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Her physician ordered measurements of blood glucose and ketone body levels and made a spot check for ketone bodies in the urine as well as ordering tests to assess the functioning of her heart and kidneys buy 100mcg rhinocort amex. THE FASTING STATE Blood glucose levels peak approximately 1 hour after eating and then decrease as tissues oxidize glucose or convert it to storage forms of fuel purchase rhinocort 100mcg with mastercard. By 2 hours after a meal generic 100mcg rhinocort visa, the level returns to the fasting range (between 80 and 100 mg/dL) discount 100 mcg rhinocort otc. This decrease in blood glucose causes the pancreas to decrease its secretion of insulin order rhinocort 100mcg amex, and the serum insulin level decreases. The liver responds to this hormonal signal by starting to degrade its glycogen stores and release glucose into the blood. If we eat another meal within a few hours, we return to the fed state. However, if we continue to fast for a 12-hour period, we enter the basal state (also known as the postabsorptive state). A person is generally considered to be in the basal state after an overnight fast, when no food has been eaten since dinner the previous evening. By this time, the serum insulin level is low and glucagon is rising. Percy Veere had not eaten much on his first day of hospitalization. Blood Glucose and the Role of the Liver on the morning of his second day of hospi- during Fasting talization was 72 mg/dL (normal, overnight fasting 80–100 mg/dL). Thus, in spite of his The liver maintains blood glucose levels during fasting, and its role is thus critical. Most neurons lack enzymes required for oxidation of fatty nearly normal levels through gluconeogene- acids, but can use ketone bodies to a limited extent. Red blood cells lack mitochon- sis using amino acid precursors. If his blood dria, which contain the enzymes of fatty acid and ketone body oxidation, and can glucose had decreased below 50 to 60 mg/dL use only glucose as a fuel. Therefore, it is imperative that blood glucose not during fasting, his brain would have been decrease too rapidly nor fall too low. Although liver glycogen levels may increase to 200 to 300 g coma and eventual death. Although many after a meal, only approximately 80 g remain after an overnight fast. Fortunately, other tissues, such as the red blood cell, are the liver has another mechanism for producing blood glucose, known as gluconeo- also totally or partially dependent on glu- genesis. In gluconeogenesis, lactate, glycerol, and amino acids are used as carbon cose for energy, they are able to function at sources to synthesize glucose. As fasting continues, gluconeogenesis progressively lower concentrations of blood glucose than adds to the glucose produced by glycogenolysis in the liver. This state occurs after an overnight (12-hour) fast. The circled numbers serve as a guide indicating the approximate order in which the processes begin to occur. Lactate is a product of glycolysis in red blood cells and exercising muscle, glyc- erol is obtained from lipolysis of adipose triacylglycerols, and amino acids are gen- erated by the breakdown of protein. Because our muscle mass is so large, most of the amino acid is supplied from degradation of muscle protein. These compounds travel in the blood to the liver, where they are converted to glucose by gluconeoge- nesis. Because the nitrogen of the amino acids can form ammonia, which is toxic to the body, the liver converts this nitrogen to urea. Urea has two amino groups for just one carbon (NH2-CO-NH2). It is a very soluble, nontoxic compound that can be readily excreted by the kidneys and thus is an efficient means for disposing of excess ammonia. As fasting progresses, gluconeogenesis becomes increasingly more important as a source of blood glucose. After a day or so of fasting, liver glycogen stores are On the second day of hospitaliza- depleted and gluconeogenesis is the only source of blood glucose. At this stage of protein–energy fatty acids, which are quantitatively the major fuel for the human body.

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The structure of apoprotein(a) is very similar to that of plasmino- ease in these women cheap 100 mcg rhinocort with amex. As a result generic rhinocort 100 mcg with amex, the accepted gen purchase rhinocort 100mcg mastercard, a precursor of the protease plasmin that degrades fibrin buy 100mcg rhinocort with mastercard, a major component of blood indications for ERT are now limited to intoler- clots discount rhinocort 100mcg with visa. Lipoprotein(a), however, cannot be converted to active plasmin. There are reports that able “hot flashes” or vaginal dryness. CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 643 B Healed Buried fissure thrombus A Atherosclerotic vessel C Plaque Atherosclerotic Mural Intraintimal fissure plaque intraluminal thrombus with small thrombus thrombus (non-occlusive) D Occlusive intraluminal thrombus Fig. Plaque capsule eroded near the “elbow” of plaque creating an early plaque fissure (A), which may heal as plaque increases in size (B) or may grow as thrombus expands, having an intraluminal portion and an intraintimal por- tion (C). If the fissure is not properly sealed, the thrombus may grow and completely occlude the vessel lumen (D), causing an acute infarction of tissues downstream of the vessel occlu- sion. STEROID HORMONES Cholesterol is the precursor of all five classes of steroid hormones: glucocorticoids, mineralcorticoids, androgens, estrogens, and progestins. These hormones are syn- thesized in the adrenal cortex, ovaries, testes, and ovarian corpus luteum. Steroid hormones are transported through the blood from their sites of synthesis to their tar- get organs, where, because of their hydrophobicity, they cross the cell membrane and bind to specific receptors in either the cytoplasm or nucleus. The bound recep- tors then bind to DNA to regulate gene transcription (see Chapter 16, section III. Because of their hydrophobicity, steroid hormones must be complexed with a serum protein. Serum albumin can act as a nonspecific carrier for the steroid hormones, but there are specific carriers as well. The cholesterol used for steroid hormone synthesis is either synthesized in the tissues from acetyl CoA, extracted from intracellular cholesterol ester pools, or taken up by the cell in the form of cholesterol-containing lipoproteins (either internalized by the LDL-recep- tor, or absorbed by the SR-B1 receptor). In general, glucocorticoids and progestins contain 21 carbons, androgens contain 19 carbons, and estrogens contain 18 car- bons. The specific complement of enzymes present in the cells of an organ deter- mines which hormones the organ can synthesize. The oxidative reactions that lead to the synthesis and secretion of glucocorticoids such as cortisol are stimulated by adrenal corticotrophic hormone (ACTH). The role of cortisol as a stress-released hormone is discussed in Chapter 43. Mineralocorticoids such as aldosterone are also synthesized in the adrenal cor- tex and are secreted in response to angiotensin II or III, rising potassium levels in the blood, or hyponatremia (low levels of sodium ions in the blood). Aldosterone stimulates sodium reuptake in the kidney, sweat glands, salivary glands, and other 644 SECTION SIX / LIPID METABOLISM Vera Leizd consulted her gynecolo- tissues, with a resultant increase in extracellular fluid volume and eventually in gist, who confirmed that her prob- blood pressure. The angiotensins are produced in response to a reduction in extra- lems were probably the result of an cellular fluid volume, which may occur as a result of such things as excessive excess production of androgens (virilization) sweating, persistent vomiting without sufficient rehydration, or bleeding without and ordered blood and urine studies to deter- adequate replacement of blood. In males, testosterone is commonly converted to dihydrotestosterone, a higher-affinity form of the hormone, within specific target tissues. This active form of the hormone stimulates the production of sperm proteins in Sertoli cells and the development of secondary sex characteristics. Estrogens such as 17- -estradiol are synthesized in the ovarian follicle and the corpus luteum, from which their secretion is stimulated by follicle-stimulating hor- mone (FSH). In the female, 17 -estradiol feeds back negatively on the synthesis and secretion of the pituitary gonadotropins, such as FSH. Estrogen and proges- terone prepare the uterine endometrium for implantation of the fertilized ovum, and among other actions promotes differentiation of the mammary gland. Progestogens such as progesterone are synthesized in the corpus luteum, and their secretion is stimulated by LH. As mentioned, in concert with estradiol, prog- esterone prepares the uterine endometrium for implantation of the fertilized ovum and acts as a differentiation factor in mammary gland development. The biosynthesis of glucocorticoids and mineralocorticoids (in the adrenal cor- tex), and that of sex steroids (in the adrenal cortex and gonads), requires four cytochrome P450 enzymes (see Chapter 24). These monooxygenases are involved in the transfer of electrons from NADPH through electron transfer protein interme- diates to molecular oxygen, which then oxidizes a variety of the ring carbons of cholesterol. Cholesterol is converted to progesterone in the first two steps of synthesis of all steroid hormones.

The APC Apoptosis is a normal part of multiple processes in complex organisms: embryo- complex activates -catenin for proteolytic genesis buy rhinocort 100mcg with amex, the maintenance of proper cell number in tissues buy cheap rhinocort 100mcg online, the removal of infected degradation discount 100mcg rhinocort amex. It acts as a transcription factor or otherwise injured cells buy cheap rhinocort 100 mcg, the maintenance of the immune system 100mcg rhinocort fast delivery, and aging. It can that increases synthesis of myc and other genes be initiated by injury, radiation, free radicals or other toxins, withdrawal of growth regulating cell cycle progression. A form of apoptosis is a normal part of embryonic development. For example, the development of the nervous system uses apoptosis to destroy neurons that have not made the proper connections with target cells. Neurons are produced in excess, and more than 50% of developing neurons are eliminated by programmed cell death. Those neurons that have made the correct connections survive by secreting growth factors that block apoptosis. CHAPTER 18 / THE MOLECULER BIOLOGY OF CANCER 329 factors or hormones, binding of pro-apoptotic cytokines, or interactions with cyto- Death receptor toxic T cells in the immune system. Apoptosis can protect organisms from the neg- ative effect of mutations by destroying cells with irreparably damaged DNA before they proliferate. Just as an excess of a growth signal can produce an excess of unwanted cells, the failure of apoptosis to remove excess or damaged cells can Mitochondrion contribute to the development of cancer. Normal Pathways to Apoptosis Apoptosis can be divided into three general phases: an initiation phase, a signal bcl-2 integration phase, and an execution phase. Apoptosis can be initiated by external signals that work through death receptors, such as tumor necrosis factor (TNF), or deprivation of growth hormones (Fig. It can also be initiated by intracellu- Active initiator lar events that affect mitochondrial integrity (e. In the signal integration phase, these pro-apoptotic signals are balanced against anti-apoptotic cell survival signals by several pathways, Execution including members of the Bcl-2 family of proteins. The execution phase is carried procaspases Proteolysis out by proteolytic enzymes called caspases. CASPASES execution caspases Caspases are cysteine proteases that cleave peptide bonds next to an aspartate residue. They are present in the cell as procaspases, zymogen-type enzyme precur- Cellular sors activated by proteolytic cleavage of the inhibitory portion of their polypeptide proteins chain. The different caspases are generally divided into two groups according to their function: initiator caspases, which specifically cleave other procaspases, and Apoptotic fragments execution caspases, which cleave other cellular proteins involved in maintaining cellular integrity (see Fig. The initiator caspases are activated through two Fig. They activate the execution caspases, which cleave protein kinases involved in cell adhesion, lamins that form the inner lining of the nuclear envelope, actin and other proteins required for cell structure, and DNA repair enzymes. They also cleave an inhibitor protein of the endonuclease CAD (caspase- activated DNase). With destruction of the nuclear envelope, additional endonucle- ases (Ca2+- and Mg2+ -dependent) also become activated. THE DEATH RECEPTOR PATHWAY TO APOPTOSIS The death receptors are a subset of TNF-1 receptors, which includes Fas/CD95, TNF- Receptor 1 (TNF-R1) and Death Receptor 3 (DR3). These receptors form a trimer that binds TNF-1 or another death ligand on its external domain and adaptor proteins to its intracellular domain (Fig. The activated TNF–receptor complex forms the scaf- fold for binding two molecules of procaspase 8, which autocatalytically cleave each other to form active caspase 8. Caspase 8 is an initiator caspase that activates execution caspases 3, 6, and 7. Caspase 8 also cleaves a Bcl-2 protein, Bid, to a form that acti- vates the mitochondrial integrity pathway to apoptosis. THE MITOCHONDRIAL INTEGRITY PATHWAY TO APOPTOSIS Apoptosis is also induced by intracellular signals indicating that cell death should occur. Examples of these signals include growth factor withdrawal, cell injury, the release of certain steroids, and an inability to maintain low levels of intracellular calcium.

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