Gluconeogenesis anabolic reaction

Avatar is my favourite science fiction movie, i think it has a lot to do with science because they talk about a new element that was very expensive but also was the strongest metal, also they are in a new planet with rich flora and natives that are similar to humans, but they are taller and stronger and also blue.
When his brother is killed in a robbery, paraplegic Marine Jake Sully decides to take his place in a mission on the distant world of Pandora. There he learns of greedy corporate figurehead Parker Selfridge’s intentions of driving off the native humanoid “Na’vi” in order to mine for the precious material scattered throughout their rich woodland. In exchange for the spinal surgery that will fix his legs, Jake gathers intel for the cooperating military unit spearheaded by gung-ho Colonel Quaritch, while simultaneously attempting to infiltrate the Na’vi people with the use of an “avatar” identity. While Jake begins to bond with the native tribe and quickly falls in love with the beautiful alien Neytiri, the restless Colonel moves forward with his ruthless extermination tactics, forcing the soldier to take a stand – and fight back in an epic battle for the fate of Pandora.

Anabolic processes tend toward "building up" organs and tissues . These processes produce growth and differentiation of cells and increase in body size, a process that involves synthesis of complex molecules . Examples of anabolic processes include the growth and mineralization of bone and increases in muscle mass. Endocrinologists have traditionally classified hormones as anabolic or catabolic, depending on which part of metabolism they stimulate. The classic anabolic hormones are the anabolic steroids , which stimulate protein synthesis, muscle growth, and insulin . The balance between anabolism and catabolism is also regulated by circadian rhythms , with processes such as glucose metabolism fluctuating to match an animal's normal periods of activity throughout the day. [3]

The secretion of hypothalamic, pituitary, and target tissue hormones is under tight regulatory control by a series of feedback and feed- forward loops. This complexity can be demonstrated using the growth hormone (GH) regulatory system as an example. The stimulatory substance growth hormone releasing hormone (GHRH) and the inhibitory substance somatostatin (SS) both products of the hypothalamus, control pituitary GH secretion. Somatostatin is also called growth hormone-inhibiting hormone (GHIH). Under the influence of GHRH, growth hormone is released into the systemic circulation, causing the target tissue to secrete insulin-like growth factor-1, IGF-1. Growth hormone also has other more direct metabolic effects; it is both hyperglycemic and lipolytic. The principal source of systemic IGF-1 is the liver, although most other tissues secrete and contribute to systemic IGF-1. Liver IGF-1 is considered to be the principal regulator of tissue growth. In particular, the IGF-1 secreted by the liver is believed to synchronize growth throughout the body, resulting in a homeostatic balance of tissue size and mass. IGF-1 secreted by peripheral tissues is generally considered to be autocrine or paracrine in its biological action.

Next comes the second ATP investment step, the phosphofructokinase 1 (PFK-1) reaction. Using ATP, this transferase adds another P i to fructose-6-phosphate (F6P), creating fructose 1,6-bisphosphate (F-1,6-BP). The product is still a reducing sugar. At a standard free energy change of -14 kJ/mol , it is also an irreversible reaction. It is an important point in glycolysis regulation, and there are several molecules that inhibit or accelerate this reaction. A high [ATP] will inhibit PFK-1, as it indicates that glycolysis is not needed – there is enough energy/ATP already. High [AMP], thus low [ATP], indicates the opposite, and the AMP will outcompete the ATP for the allosteric site on PFK-1. It can also be noted that in low ATP instances, thus high [ADP], two ADP can react together to form one ATP. However, AMP is a side product of this “desperate” reaction, and it contributes to activating PFK-1. PFK-1 is more sensitive to AMP than to ATP. This occurs mostly in the muscle cells. In the liver, there is another enzyme, PFK-2 . Instead of making F-1,6-P, this enzyme forms fructose- 2 ,6-biphosphate. It is not a reducing sugar. This compound is an activator of PFK-1. The PFK-1 reaction itself is rather slow, and since a pathway’s speed is determined by the slowest step, then PFK-1 must be accelerated. Feed forward control takes place when a build-up of F6P from the previous reaction occurs. rising F6P will open the PFK-2 path, creating F-2,6-P. This is an effective allosteric activator of PFK-1, thus speeding up the overall reaction.

Gluconeogenesis anabolic reaction

gluconeogenesis anabolic reaction

Next comes the second ATP investment step, the phosphofructokinase 1 (PFK-1) reaction. Using ATP, this transferase adds another P i to fructose-6-phosphate (F6P), creating fructose 1,6-bisphosphate (F-1,6-BP). The product is still a reducing sugar. At a standard free energy change of -14 kJ/mol , it is also an irreversible reaction. It is an important point in glycolysis regulation, and there are several molecules that inhibit or accelerate this reaction. A high [ATP] will inhibit PFK-1, as it indicates that glycolysis is not needed – there is enough energy/ATP already. High [AMP], thus low [ATP], indicates the opposite, and the AMP will outcompete the ATP for the allosteric site on PFK-1. It can also be noted that in low ATP instances, thus high [ADP], two ADP can react together to form one ATP. However, AMP is a side product of this “desperate” reaction, and it contributes to activating PFK-1. PFK-1 is more sensitive to AMP than to ATP. This occurs mostly in the muscle cells. In the liver, there is another enzyme, PFK-2 . Instead of making F-1,6-P, this enzyme forms fructose- 2 ,6-biphosphate. It is not a reducing sugar. This compound is an activator of PFK-1. The PFK-1 reaction itself is rather slow, and since a pathway’s speed is determined by the slowest step, then PFK-1 must be accelerated. Feed forward control takes place when a build-up of F6P from the previous reaction occurs. rising F6P will open the PFK-2 path, creating F-2,6-P. This is an effective allosteric activator of PFK-1, thus speeding up the overall reaction.

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