Abstract Title:

Changes in calcium fluxes in mitochondria, microsomes, and plasma membrane vesicles of livers from monosodium l-glutamate-obese rats.

Abstract Source:

Metabolism. 2011 Apr 11. Epub 2011 Apr 11. PMID: 21489575

Abstract Author(s):

Monique Cristine de Oliveira, Rosana Torrezan, Cecília Edna Mareze da Costa, Célia Regina Ambiel, Rodrigo Polimeni Constantin, Emy Luiza Ishii-Iwamoto, Clairce Luzia Salgueiro-Pagadigorria

Article Affiliation:

Laboratory of Biological Oxidations, Department of Biochemistry, University of Maringá, 87020900 Maringá, Brazil.


The purpose of this work was to evaluate if the fat liver accumulation interferes with intracellular calcium fluxes and the liver glycogenolytic response to a calcium-mobilizingα(1)-adrenergic agonist, phenylephrine. The animal model of monosodium l-glutamate (MSG)-induced obesity was used. The adult rats develop obesity and steatosis. Calcium fluxes were evaluated through measuring the (45)Ca(2+) uptake by liver microsomes, inside-out plasma membrane, and mitochondria. In the liver, assessments were performed on the calcium-dependent glycogenolytic response to phenylephrine and the glycogen contents. The Ca(2+) uptake by microsomes and plasma membrane vesicles was reduced in livers from obese rats as a result of reduction in the Ca(2+)-ATPase activities. In addition, the plasma membrane Na(+)/K(+)-ATPase was reduced. All these matched effects could contribute to elevated resting intracellular calcium levels in the hepatocytes. Livers from obese rats, albeit smaller and with similar glycogen contents to those of control rats, released higher amounts of glucosein response to phenylephrine infusion, which corroborates these observations. Mitochondria from obese rats exhibited a higher capacity of retaining calcium, a phenomenon that could be attributed to a minor susceptibility of the mitochondrial permeability transition pore opening.

Study Type : Animal Study

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