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Metabolic pathways interact in a complex way in order to allow an adequate regulation. This interaction includes the enzymatic control of each pathway, each organ's metabolic profile and hormone control.
hexokinase: is inhibited by glucose-6-P (product inhibition) phosphofructokinase: is inhibited by ATP and citrate (which signals the abundance of citric acid cycle intermediates). It is also inhibited by H+, which becomes important under anaerobiosis (lactic fermentation produces lactic acid, resulting on a lowering of the pH ). Probably this mechanism prevents the cell from using all its ATP stock in the phosphofrutokinase reaction, which would prevent glucose activation by hexokinase. It is stimulated by its substrate (fructose-6-phosphate), AMP and ADP (which signal the lack of available energy), etc. pyruvate kinase: inhibited by ATP and acetyl-CoA
Regulation of gluconeogenesis
Flow is regulated in the gluconeogenesis-specific reactions. Pyruvate carboxilase is activated by acetyl-CoA, which signals the abundance of citric acid cycle intermediates, i.e., a decreased need of glucose.
pyruvate dehydrogenase: is inhibited by its products, acetyl-CoA and NADH citrate synthase: is inhibited by its product, citrate. It is also inhibited by NADH and succinyl-CoA (which signal the abundance of citric acid cycle intermediates). isocitrate dehydrogenase and -ketoglutarate dehydrogenase: like citrate synthase, these are inhibited by NADH and succinyl-CoA. Isocitrate dehydrogenase is also inhibited by ATP and stimulated by ADP. All aforementioned dehydrogenases are stimulated by Ca2+. This makes sense in the muscle, since Ca2+ release from the sarcoplasmic reticulum triggers muscle contraction, which requires a lot of energy. This way, the same "second messenger" activates an energy-demanding task and the means to produce that energy.
Metabolic flow through the pentose phosphate pathway is controled by the activity of glucose-6phosphate dehydrogenase, which is controlled by NADP+ availability.
Liver
The maintenance of a fairly steady concentration of glucose in the blood is one of the liver's main functions. This is accomplished through gluconeogenesis and glycogen synthesis and degradation. It synthesizes ketone bodies when acetyl-CoA is plenty. It is also the site of urea synthesis.
Adipose tissue
It synthesizes fatty acids and stores them as triacylglycerols. Glucagon activates a hormonesensitive lipase, which hydrolizes triacylglycerols yielding glycerol and fatty acids. These are then released into the bloodstream in lipoproteins.
Muscle
Muscles use glucose, fatty acids, ketone bodies and aminoacids as energy source. It also contains a reserve of creatine-phosphate, a compound with a high phosphate-transfer potential that is able to phosphorilate ADP to ATP, thereby producing energy without using glucose. The amount of creatine in the muscle is enough to sustain about 3-4 s of exertion. After this period, the muscle uses glycolysis, first anaerobically (since it is much faster than the citric acid cycle), and later (when the increased acidity slows phosphofrutokinase enough for the citric acid cycle to become non-rate-limiting) in aerobic conditions.
Kidney
It can perform gluconeogenesis and release glucose into the bloodstream. It is also responsible for the excretion of urea, electrolytes, etc. Metabolic acidosis may be increased by the action of the urea cycle, since urea synthesis (which takes place in the liver) uses HCO3-, thereby further lowering blood pH. Under these circunstances, nitrogen may be eliminated by the joint action of kidney and liver: excess nitrogen is first incorporated in glutamine by glutamine synthetase. Kidney glutaminase then cleaves glutamine in glutamate e NH3, which the kidney immediately excretes. This process allows nitrogen excretion without affecting blood bicarbonate levels.
Hormone control
Hormone control is mainly effected through the action of two hormones synthesized by the pancreas: insulin and glucagon. Insulin is released by the pancreas when blood glucose levels are high, i.e., after a meal. Insulin stimulates glucose uptake by the muscle, glycogen synthesis, and triacylglyceride synthesis by the adipose tissue. It inhibits gluconeogenesis and glycogen degradation. Glucagon is released by pancreas when blood glucose levels drop too much. Its effects are opposite those of insulin: in liver, glucagon stimulates glycogen degradation and the absorption of gluconeogenic aminoacids. It inhibits glycogen synthesis and promotes the release of fatty acids by adipose tissue.
Further reading
Biochemistry, by Donald Voet & Judith Voet An excellent text. It presents Biochemistry with frequent references to organic chemistry and biochemical logic. Highly reccommended for students of Biochemistry, Chemistry and Pharmaceutical Sciences. Textbook of Biochemistry with Clinical Correlations, Thomas Devlin Strongly advised to students in Nursing, Medicine, Dentistry, etc. Plenty of examples of application of biochemical knowledge to clinical cases. Biochemistry, Stryer A widely used classical text, frequently updated and re-issued. Principles of Biochemistry, Lehninger A widely used classical text, frequently updated and re-issued.