Date: 2020-07-07 01:24:38
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Metabolic Gridlock Explained
In a review published in Cell, it was concluded that mitochondria function optimally when acetyl-CoA is produced from either glucose or fatty acids at a time.
Several molecular mechanisms were mentioned here but the picture would not be complete without mentioning mitochondria.
Fasting or ketogenic diet feeds mitochondria with fatty acid. Historically, summertime connected with ripe fruits would feed mitochondria with glucose.
Clear and decisive shifts between substrates prevent mitochondrial damage. Besides, glucose and fatty acids often trigger antagonistic signalling pathway. Being fuelled by one dominant substrate at a time allows for your pathways to send clear signals which guide energy homeostasis.
Because insulin orchestrates systemic flux and disposal of glucose, fatty acids, and amino acids, resistance to the actions of the hormone gives rise to a metabolic storm of aberrant nutrient partitioning.
Among the key features of this storm is an apparent stiffness in mitochondrial substrate selection, such that various organs and cell types fail to appropriately adjust fuel choice in response to nutritional circumstances.
This phenomenon, dubbed “metabolic inflexibility,” has gained growing attention as a hallmark of cardiometabolic disease and a potential cause of cellular dysfunction. Thus, emerging evidence implies that metabolic health deteriorates as mitochondria lose their capacity to switch freely between alternative forms of carbon energy.
Fasting or ketogenic diet feeds mitochondria with fatty acid. Historically, summertime connected with ripe fruits would feed mitochondria with glucose. Clear and decisive shifts between substrates prevent mitochondrial damage.
Besides, glucose and fatty acids often trigger antagonistic signalling pathway. Being fuelled by one dominant substrate at a time allows for your pathways to send clear signals which guide energy homeostasis.
Glucose and fatty acids serve as the primary catabolic substrates that provide acetyl-CoA to the tricarboxylic acid cycle. The pathways of glucose and fat oxidation are reciprocally regulated by several key metabolic intermediates and signals.
During fasting, elevated acetyl-CoA derived from high rates of β-oxidation lowers glucose oxidation by allosterically inhibiting PDH and by activating its inhibitory kinase, PDK. Conversely, feeding and glucose surplus restrict fat oxidation by increasing production of malonyl-CoA, which inhibits CPT1.
Citrate acts as a signal of plenty that limits glycolytic flux by inhibiting PFK and lowers β-oxidation by giving rise to cytoplasmic acetyl-CoA and malonyl-CoA via CL and ACC, respectively. During periods of energy deficit, an increase in the cellular AMP/ATP ratio activates AMPK, which phosphorylates and inhibits ACC while also activating MCD, thereby relieving malonyl-CoA-mediated inhibition of CPT-1 and promoting fat oxidation.
Catabolism of branched-chain amino acids (BCAA) is regulated by BCKD, which is feedback inhibited by acyl-CoA products of the complex due to activation of its inhibitory kinase, BCK. Increased cellular concentrations of pyruvate, BCAA, and fatty acyl-CoAs promote their own catabolism by antagonizing the inhibitory actions of PDK, BCK, and malonyl-CoA, respectively.
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