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ZOOMING IN Which division of the autonomic nervous system has ganglia closer to the effector organ? THE NERVOUS SYSTEM: THE SPINAL CORD AND SPINAL NERVES 195 Table 9•3 Divisions of the Autonomic Nervous System CHARACTERISTICS DIVISIONS Sympathetic Nervous System Parasympathetic Nervous System Origin of fibers Thoracic and lumbar regions of the spinal Brain stem and sacral regions of the cord quality extra super avana 260mg; thoracolumbar spinal cord order 260 mg extra super avana with amex; craniosacral Location of ganglia Sympathetic chains and three single collateral Terminal ganglia in or near the effector ganglia (celiac 260 mg extra super avana visa, superior mesenteric buy 260 mg extra super avana with amex, infe- organ rior mesenteric) Neurotransmitter Adrenaline and noradrenaline cheap extra super avana 260mg mastercard; adrenergic Acetylcholine; cholinergic Effects (see Table 9-4) Response to stress; fight-or-flight response Reverses fight-or-flight (stress) response; stimulates some activities Parasympathetic Nervous System The parasympa- because in the most primitive terms, the person must decide thetic motor pathways begin in the craniosacral (kra-ne-o- to stay and “fight it out” with the enemy or to run away from SAK-ral) areas, with fibers arising from cell bodies in the danger. If you think of what happens to a person who is brainstem (midbrain and medulla) and the lower (sacral) frightened or angry, you can easily remember the effects of part of the spinal cord. From these centers, the first fibers impulses from the sympathetic nervous system: extend to autonomic ganglia that are usually located near 9 ◗ Increase in the rate and force of heart contractions. The pathways then continue along post- tive heartbeat and partly to constriction of small arter- ganglionic neurons that stimulate the involuntary tissues. The neurons of the parasympathetic system release the neurotransmitter acetylcholine, leading to the de- ◗ Dilation of blood vessels to skeletal muscles, bringing scription of this system as cholinergic (activated by more blood to these tissues. Functions of the Autonomic ◗ Stimulation of the central portion of the adrenal gland. This produces hormones, including epinephrine, that Nervous System prepare the body to meet emergency situations in many Most organs are supplied by both sympathetic and parasym- ways (see Chapter 12). The sympathetic nerves and pathetic fibers, and the two systems generally have opposite hormones from the adrenal gland reinforce each other. The sympathetic part of the ANS tends to act as an ◗ Increase in basal metabolic rate. It promotes what is called the fight-or-flight response (for near objects). Effects of the Sympathetic and Parasympathetic Systems on Table 9•4 Selected Organs Effector Sympathetic System Parasympathetic System Pupils of eye Dilation Constriction Sweat glands Stimulation None Digestive glands Inhibition Stimulation Heart Increased rate and strength of beat Decreased rate of beat Bronchi of lungs Dilation Constriction Muscles of digestive system Decreased contraction (peristalsis) Increased contraction Kidneys Decreased activity None Urinary bladder Relaxation Contraction and empty- ing Liver Increased release of glucose None Penis Ejaculation Erection Adrenal medulla Stimulation None Blood vessels to: Skeletal muscles Dilation Constriction Skin Constriction None Respiratory system Dilation Constriction Digestive organs Constriction Dilation 196 CHAPTER NINE Box 9-3 A Closer Look Cell Receptors: Getting the MessageCell Receptors: Getting the Message eurons use neurotransmitters to communicate with other found on effector cells of the parasympathetic nervous sys- Ncells at synapses. ACh can either stimulate or inhibit muscarinic recep- “docking sites,” the receptors on the receiving (postsynaptic) tors depending on the effector organ. A neurotransmitter fits into its receptor like stimulates digestive organs but inhibits the heart. Once the neurotransmitter binds, the receptor The second class of receptors is the adrenergic receptors, initiates events that change the postsynaptic cell’s activity. They are found Different receptors’ responses to the same neurotransmitter on effector cells of the sympathetic nervous system. They are may vary, and a cell’s response depends on the receptors it further subdivided into alpha ( ) and beta ( ), each with contains. When norepineph- Among the many different classes of identified receptors, rine (or epinephrine) binds to adrenergic receptors, it can ei- two are especially important and well-studied. The first is the ther stimulate or inhibit, depending on the organ. For exam- cholinergic receptors, which bind acetylcholine (ACh). With some exceptions, 1 and 1 receptors each named for drugs that bind to them and mimic ACh’s ef- usually stimulate, whereas 2 and 2 receptors inhibit. For example, “beta- ◗ Nicotinic receptors (which bind nicotine) are found on blockers” regulate the heart in cardiac disease by preventing skeletal muscle cells and stimulate muscle contraction when 1 receptors from binding epinephrine, the neurotransmitter ACh is present. Saliva, for example, flows more easily and pro- systems not directly involved in the response to stress, fusely, and its quantity and fluidity increase. If you try to eat Most organs of the body receive both sympathetic and while you are angry, you may note that your saliva is thick parasympathetic stimulation, the effects of the two sys- and so small in amount that you can swallow only with dif- tems on a given organ generally being opposite. Under these circumstances, when food does reach 4 shows some of the actions of these two systems. Box 9- the stomach, it seems to stay there longer than usual. The parasympathetic system brings about con- striction of the pupils, slowing of the heart rate, and con- striction of the bronchial tubes. It also stimulates the for- Checkpoint 9-15 Which division of the ANS stimulates a stress response, and which division reverses the stress response? Learning the meanings of these parts can help you remember words and interpret unfamiliar terms.

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The purpose of these phosphate transfers is to activate both carbon 5 and the hydroxyl group on carbon 3 for further reactions in which these groups will leave the molecule discount extra super avana 260 mg with amex. The phosphate group attached to the C-3 hydroxyl group of mevalonate in the 3- phospho-5-pyrophosphomevalonate intermediate is removed along with the car- boxyl group on C-1 proven extra super avana 260mg. This produces a double bond in the 5-carbon product quality extra super avana 260 mg, ∆3- isopentenyl pyrophosphate buy cheap extra super avana 260mg on line, the first of two activated isoprenes necessary for the synthesis of cholesterol extra super avana 260mg on line. The second activated isoprene is formed when ∆3- isopentenyl pyrophosphate is isomerized to dimethylallyl pyrophosphate (see Fig. Stage 3: Condensation of Six Activated 5-Carbon Isoprenes to Form the 30-Carbon Squalene The next stage in the biosynthesis of cholesterol involves the head-to-tail conden- sation of isopentenylpyrophosphate and dimethylallyl pyrophosphate. In this reac- tion, one pyrophosphate group is displaced, and a 10-carbon chain, known as ger- anyl pyrophosphate, is generated (Fig. After this, two molecules of farne- form covalent bonds with proteins, syl pyrophosphate undergo a head-to-head fusion, and both pyrophosphate groups particularly the G proteins and cer- are removed to form squalene, a compound first isolated from the liver of sharks tain protooncogene products involved in signal (genus Squalus). Squalene contains 30 carbons (24 in the main chain and 6 in the transduction. These hydrophobic groups methyl group branches; see Fig. The formation of activated isoprene units (∆3-isopentenyl pyrophosphate and dimethylallyl pyrophosphate) from mevalonic acid. Stage 4: Conversion of Squalene to the Four-Ring Steroid Nucleus The enzyme squalene monooxygenase adds a single oxygen atom from O2 to the end of the squalene molecule, forming an epoxide. NADPH then reduces the other oxygen atom of O2 to H2O. The unsaturated carbons of the squalene 2, 3- epoxide are aligned in a way that allows conversion of the linear squalene epoxide into a cyclic structure. The cyclization leads to the formation of lanosterol, a sterol with the four-ring structure characteristic of the steroid nucleus. A series of complex CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 627 O O O O O P P O– + P P O– O– O– O– O– Dimethlylallyl pyrophosphate ∆3-isopentenyl pyrophosphate PPi O O O P P O– O– O– Geranyl pyrophosphate O O O P P O– O– O– PPi O O O P P O– O– O– Squalene Farnesyl pyrophosphate NADPH + H+ Squalene O2 NADPH + H+ Farnesyl pyrophosphate monooxygenase H2O NADP+ NADP+ 2PP i 3 2 Squalene O Fig. The activation of the isoprene Squalene 2,3-epoxide units drives their condensation to form geranyl pyrophosphate, farnesyl pyrophosphate, and Cyclase squalene. SEVERAL FATES OF CHOLESTEROL HO Lanosterol Almost all mammalian cells are capable of producing cholesterol. Most of the biosynthesis of cholesterol, however, occurs within liver cells, although the gut, the Many reactions adrenal cortex, and the gonads (as well as the placenta in pregnant women) also pro- duce significant quantities of the sterol. Although a fraction of hepatic cholesterol is used for the synthesis of hepatic membranes, the bulk of synthesized cholesterol is secreted from the hepatocyte as one of three moieties: cholesterol esters, biliary cholesterol, or bile acids. Cholesterol ester production in the liver is catalyzed by acyl-CoA-cholesterol acyl transferase (ACAT). ACAT catalyzes the transfer of a fatty acid from coenzyme A to the hydroxyl group on carbon 3 of cholesterol (Fig. Cholesterol esters are more hydrophobic than is free cholesterol. The HO liver packages some of the esterified cholesterol into the hollow core of lipopro- Cholesterol teins, primarily VLDL. VLDL is secreted from the hepatocyte into the blood and Fig. The conversion of squalene to cho- transports the cholesterol esters (and triacylglycerols, phospholipids, apoproteins, lesterol. These tissues then use the cholesterol for the synthesis of membranes, cate how the cyclization reaction occurs. The residual cholesterol esters not used in these ways are stored in the liver for later use. The hepatic cholesterol pool also serves as a source of cholesterol for the synthesis of the relatively hydrophilic bile acids and their salts. These derivatives of choles- terol are highly effective detergents because they contain both polar and nonpolar regions. They are introduced in the biliary ducts of the liver. They are stored and HO Cholesterol concentrated in the gallbladder and later discharged into the gut in response to the ingestion of food.

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The cAMP- by decreasing the lipolytic activity dependent protein kinase also phosphorylates glycogen synthase discount extra super avana 260 mg fast delivery, inactiving the enzyme effective extra super avana 260 mg. Phosphorylated phosphorylase kinase phosphorylates glycogen phosphorylase generic 260 mg extra super avana with visa. Phos- such as Di Abietes extra super avana 260mg for sale, who have a deficiency of phorylated glycogen phosphorylase catalyzes the phosphorolysis of glycogen buy generic extra super avana 260mg line, producing glu- insulin, have an increase in lipolysis and a cose 1-phosphate. These events occur during fasting and produce glucose to maintain a rela- subsequent increase in the concentration of tively constant level of blood glucose. The liver, in turn, uses some of these fatty acids to syn- thesize triacylglycerols, which then are used because acetyl CoA carboxylase is inactive, malonyl CoA levels are low, and CPTI in the hepatic production of VLDL. VLDL is (carnitine:acyltransferase I) is active (see Fig. Acetyl CoA, produced by - not stored in the liver but is secreted into the oxidation, is converted to ketone bodies. Ketone bodies are used as an energy source blood, raising its serum concentration. Her hypertriglyc- of acetyl CoA in the liver (derived from fat oxidation) inhibit pyruvate dehydroge- eridemia is the result, therefore, of both nase (which prevents pyruvate from being converted to acetyl CoA) and activate overproduction of VLDL by the liver and pyruvate carboxylase, which produces oxaloacetate for gluconeogenesis. The decreased breakdown of VLDL triacylglyc- oxaloacetate does not condense with acetyl CoA to form citrate for two reasons. The serum begins to appear cloudy when The first is that under these conditions (a high rate of fat oxidation in the liver mito- the triacylglycerol level reaches 200 mg/dL. The high NADH level inhibits isocitrate dehy- ther, the degree of serum opalescence drogenase. As a result, citrate accumulates and inhibits citrate synthase from pro- increases proportionately. The second reason that citrate synthesis is depressed is that the CHAPTER 36 / INTEGRATION OF CARBOHYDRATES AND LIPID METABOLISM 675 Glycolysis Gluconeogenesis Glucose glucokinase glucose 6–phosphatase (high Km) Glucose 6–phosphate Fructose 6–phosphate F–2,6–P phosphofructokinase-1 fructose 1,6–bisphosphatase + – Fructose 1,6–bisphosphate Dihydroxyacetone Glyceraldehyde phosphate 3–phosphate Phosphoenolpyruvate phosphoenolpyruvate + cAMP carboxykinase pyruvate pyruvate kinase– P kinase Oxaloacetate (inactive) (active) pyruvate carboxylase Acetyl CoA+ P Pyruvate i Fig. Regulation of gluconeogenesis and glycolysis during fasting. The gluconeogenic enzymes phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase, and glucose 6-phosphatase are induced. Fructose 1,6-bisphosphatase is also active because, during fast- ing, the level of its inhibitor, fructose 2,6-bisphosphate, is low. The corresponding enzymes of glycolysis are not very active during fasting. The rate of glucokinase is low because it has a high Km for glucose and the glucose concentration is low. Phosphofructokinase-1 is not very active because the concentration of its activator fructose 2,6-bisphosphate is low. Pyru- vate kinase is inactivated by cAMP-mediated phosphorylation. Fuel Utilization by Various Tissues during Starvation (Fasting) Tissue Glucose Fatty Acids Ketone Bodies Nervous system Skeletal muscle Heart muscle Liver Intestinal epithelial cells Kidney 676 SECTION SIX / LIPID METABOLISM Fasted state hormone sensitive lipase TG (inactive) Blood protein kinase hormone + sensitive cAMP lipase– P (active) + Low insulin/high glucagon ATP FA FA other FA FA lipases FA FA Glycerol Glycerol Adipose cell Fig. Regulation of hormone-sensitive lipase (HSL) in adipose tissue. During fasting, the glucagon/insulin ratio rises, causing cAMP levels to be elevated. Protein kinase A is acti- vated and phosphorylates HSL, activating this enzyme. HSL-P initiates the mobilization of adipose triacylglycerol by removing a fatty acid (FA). Other lipases then act, producing fatty acids and glycerol. Insulin stimulates the phosphatase that inactivates HSL in the fed state. Regulation of the Use of Glucose and Fatty Acids by Muscle During exercise, the fuel that is used initially by muscle cells is muscle glycogen. As exercise continues and the blood supply to the tissue increases, glucose is taken up from the blood and oxidized. Liver glycogenolysis and gluconeogenesis replenish the blood glucose supply. However, as insulin levels drop, the concentration of GLUT4 transporters in the membrane is reduced, thereby reducing glucose entry from the cir- Muscle GLUT4 transporters also culation into the muscle. Thus, if produces NADH and acetyl CoA, which slow the flow of carbon from glucose energy levels are very low, and AMP levels through the reaction catalyzed by pyruvate dehydrogenase (see Fig.

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