2001
DOI: 10.1046/j.1365-2796.2001.00779.x
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Increased erythrocyte content of Ca2+ in patients with Tarui's disease

Abstract: Abstract. Waldenstro Èm A, Engstro Èm I, Ronquist G

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Cited by 10 publications
(7 citation statements)
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“…Findings of an enhanced hydrolysis of ATP, combined with an increased glycolytic flux suggested an accelerated ATP‐dependent Ca 2+ ‐extrusion machinery due to an increased membrane leakiness of Ca 2+ in these cells. This membrane leakiness should be understood as a co‐phenomenon to the PFK‐M deficiency [71, 72]. This co‐phenomenon, leading to Ca 2+ ‐induced membrane stiffness, i.e.…”
Section: Tarui's Diseasementioning
confidence: 99%
“…Findings of an enhanced hydrolysis of ATP, combined with an increased glycolytic flux suggested an accelerated ATP‐dependent Ca 2+ ‐extrusion machinery due to an increased membrane leakiness of Ca 2+ in these cells. This membrane leakiness should be understood as a co‐phenomenon to the PFK‐M deficiency [71, 72]. This co‐phenomenon, leading to Ca 2+ ‐induced membrane stiffness, i.e.…”
Section: Tarui's Diseasementioning
confidence: 99%
“…The microcalorimeter is the earliest method for direct cellular thermosensing . It has been used to monitor heat production property of various cell types such as erythrocyte, hepatocytes, lymphocytes, thrombocytes, muscle cells and adipocytes . However the readout is only an overall outcome of the cells in the measuring cup, while 10 4 –10 5 cells are sufficient for one measurement .…”
Section: Introductionmentioning
confidence: 99%
“…Elles pourraient ê tre rapproché es des aspects de mitochondries volumineuses avec inclusions en galons vues chez des sportifs sans qu'il y ait d'anomalies biochimiques. Enfin, la responsabilité d'une augmentation du Ca 2+ intracellulaire a é té suggé ré e (Waldenströ m et al, 2001). Dans la forme myopathique (GSD VIIb), plusieurs hypothè ses pourraient ê tre formulé es, comme une destruction des fibres secondaire aux é pisodes ré pé té s de rhabdomolyse ou à l'é puisement mé tabolique non compensé lors du vieillissement musculaire ou du fait d'une mitochondriopathie secondaire (Sivakumar et al, 1996), un dé ficit enzymatique plus marqué (exclu par les dosages des cas rapporté s) ou l'accumulation au fil du temps du glycogè ne normal ou surtout r e v u e n e u r o l o g i q u e 1 6 9 ( 2 0 1 3 ) 6 1 3 -6 2 4 d'amylopectine qui comprimerait et dé placerait les fibres et les organelles (polysaccharide anormal synthé tisé par insuffisance relative de l'enzyme branchant comparé à l'hyperactivation du glycogè ne synthase induite par l'accumulation de fructose-6-phosphate et glucose-6-phosphate) (Danon et al, 1988).…”
Section: Discussionunclassified