C pathway by vasopressin, diacylglycerol analogs, or phorbol 12-myristate 13-acetate derivates despite the reduced basal content in cellular Mg²⁺. Experiments performed in purified plasma membrane from diabetic livers located the defect at the level of the bidirectional Na⁺/Mg²⁺ exchanger operating in the basolateral domain of the hepatocyte cell membrane, which could extrude but not accumulate Mg²⁺ in exchange for Na⁺. The impairment of Mg²⁺ uptake mechanism, in addition to the decrease in cellular ATP level, can contribute to explaining the decrease in liver Mg²⁺ content observed under diabetic conditions.

magnesium; adrenergic signaling; protein kinase c; adenosine 5'-triphosphate; plasma membrane