Insulin and tca cycle

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Insulin and tca cycle

Colin Ward The tricarboxylic acid TCA cycle, also known as the citric acid cycle or Krebs cycle, is a key metabolic pathway that unifies carbohydrate, fat, and protein metabolism. Commonly referred to as the Krebs cycle, it takes its name from its discoverer Hans Adolf Krebs, a German-born British medical scientist, who discovered the cycle in while working at the University of Sheffield.

The discovery won him the Nobel Prize in Physiology and Medicine. The cycle is a series of biochemical reactions employed to generate energy through the oxidation of acetate in the form of acetyl-CoA.

Insulin and tca cycle

The cycle comprises eight sequential enzymic reactions that reduce each 2 carbon acetate moiety to two molecules of CO2. Energy production via the TCA cycle and oxidative phosphorylation takes place in specialized organelles called mitochondria.

Enzymes involved in the TCA cycle Figure 1. Overview of the citric acid cycle[1]. See text for details. Click to enlarge As shown in Figure 1 there are eight enzymic steps in the TCA cycle and details of the chemical reactions involved can be found elsewhere [1] [2].

The cycle begins with an irreversible aldol condensation reaction where the two-carbon acetyl group from acetyl-CoA is transferred to the four carbon dicarboxylic acid oxaloacetate, to form the six-carbon tricarboxylic acid citrate.

This reaction is catalyzed by the enzyme citrate synthase[1][2]. In the second reaction, citrate is converted to isocitrate in a two step process catalyzed by the enzyme acontinase.

Here a water molecule is removed dehydration reaction from the citric acid forming the intermediate cis-aconitate which is then rehydrated to form isocitrate.

This is another rate-limiting, irreversible stage in the cycle[1]. The fifth reaction of the TCA cycle is a substrate-level phosphorylation catalyzed by the enzyme succinyl-CoA synthetase. In this reaction a free phosphate group attacks the succinyl-CoA molecule releasing the CoA hydrolysis and generating a succinyl phosphate intermediate.

In a condensation reaction, the phosphate is then transferred to GDP to form GTP and the 4-carbon dicarboxylic acid, succinate[1][2]. In the sixth reaction succinate is oxidized to fumarate by the enzyme succinate dehydrogenase an enzyme that functions in both the TCA cycle and the electron transport chain [1].

Again this is a two step process where the prosthetic group FAD of succinate dehydrogenase is reduced to FADH2 before the reducing equivalents are transferred to coenzyme Q forming QH2[1][2]. The last two seventh and eighth steps of the TCA cycle involve the hydration of fumarate to malate by the enzyme fumarase and the oxidation of malate to oxaloacetate by the enzyme malate dehydrogenase.

Both of these reactions are readily reversible and a new molecule of oxaloacetate has been generated for the next round of the cycle. The carbons donated by acetyl-CoA become part of the oxaloacetate carbon backbone used in the next turn of the cycle.

Loss of the acetyl-CoA-donated carbons as CO2 requires several turns of the citric acid cycle[2].Question: A patient presents complaining of severe pain and "burning" in an extremity.

You note that the extremity is pale and cool to the touch, with mottled skin and without a palpable pulse. The Medical Biochemistry Page is a portal for the understanding of biochemical, metabolic, and physiological processes with an emphasis on medical relevance.

Reduced tricarboxylic acid cycle flux in type 2 diabetes mellitus? leading to muscular insulin sensitivity and ultimately type 2 diabetes mellitus.

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a reduced TCA cycle flux in type 2 diabetic patients may be the consequence of a more sedentary, inactive lifestyle. So far, most studies that report mitochondrial dysfunction in type 2. Elevated TCA cycle function in the pathology of diet-induced hepatic insulin resistance and fatty liver.

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The citric acid cycle (CAC) – also known as the tricarboxylic acid (TCA) cycle or the Krebs cycle – is a series of chemical reactions used by all aerobic organisms to release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats.

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