By I. Gamal. Mississippi State University.

Shingosine is derived from serine and a specific fatty acid order 20mg forzest with visa injections for erectile dysfunction that truly work, palmitate quality 20 mg forzest erectile dysfunction ginseng. Ceramides are amides formed from sphingosine by attaching a fatty acid to the O O O CH2 R1 O CH2 R1 R2 C O CH O CH R2 C O CH O + 3 CH CH N CH CH O– 2 2 2 3 2 – CH3 – O O Choline Phosphatidylcholine Phosphatidic acid Fig. Phospholipids found in membranes, such as phosphatidylcholine, have a polar group attached to the phosphate. CHAPTER 5 / STRUCTURES OF THE MAJOR COMPOUNDS OF THE BODY 65 Phosphorylcholine Palmitoleic acid is an 7 fatty acid. It has one double bond between O CH + 3 the 9th and 10th carbons. It has 16 Ceramide OCH2 CH2 N CH3 carbons, like palmitic acid, so the double – CH3 bond must be at the 7th carbon from the O end. Sphingomyelin Galactose Ceramide Gal Galactocerebroside Oligosaccharide Ceramide Glc Gal GalNAc NANA Ganglioside Site of added sugar CH2OH H NH H OH C O CH (CH2)n CH CH3 (CH2)12 CH3 Ceramide Fig. The structure of ceramide is shown at the bottom of the figure. The portion of ceramide shown in blue is sphingosine. Different groups are added to the hydroxyl group of ceramide to form sphingomyelin, galactocerebrosides, and gangliosides. NANA N-acetylneuraminic acid, also called sialic acid; Glc glucose; Gal galactose; GalNAc N-acetylgalac- tosamine. Various sphingolipids are then formed by attaching different groups to the hydroxyl group on ceramide. As reflected in the names for cerebrosides and gangliosides, these sphingolipids contain sugars attached to the hydroxyl group of ceramide through glycosidic bonds. They are glycolipids (more specifically, gly- cosphingolipids). Sphingomyelin, which contains a phophorylcholine group attached to ceramide, is a component of cell membranes and the myelin sheath around neurons. Steroids Steroids contain a four-ring structure called the steroid nucleus (Fig. Choles- terol is the steroid precursor in human cells from which all of the steroid hormones are synthesized by modifications to the ring or C20 side chain. Although cholesterol is not very water soluble, it is converted to amphipathic water-soluble bile salts such as cholic acid. Bile salts line the surfaces of lipid droplets called micelles in the lumen of the intestine, where they keep the droplets emulsified in the aqueous environment. Cholesterol is one of the compounds synthesized in the human from branched 5- carbon units with one double bond called an isoprenyl unit (see Fig. Isoprenyl 66 SECTION TWO / CHEMICAL AND BIOLOGICAL FOUNDATIONS OF BIOCHEMISTRY 21 22 24 26 CH3 CH2 CH2 CH3 20CH 23CH2 25CH CH3 – CH3 27 COO 18 12 17 HO OH 11 13 16 C 19CH3 14 15 1 9 2 10 8 A 3 7 4 6 HO HO HO OH Cholesterol Cholic acid 17β–Estradiol Fig. The bile salt, cholic acid, and the steroid hormone 17 -estradiol are derived from cholesterol and contain the steroid ring structure. What structural features account units are combined in long chains to form other structures, such as the side chains of for the differences in the solubility coenzyme Q in humans and vitamin A in plants. NITROGEN-CONTAINING COMPOUNDS Nitrogen, as described in Section IB2, is an electronegative atom with two unshared electrons in its outer valence shell. At neutral pH, the nitrogen in amino groups is usually bonded to four other atoms and carries a positive charge. However, the pres- ence of nitrogen atom in an organic compound will increase its solubility in water, whether the nitrogen is charged or uncharged. Amino Acids Amino acids are compounds that contain an amino group and a carboxylic acid group. In proteins, the amino acids are always L- amino acids (the amino group is attached Although D-amino acids are not to the carbon in the L-configuration) (Fig. These same amino acids also serve usually incorporated into proteins as precursors of nitrogen-containing compounds in the body, such as phosphatidyl- in living organisms, they serve choline (see Fig. How- many other functions in bacteria, such as ever, our metabolic reactions occasionally produce an amino acid that has a or synthesis of cross-links in cell walls. How- ever, only amino acids are incorporated into proteins.

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Its main function is to deliver oxygen to the tissues through the binding of oxygen to hemoglobin cheap 20mg forzest otc erectile dysfunction pills for diabetes. When the number of red blood cells is reduced order 20 mg forzest free shipping impotence medical definition, an anemia is said to have developed. This can be attributable to many causes, including nutri- tional deficiencies or mutations (hereditary anemias). The morphology of the red blood cell can sometimes aid in distinguishing between the various types of anemia. Red blood cell metabolism is geared toward preserving the ability of these cells to transport oxygen, as well as to regulate oxygen binding to hemoglobin. Glycol- ysis provides energy and NADH to protect the oxidation state of the heme-bound iron. The hexose monophosphate shunt pathway generates NADPH to protect red blood cell membranes from oxidation. Heme synthesis, which uses succinyl CoA and glycine for all of the carbon and nitrogen atoms in the structure, occurs in the precursors of red blood cells. Inherited defects in heme synthesis lead to a class of diseases known as the porphyrias. Because the red blood cell normally passes through the very narrow capillaries, its membrane must be easily deformable. This deformability is, in part, attributable to the complex cytoskeletal structure that sur- rounds the erythrocyte. Mutations in these structural proteins can lead to less deformable cells. Among other functions, the hematologic system is responsible for hemostasis as well as for maintaining a constant blood volume (see Chapter 45). A tear in the wall 781 of a vessel can lead to blood loss, which, when extensive, can be fatal. Repairing ves- sel damage, whether internal or external, is accomplished by a complicated series of zymogen activations of circulating blood proteins resulting in the formation of a fibrin clot (the coagulation cascade). Platelets play a critical role in hemostasis not only through their release of procoagulants but through their ability to form aggregates within the thrombus (clot) as well. Clots function as a plug, allowing vessel walls to repair and preventing further blood loss. Conversely, inappropriate clot formation in vessels that supply blood to vital organs or tissues can have devastating consequences, such as an acute cerebral or myocardial infarction. Because clotting must be tightly con- trolled, intricate mechanisms exist that regulate this important hematologic function. The liver is an altruistic organ that provides multiple services for other tissues (see Chapter 46). It supplies glucose and ketone bodies to the rest of the body when fuel stores are limiting. It disposes of ammonia as urea when amino acid degradation occurs. It is the site of detoxification of xenobiotics, and it synthesizes many of the proteins found in the blood. The liver synthesizes fatty acids and cholesterol and dis- tributes them to other tissues in the form of very-low-density lipoprotein (VLDL). The liver also synthesizes bile acids for fat digestion in the intestine. The liver recy- cles cholesterol and triglyceride through its uptake of intermediate density lipopro- tein (IDL), chylomicron and VLDL remnants, and low-density lipoprotein (LDL) particles. Because of its protective nature and its strategic location between the gut and the systemic circulation, the liver has “first crack” at all compounds that enter the blood through the enterohepatic circulation. Thus, xenobiotic compounds can be detoxified as they enter the liver before they have a chance to reach other tissues. Muscle cells contain unique pathways that allow them to store energy as creatine phosphate and to closely regulate their use of fatty acids as an energy source (see Chapter 47). The adenosine monophosphate (AMP)-activated protein kinase is an important regulator of muscle energy metabolism. Muscle is comprised of different types of contractile fibers that derive their energy from different sources.

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The phosphorylated form of pose cells do not take glucose up at a normal this enzyme is active and cleaves fatty acids from triacylglycerols (Fig proven 20mg forzest psychological erectile dysfunction drugs. As a hormone) also activate this enzyme (see Chapter 43) cheap 20mg forzest with mastercard erectile dysfunction treatment natural way. Glyceroneogenesis and resyn- result, her blood glucose levels are elevated. However, in this case, she produces insulin, but her tissues are resistant to its actions. Mechanisms That Affect Ketone Body Production by the Liver Would Ann Sulin’s serum triacyl- glycerol level be elevated? As fatty acids are released from adipose tissue during fasting, they travel in the blood complexed with albumin. These fatty acids are oxidized by various tissues, particularly muscle. In the liver, fatty acids are transported into mitochondria 674 SECTION SIX / LIPID METABOLISM Because the adipose tissue of indi- Glucagon viduals with type 2 diabetes melli- + tus is relatively resistant to insulin’s inhibition of HSL and its stimulation G-protein of LPL, Ann Sulin’s serum triacylglycerol + level would be elevated for the same rea- sons as those that caused the hypertriglyc- eridemia in Di Abietes. Cell adenylate membrane cyclase 1 ATP cAMP protein kinase A regulatory (inactive) 2 subunit-cAMP glycogen synthase– P ADP (inactive) phosphorylase ATP 4 kinase active protein kinase A (inactive) ATP 3 glycogen synthase ADP (active) phosphorylase kinase– P (active) Glycogen 5 Pi ATP ADP 6 phosphorylase b phosphorylase a (inactive) (active) P Glucose-1-P Glucose-6-P Liver Blood glucose Fig. Regulation of the enzymes of glycogen degradation in the liver. Glucagon (or epinephrine) binds to its cell membrane receptor, initially activating a G protein, which acti- vates adenylate cyclase. As cAMP levels rise, inhibitory subunits are removed from pro- Insulin normally inhibits lipolysis tein kinase A, which now phosphorylates phosphorylase kinase (step 3). The cAMP- by decreasing the lipolytic activity dependent protein kinase also phosphorylates glycogen synthase, inactiving the enzyme. Phosphorylated phosphorylase kinase phosphorylates glycogen phosphorylase. Phos- such as Di Abietes, who have a deficiency of phorylated glycogen phosphorylase catalyzes the phosphorolysis of glycogen, 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.

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