ArticleBiochemistry research international2012
Reduced TCA Flux in Diabetic Myotubes: Determined by Single Defects?
Article in Biochemistry research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Chronic Hyperglycaemia Inhibits Tricarboxylic Acid Cycle in Rat Cardiomyoblasts Overexpressing Glucose Transporter Type 4.International journal of molecular sciences · 2022Article
- A Comparative Analysis of Metabolic Profiles of Embryonic Skeletal Muscle from Lantang and Landrace Pigs.Animals : an open access journal from MDPI · 2022Article
- Altered tricarboxylic acid cycle flux in primary myotubes from severely obese humans.International journal of obesity (2005) · 2019Article
- Metabolic effects of mulberry branch bark powder on diabetic mice based on GC-MS metabolomics approach.Nutrition & metabolism · 2019Article
- Increased pyruvate dehydrogenase kinase expression in cultured myotubes from obese and diabetic individuals.European journal of nutrition · 2015Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The diabetic phenotype is complex, requiring elucidation of key initiating defects. Diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux but at present it is unclear in which part of the TCA cycle the defect is localised. In order to localise the defect we studied ATP production in isolated mitochondria from substrates entering the TCA cycle at various points. ATP production was measured by luminescence with or without concomitant ATP utilisation by hexokinase in mitochondria isolated from myotubes established from eight lean and eight type 2 diabetic subjects. The ATP production of investigated substrate combinations was significantly reduced in mitochondria isolated from type 2 diabetic subjects compared to lean. However, when ATP synthesis rates at different substrate combinations were normalized to the corresponding individual pyruvate-malate rate, there was no significant difference between groups. These results show that the primary reduced TCA cycle flux in diabetic myotubes is not explained by defects in specific part of the TCA cycle but rather results from a general downregulation of the TCA cycle.
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Registered trials
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