Isolated mitochondria from liver or brown adipose tissue of obese ob/ob mice demonstrated increased rates of Ca2+ uptake and release compared with those of lean mice. This enhanced transport activity was not found in mitochondria from kidney or skeletal muscle. Respiration-induced membrane potential was the same in mitochondria from lean and ob/ob mice. It is therefore concluded that the increased Ca2+ uptake rates reflect an activation of the Ca2+ uniporter rather than a change in the electrophoretic driving force. As mitochondria from pre-obese ob/ob mice did not show elevated rates of Ca2+ transport, the activated transport in the obese animals was thus a consequence of the state of obesity rather than being a direct effect of the ob/ob genotype. It is suggested that the enhanced activity of the Ca2+-transport pathways in liver and brown adipose tissue may alter metabolic functions in these tissues by modifying cytoplasmic or intramitochondrial Ca2+ concentrations.
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Research Article| July 15 1983
Mitochondrial Ca2+ transport in lean and genetically obese (ob/ob) mice
Biochem J (1983) 214 (1): 163–170.
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D R Fraser, P Trayhurn; Mitochondrial Ca2+ transport in lean and genetically obese (ob/ob) mice. Biochem J 15 July 1983; 214 (1): 163–170. doi: https://doi.org/10.1042/bj2140163
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