Active and inactive forms of pyruvate dehydrogenase in rat heart and kidney: Effect of diabetes, fasting, and refeeding on pyruvate dehydrogenase interconversion
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Fisetin protects against streptozotocin-induced diabetic cardiomyopathy in rats by suppressing fatty acid oxidation and inhibiting protein kinase R
2021, Saudi Pharmaceutical JournalCitation Excerpt :In diabetic hearts, the activity of PFK is allosterically inhibited by the high citrate levels (Da Silva et al., 2012). Likewise, the diabetic cardiac activity of PDH kinase (PFK) is inhibited by the higher activity of PDH kinase (PDK4) which is activated in response to high levels of β-oxidation and accumulation of acetyl CoA/CoA, NADH/ NAD, and ATP/ADP (Wieland et al., 1971; Kuo et al., 1985; Stanley et al., 1997). This was also confirmed in the diabetic hearts of this study where the higher activity of medium-chain acyl-coenzyme A dehydrogenase (MCAD), a mitochondrial fatty acid β-oxidation enzyme, and PDK4 and lower activities of PDH and PFK were observed, thus confirming a cardiac shift toward FAs metabolism.
Ca<sup>2+</sup>-dependent inhibition of branched-chain α-ketoacid dehydrogenase kinase by thiamine pyrophosphate
2018, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This relationship is reversed in the fasted state. Inactivation of the PDH complex conserves pyruvate, lactate, and alanine for gluconeogenesis [28] while activation of the BCKDH complex generates substrates for gluconeogenesis and ketogenesis from BCAAs [29,30]. On the other hand, when the energy expenditure is extremely enhanced by exercise, both complexes are simultaneously activated in skeletal muscles [31,32].
Temporal partitioning of adaptive responses of the murine heart to fasting
2018, Life SciencesCitation Excerpt :Collectively, these data are consistent with whole body adaptation to this fasting protocol, with maintenance of glucose homeostasis. Prior studies have reported that fasting induces fatty acid responsive genes, thus facilitating myocardial fatty acid oxidation [11,31,37]. However, few studies have defined the time course of these events.
Trimetazidine-Induced Enhancement of Myocardial Recovery during Reperfusion: A Comparative Study in Diabetic and Non-diabetic Rat Hearts
2006, Archives of Medical ResearchCitation Excerpt :In diabetics, removal of the normal insulin inhibition on lipolysis in adipocytes leads to increment of free fatty acid concentration in plasma (22). Elevated FFA rates in plasma feed back to inhibit glucose uptake (23), glucose oxidation (24), and increase β-oxidation in the heart (25), relative to non-diabetics. High rates of fatty acid β-oxidation inhibit glucose and pyruvate oxidation and exacerbate production and accumulation of H+, leading to intracellular acidosis (24).
A radiochemical pyruvate dehydrogenase assay: Activity in heart
2003, Analytical BiochemistryRegulation of the activity of the pyruvate dehydrogenase complex
2002, Advances in Enzyme Regulation