Мне насрать как и чем какой мудак зарабатывает. Хоть мочу внутривенно пусть советует, хоть кетоз.
Вы не в состоянии понять разницу между здоровыми людьми, которые от безделья качаются, и людьми с нарушенным обменом веществ, не в состоянии прочитать что-то серьезнее качковской писанины, и имеете наглость судить о моих знаних.
Идите нахуй, мудак.
Among fasting patients with fatty acid oxidation defects, the free fatty acids cannot be metabolized because of the existing metabolic block; as a result, they are stored in the cytoplasm as triglycerides, thereby resulting in progressive lipid storage myopathy with weakness, hypertrophic and/or dilated cardiomyopathy, and fatty liver. In addition, with fasting, glucose and glycogen stores are depleted and ketone bodies are not generated because of the existing metabolic block. As a result, the ratio of serum free fatty acids to ketones increases from the normal ratio of 1:1 to more than 2:1, which is highly suggestive of a block in beta-oxidation [1,9 (http://www.uptodate.com/contents/approach-to-the-metabolic-myopathies/abstract/1,9)].
Ninety percent of the hepatic acetyl-CoA, however, is converted into ketones, which are an important source of energy for all tissues, particularly the brain. During prolonged fasting, ketones provide an important source of energy in brain tissue because the blood-brain barrier is impermeable to long-chain fatty acids [18 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/18)]. The intramitochondrial beta-oxidation of fatty acids requires the existence of chain-length specific enzymes. The complete oxidation of fatty acids is mediated by at least 11 enzymes (table 1 (http://www.uptodate.com/contents/image?imageKey=RHEUM%2F26842&topicKey=PEDS%2F6212&source=see_link)) [19,20 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/19,20)].
In metabolic defects of intramitochondrial fatty acid oxidation, mitochondrial beta-oxidation of DCAs is impaired at a time when the production of DCAs is increased due to the recruitment of peroxisomal omega-oxidation [22 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/22)], hence the detection of DCAs in the urine. However, DCAs are also produced in other settings, including normal fasting, diabetic ketoacidosis, and diets containing medium-chain triglycerides. In addition, thioesterases catalyze the deacylation of coenzyme A and the conjugation of the acyl groups to glycine and to carnitine (http://www.uptodate.com/contents/l-carnitine-drug-information?source=see_link) [23,24 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/23,24)]. Thus, the detection of acylcarnitine derivatives in serum, and the detection of dicarboxylic acids and acylglycines in urine, has proven useful in the diagnosis of inborn errors of fatty acid oxidation [25,26 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/25,26)].
Impairments at any of the important regulatory steps of lipid metabolism can lead to a myopathy and, in some cases, involvement of other organs. (See "Causes of metabolic myopathies" (http://www.uptodate.com/contents/causes-of-metabolic-myopathies?source=see_link).)
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no subject
Date: 2011-12-19 04:37 pm (UTC)Вы не в состоянии понять разницу между здоровыми людьми, которые от безделья качаются, и людьми с нарушенным обменом веществ, не в состоянии прочитать что-то серьезнее качковской писанины, и имеете наглость судить о моих знаних.
Идите нахуй, мудак.
Among fasting patients with fatty acid oxidation defects, the free fatty acids cannot be metabolized because of the existing metabolic block; as a result, they are stored in the cytoplasm as triglycerides, thereby resulting in progressive lipid storage myopathy with weakness, hypertrophic and/or dilated cardiomyopathy, and fatty liver. In addition, with fasting, glucose and glycogen stores are depleted and ketone bodies are not generated because of the existing metabolic block. As a result, the ratio of serum free fatty acids to ketones increases from the normal ratio of 1:1 to more than 2:1, which is highly suggestive of a block in beta-oxidation [1,9 (http://www.uptodate.com/contents/approach-to-the-metabolic-myopathies/abstract/1,9)].
Ninety percent of the hepatic acetyl-CoA, however, is converted into ketones, which are an important source of energy for all tissues, particularly the brain. During prolonged fasting, ketones provide an important source of energy in brain tissue because the blood-brain barrier is impermeable to long-chain fatty acids [18 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/18)]. The intramitochondrial beta-oxidation of fatty acids requires the existence of chain-length specific enzymes. The complete oxidation of fatty acids is mediated by at least 11 enzymes (table 1 (http://www.uptodate.com/contents/image?imageKey=RHEUM%2F26842&topicKey=PEDS%2F6212&source=see_link)) [19,20 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/19,20)].
In metabolic defects of intramitochondrial fatty acid oxidation, mitochondrial beta-oxidation of DCAs is impaired at a time when the production of DCAs is increased due to the recruitment of peroxisomal omega-oxidation [22 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/22)], hence the detection of DCAs in the urine. However, DCAs are also produced in other settings, including normal fasting, diabetic ketoacidosis, and diets containing medium-chain triglycerides. In addition, thioesterases catalyze the deacylation of coenzyme A and the conjugation of the acyl groups to glycine and to carnitine (http://www.uptodate.com/contents/l-carnitine-drug-information?source=see_link) [23,24 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/23,24)]. Thus, the detection of acylcarnitine derivatives in serum, and the detection of dicarboxylic acids and acylglycines in urine, has proven useful in the diagnosis of inborn errors of fatty acid oxidation [25,26 (http://www.uptodate.com/contents/energy-metabolism-in-muscle/abstract/25,26)].
Impairments at any of the important regulatory steps of lipid metabolism can lead to a myopathy and, in some cases, involvement of other organs. (See "Causes of metabolic myopathies" (http://www.uptodate.com/contents/causes-of-metabolic-myopathies?source=see_link).)