Nad to nadh anabolic or catabolic

All energy yielding process are ultimately dependent upon enzymatically catalyzed redox reactions. The most important one for energy metabolism involve biological membranes with bound electron transport processes like photosynthesis and oxidative phosphorylation. Biological oxidation is the primary provider of energy for cellular anabolism, the reductive synthesis of metabolites, by furnishing mobile hydrogens, and phosporylating energy by combining hydrogens with oxygen to form water coupling this process to the production of ATP in the form of oxidative phosphorylation. Central to the oxidation-reduction processes are the vitamin B group containing coenzymes nicotinamide-adenine dinucleotide (NAD) and nicotinamide-adenine dinucleotide phosphate ( NADP , (C00006; oxidized form); NAD (C00003; oxidized form; not phosphorylated at the adenosine ribosyl C2 position).  Being part of the appropriate enzymes the oxidized nicotinamide ring of NAD + or NADP + extracts a hydride (H: - ) from a wide variety of simple metabolites in a process known as dehydrogenation . The enzymes catalyzing the reduction of nicotinamide containing coenzymes are called dehydrogenases . In a typical reaction two hydrogen atoms (including their electrons) are removed from the substrate to produce the oxidized form of the donor. The fate of the two hydrogens differs: one hydrogen with two electrons (H: - ), a hydride ion, is transferred to the nicotinamide ring to produce reduced NADH or NADPH while the other hydrogen is released into solution as a free proton (H + ). The generic form of a redox reaction mechanism catalyzed by enzymes with NAD as cofactor is shown.

Because of the adverse side effects associated with high doses of niacin (see Safety ), it has most often been used in combination with other lipid-lowering medications in slightly lower doses (54) . In particular, LDL cholesterol-lowering statins like simvastatin form the cornerstone of treatment of hyperlipidemia , a major risk factor for CHD. The HDL- Atherosclerosis Treatment Study (HATS), a three-year randomized controlled trial in 160 patients with documented CHD and low HDL levels found that a combination of simvastatin and niacin (2 to 3 grams/day) increased HDL levels, inhibited the progression of coronary artery stenosis (narrowing), and decreased the frequency of cardiovascular events, including myocardial infarction and stroke (58) . Patients with metabolic syndrome display a number of metabolic disorders, including dyslipidemia and insulin resistance , that put them at increased risk for type 2 diabetes mellitus , cardiovascular disease, and mortality. A subgroup analysis of the HATS patients with metabolic syndrome showed a reduction in rate of primary clinical events even though glucose and insulin metabolism were moderately impaired by niacin (59) . Moreover, a review of niacin safety and tolerability among the HATS subjects showed glycemic control in diabetic patients returned to pretreatment values following eight months of disease management with medication and diet (60) . Similarly, the cardiovascular benefit of long-term niacin therapy outweighed the modest increase in risk of newly onset type 2 diabetes in patients from the CDP study (61) .

Table 1. Oxidative pathways of glycolysis employed by various bacteria. Bacterium Embden-Meyerhof pathway Phosphoketolase (heterolactic) pathway Entner Doudoroff pathway Acetobacter aceti - + - Agrobacterium tumefaciens - - + Azotobacter vinelandii - - + Bacillus subtilis major minor - Escherichia coli + - - Lactobacillus acidophilus + - - Leuconostoc mesenteroides - + - Pseudomonas aeruginosa - - + Vibrio cholerae minor - major Zymomonas mobilis - - +

However, there are several other lesser-known mechanisms of generating NADPH, all of which depend on the presence of mitochondria. The key enzymes in these processes are: NADP-linked malic enzyme , NADP-linked isocitrate dehydrogenase , NADP-linked glutamate dehydrogenase and nicotinamide nucleotide transhydrogenase. [1] The isocitrate dehydrogenase mechanism appears to be the major source of NADPH in fat and possibly also liver cells. [2] Also, in mitochondria, NADH kinase produces NADPH and ADP, using NADH and ATP as substrates.

Nad to nadh anabolic or catabolic

nad to nadh anabolic or catabolic

However, there are several other lesser-known mechanisms of generating NADPH, all of which depend on the presence of mitochondria. The key enzymes in these processes are: NADP-linked malic enzyme , NADP-linked isocitrate dehydrogenase , NADP-linked glutamate dehydrogenase and nicotinamide nucleotide transhydrogenase. [1] The isocitrate dehydrogenase mechanism appears to be the major source of NADPH in fat and possibly also liver cells. [2] Also, in mitochondria, NADH kinase produces NADPH and ADP, using NADH and ATP as substrates.

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