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For CYP2E1 order 100mg kamagra soft free shipping, RH is ethanol are found in actively drinking patients cheap 100 mg kamagra soft. The protein is also stabilized against degra- (CH3CH2OH) and ROH is acetaldehyde dation kamagra soft 100 mg cheap. In general cheap kamagra soft 100mg mastercard, the mechanism for induction of P450 enzymes by their substrates (CH3COH) order 100mg kamagra soft overnight delivery. Whether ethanol induction of CYP2E1 follows this general P450 is an Fe-heme similar to that pattern has not yet been shown. In inducers is responsible for several types of drug interactions. For example, phe- CYP2E1, the “2” refers to the gene family, nobarbital, a barbiturate long used as a sleeping pill or for treatment of epilepsy, which comprises isoenzymes with greater is converted to an inactive metabolite by cytochrome P450 monooxygenases CYP2B1 and than 40% amino acid sequence identity. After treatment with phenobarbital, CYP2B2 is increased 50- to 100-fold. Individ- “E” refers to the subfamily, a grouping of uals who take phenobarbital for prolonged periods develop a drug tolerance as CYP2B2 isoenzymes with greater than 55 to 60% is induced, and the drug is metabolized to an inactive metabolite more rapidly. Conse- sequence identity, and the “1” refers to the quently, these individuals use progressively higher doses of phenobarbital. Ethanol is an inhibitor of the phenobarbital-oxidizing P450 system. When large amounts of ethanol are consumed, the inactivation of phenobarbital is directly or indi- rectly inhibited. Therefore, when high doses of phenobarbital and ethanol are consumed at the same time, toxic levels of the barbiturate can accumulate in the blood. CHAPTER 25 / METABOLISM OF ETHANOL 463 Although induction of CYP2E1 increases ethanol clearance from the blood, it has As blood ethanol concentration negative consequences. Acetaldehyde may be produced faster than it can be metab- rises above 18 mM (the legal intox- olized by acetaldehyde dehydrogenases, thereby increasing the risk of hepatic injury. In addition, cytochrome P450 enzymes are capable of generating free radicals, and central nervous system are affected. Induction of CYP2E1 increases the rate of ethanol clearance from the blood, thereby E. Variations in the Pattern of Ethanol Metabolism contributing to increased alcohol tolerance. However, the apparent ability of a chronic The routes and rates of ethanol oxidation vary from individual to individual. Dif- alcoholic to drink without appearing inebri- ferences in ethanol metabolism may influence whether an individual becomes a ated is partly a learned behavior. Factors that determine the rate and route of ethanol oxidation in individuals include: • Genotype—Polymorphic forms of alcohol dehydrogenases and acetaldehyde dehydrogenases can greatly affect the rate of ethanol oxidation and the accumu- lation of acetaldehyde. CYP2E1 activity may vary as much as 20-fold between individuals, partly because of differences in the inducibility of different allelic variants. After chronic consumption of ethanol, gastric ADH decreases in both men and women, but the gender differences become even greater. Gender differ- ences in blood alcohol levels also occur because women are normally smaller. Furthermore, in females, alcohol is distributed in a 12% smaller water space because a woman’s body composition consists of more fat and less water than that of a man. Small amounts of ethanol are metabo- lized most efficiently through the low Km pathway of class I ADH and class II ALDH. Little accumulation of NADH occurs to inhibit ethanol metabolism via these dehydrogenases. However, when higher amounts of ethanol are consumed in a short period, a disproportionately greater amount is metabolized through MEOS. MEOS, which has a much higher Km for ethanol, functions principally at high concentrations of ethanol. A higher activity of MEOS would be expected to correlate with tendency to develop alcohol-induced liver disease, because both acetaldehyde and free radical levels would be increased. The Energy Yield of Ethanol Oxidation The ATP yield from ethanol oxidation to acetate varies with the route of ethanol metabolism. If ethanol is oxidized by the major route of cytosolic ADH and mito- chondrial ALDH, one cytosolic and one mitochondrial NADH are generated with a maximum yield of 5 ATP. Oxidation of acetyl CoA in the TCA cycle and electron transport chain leads to the generation of 10 high-energy phosphate bonds. How- ever, activation of acetate to acetyl CoA requires two high-energy phosphate bonds (one in the cleavage of ATP to AMP pyrophosphate and one in the cleavage of pyrophosphate to phosphate), which must be subtracted.

Cholesterol is obtained from the diet or synthesized by a pathway that occurs in most cells of the body kamagra soft 100 mg online, but to a greater extent in cells of the liver and intestine cheap kamagra soft 100mg otc. The precursor for cholesterol synthesis is acetyl CoA discount kamagra soft 100 mg on-line, which can be produced from glucose order kamagra soft 100mg free shipping, fatty acids discount 100mg kamagra soft amex, or amino acids. Two molecules of acetyl CoA form ace- toacetyl CoA, which condenses with another molecule of acetyl CoA to form hydroxymethylglutaryl CoA (HMG-CoA). This reaction, catalyzed by HMG-CoA reductase, is the major rate- limiting step of cholesterol synthesis. Mevalonate produces isoprene units that condense, eventually forming squalene. Cyclization of squalene produces the steroid ring system, and a number of subsequent reactions generate cholesterol. The adrenal cortex and the gonads also synthesize cholesterol in significant amounts and use it as a precursor for steroid hormone synthesis. Cholesterol is packaged in chylomicrons in the intestine and in very-low-den- sity lipoprotein (VLDL) in the liver. It is transported in the blood in these lipopro- tein particles, which also transport triacylglycerols. As the triacylglycerols of the blood lipoproteins are digested by lipoprotein lipase, chylomicrons are converted to chylomicron remnants, and VLDL is converted to intermediate-density lipoprotein (IDL) and subsequently to low-density lipoprotein (LDL). These prod- ucts return to the liver, where they bind to receptors in cell membranes and are taken up by endocytosis and digested by lysosomal enzymes. LDL is also endocy- tosed by nonhepatic (peripheral) tissues. Cholesterol and other products of lyso- somal digestion are released into the cellular pools. The liver uses this recycled cholesterol, and the cholesterol that is synthesized from acetyl CoA, to produce VLDL and to synthesize bile salts. Intracellular cholesterol obtained from blood lipoproteins decreases the synthesis of cholesterol within cells, stimulates the storage of cholesterol as cholesterol esters, and decreases the synthesis of LDL receptors. LDL receptors are found on the sur- face of the cells and bind various classes of lipoproteins prior to endocytosis. Although high-density lipoprotein (HDL) contains triacylglycerols and choles- terol, its function is very different from that of the chylomicrons and VLDL, which transport triacylglycerols. HDL exchanges proteins and lipids with the other lipoproteins in the blood. HDL transfers apolipoprotein E (apoE) and apoCII to chylomicrons and VLDL. After digestion of the VLDL triacylglycerols, apoE and apoC are transferred back to HDL. In addition, HDL obtains cholesterol from 619 II 620 SECTION SIX / LIPID METABOLISM other lipoproteins and from cell membranes and converts it to cholesterol esters by the lecithin:cholesterol acyltransferase (LCAT) reaction. Then HDL either directly transports cholesterol and cholesterol esters to the liver or transfers cho- lesterol esters to other lipoproteins via the cholesterol ester transfer protein (CETP). Ultimately, lipoprotein particles carry the cholesterol and cholesterol esters to the liver, where endocytosis and lysosomal digestion occur. Elevated levels of cholesterol in the blood are associated with the formation of atherosclerotic plaques that can occlude blood vessels, causing heart attacks and strokes. Although high levels of LDL cholesterol are especially atherogenic, high levels of HDL cholesterol are protective because HDL particles are involved in the process of removing cholesterol from tissues, such as the lining cells of ves- sels, and returning it to the liver. Bile salts, which are produced in the liver from cholesterol obtained from the blood lipoproteins or synthesized from acetyl CoA, are secreted into the bile. They are stored in the gallbladder and released into the intestine during a meal. The bile salts emulsify dietary triacylglycerols, thus aiding in digestion. The digestive products are absorbed by intestinal epithelial cells from bile salt micelles, tiny microdroplets that contain bile salts at their water interface. After the contents of the micelles are absorbed, most of the bile salts travel to the ileum, where they are resorbed and recycled by the liver. Less than 5% of the bile salts that enter the lumen of the small intestine are eventually excreted in the feces. Although the fecal excretion of bile salts is relatively low, it is a major means by which the body disposes of the steroid nucleus of cholesterol.

As glucose is being oxidized to CO kamagra soft 100 mg free shipping, it is first oxidized to pyruvate in the path- In the liver and most other tissues purchase 100mg kamagra soft with visa, 2 glucose order 100mg kamagra soft with mastercard, fats discount 100 mg kamagra soft with mastercard, and other fuels are oxi- way of glycolysis discount kamagra soft 100 mg online. The acetyl group enters dized to the 2-carbon acetyl group the tricarboxylic acid (TCA) cycle, where it is completely oxidized to CO2. Energy O from the oxidative reactions is used to generate ATP. Liver glycogen stores reach a maximum of approximately 200 to 300 g after a CH3 C of acetyl CoA. CoA, which makes the acetyl group high-carbohydrate meal, whereas the body’s fat stores are relatively limitless. As the more reactive, is a cofactor (coenzyme A) glycogen stores begin to fill, the liver also begins converting some of the excess glu- derived from the vitamin pantothenate. Both the glycerol and the fatty acid moieties of acetyl group of acetyl CoA is completely oxi- the triacylglycerols can be synthesized from glucose. The fatty acids are also dized to CO2 in the TCA cycle (see Fig 1. Adenosine triphosphate (ATP) is the final obtained preformed from the blood. The liver does not store triacylglycerols, how- product of these oxidative pathways. It con- ever, but packages them along with proteins, phospholipids, and cholesterol into the tains energy derived from the catabolic lipoprotein complexes known as very-low-density lipoproteins (VLDL), which are energy-producing oxidation reactions and secreted into the bloodstream. Some of the fatty acids from the VLDL are taken up transfers that energy to anabolic and other energy-requiring processes in the cell. Glucose Metabolism In Other Tissues The glucose from the intestine that is not metabolized by the liver travels in the Fuel metabolism is often discussed blood to peripheral tissues (most other tissues), where it can be oxidized for as though the body consisted only of brain, skeletal and cardiac mus- energy. Glucose is the one fuel that can be used by all tissues. Many tissues store cle, liver, adipose tissue, red blood cells, kid- small amounts of glucose as glycogen. Muscle has relatively large glycogen ney, and intestinal epithelial cells (“the gut”). These are the dominant tissues in terms of Insulin greatly stimulates the transport of glucose into the two tissues that have overall fuel economy, and they are the tissues the largest mass in the body, muscle and adipose tissue. Of course, all tissues on the transport of glucose into other tissues. BRAIN AND OTHER NEURAL TISSUES The brain and other neural tissues are very dependent on glucose for their energy needs. They generally oxidize glucose via glycolysis and the TCA cycle completely to CO2 and H2O, generating ATP (see Fig. Except under conditions of starvation, glucose is their only major fuel. Glucose is also a major precursor of neurotransmitters, the chemicals that convey electrical impulses (as ion gradients) between neurons. If our blood glucose drops much below normal levels, we become dizzy and light-headed. If blood glucose continues to drop, we become comatose and ultimately die. Under normal, nonstarving conditions, the brain and the rest of the nervous system require roughly 150 g glucose each day. RED BLOOD CELLS Glucose is the only fuel used by red blood cells, because they lack mitochondria. Fatty acid oxidation, amino acid oxidation, the TCA cycle, the electron transport chain, and oxidative phosphorylation (ATP generation that is dependent on oxygen 26 SECTION ONE / FUEL METABOLISM and the electron transport chain) occur principally in mitochondria. Glucose, in con- trast, generates ATP from anaerobic glycolysis in the cytosol and, thus, red blood Glycogen cells obtain all their energy by this process. In anaerobic glycolysis, the pyruvate formed from glucose is converted to lactate and then released into the blood (see [ATP] Fig. Glucose Without glucose, red blood cells could not survive. Red blood cells carry O2 Lactate Fatty acids from the lungs to the tissues. Without red blood cells, most of the tissues of the body Acetyl CoA would suffer from a lack of energy because they require O2 to completely convert their fuels to CO2 and H2O. MUSCLE Exercising skeletal muscles can use glucose from the blood or from their own glycogen stores, converting glucose to lactate through glycolysis or oxidizing it completely to CO2 and H2O.

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