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By A. Agenak. San Joaquin College of Law.

This disease affects both chylomicron assembly in the intestine and VLDL assembly in the liver purchase 180mg diltiazem fast delivery symptoms brain tumor. Both particles require a B apoprotein for their assembly (ApoB-48 for chylomicrons buy generic diltiazem 180mg symptoms nausea headache fatigue, ApoB-100 for VLDL), and MTP binds to the B apoproteins. For both chylomicron and VLDL assembly, a small ApoB–containing particle is first produced within the lumen of the ER. The appro- priate apoB is made on the rough endoplasmic reticulum (RER) and is inserted into the ER lumen during its synthesis (see Chapter 15, section IX). As the protein is being translated, lipid (a small amount of triglyceride) begins to associate with the protein, and the lipid association is catalyzed by MTP. This leads to the generation of small ApoB-containing particles; these particles are not formed in patients with abetalipoproteinemia. Thus, it appears as though MTP activity is necessary to trans- fer triacylglycerol formed within the ER to the ApoB protein. The second stage of particle assembly is the fusion of the initial ApoB particle with triacylglycerol droplets within the ER. MTP also may be required for the transfer of triacylglycerol from the cytoplasm to the lumen of the ER to form this lipid droplet. The symptoms of abetalipoproteinemia include lipid malabsorption (and its accompanying symptoms, such as steatorrhea and vomiting), which can result in caloric deficiencies and weight loss. Because lipid-soluble vitamin distribution occurs through chylomicron circulation, signs and symptoms of deficiencies in the lipid-soluble vitamins may be seen in these patients. ER Lumen ApoB-48 ApoB Larger particle ApoB To Golgi particle for maturation MTP MTP and secretion LIPID TG Ribosome Cytoplasm Fig. A model of microsomal triglyceride transfer protein (MTP) action. MTP is required to transfer lipid to apoB-48 as it is synthesized, and to transfer lipid from the cyto- plasm to the ER lumen. CHAPTER 32 / DIGESTION AND TRANSPORT OF DIETARY LIPIDS 593 Suggested References Berriot-Varoqueaux N, Aggerbeck LP, Samson-Bouma ME, Wetterau JR. The role of the microsomal triglyceride transfer protein in abetalipoproteinemia. Introduction: structure and metabolism of plasm lipoproteins. The Metabolic and Molecular Bases of Inherited Disease, vol II, 8th Ed. In: Nutritional Biochemistry and Metabolism with Clinical Applications. Nutritional Biochemistry and Metabolism with Clin- ical Applications. The most abundant component of chylomicrons is which of the following? The conversion of nascent chylomicrons to mature chylomicrons requires which of the following? The apoproteins B-48 and B-100 are similar with respect to which of the following? Bile salts must reach a particular concentration within the intestinal lumen before they are effective agents for lipid digestion. Type III hyperlipidemia is caused by a deficiency of apoprotein E. Analysis of the serum of patients with this disorder would exhibit which of the following? This section describes a number of such tissues and, in some cases, how the tissues inter- act with the rest of the body to coordinate their functions. A The previous chapters of this text have focused primarily on insulin and glucagon as the major mediators for regulating metabolic pathways; however, a large number of other hormones also regulate the storage and utilization of metabolic fuels (see Chapter 43). These hormones primarily counteract the effects of insulin and are called counter-regulatory hormones. They include growth hormone; thyroid hormone; glucocorticoids, such as cortisol; small peptides, such as the somatostatins; and small molecules, such as the catecholamines. Growth hor- mone works, in part, by inducing the synthesis of the insulin-like growth factors.

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This polymerase can withstand the only a few minutes and in 20 heating and cooling cycles purchase diltiazem 180 mg without prescription treatment of strep throat, the DNA is amplified heat required for separation of DNA strands trusted diltiazem 60mg medications by mail. USE OF RECOMBINANT DNA TECHNIQUES FOR DIAGNOSIS OF DISEASE A. DNA Polymorphisms Polymorphisms are variations among individuals of a species in DNA sequences of the genome. They serve as the basis for using recombinant DNA techniques in the diagnosis of disease. The human genome probably contains millions of different polymorphisms. Some polymorphisms involve point mutations, the substitution of one base for another. Deletions and insertions are also responsi- ble for variations in DNA sequences. Some polymorphisms occur within the cod- ing region of genes. Others are found in noncoding regions closely linked to genes involved in the cause of inherited disease, in which case they can be used as a marker for the disease. CHAPTER 17 / USE OF RECOMBINANT DNA TECHNIQUES IN MEDICINE 307 B. Detection of Polymorphisms The mutation that causes sickle cell anemia abolishes a restriction site 1. RESTRICTION FRAGMENT LENGTH POLYMORPHISMS for the enzyme MstII in the -globin gene. The consequence of this mutation is Occasionally, a point mutation occurs in a recognition site for one of the restric- that the restriction fragment produced by tion enzymes. The restriction enzyme therefore can cut at this restriction site in MstII that includes the 5 -end of the -globin DNA from most individuals, but not in DNA from individuals with this mutation. Mutations also can create restriction sites that are not commonly fragments provides a direct test for the muta- present. In this case, the restriction fragment from this region of the genome will tion. In Will Sichel’s case, both alleles for - be smaller for a person with the mutation than for most individuals. These vari- globin lack the MstII site and produce 1. Carriers have both a normal and a mutant In some cases, the mutation that causes a disease affects a restriction site within allele. Therefore, their DNA will produce both the coding region of a gene. However, in many cases, the mutation affects a restric- the larger and the smaller MstII restriction tion site that is outside the coding region but tightly linked (i. When Will Sichel’s sister Carrie the DNA molecule) to the abnormal gene that causes the disease. This RFLP could Sichel was tested, she was found to have still serve as a biologic marker for the disease. Both types of RFLPs can be used for both the small and the large restriction frag- genetic testing to determine whether an individual has the disease. DETECTION OF MUTATIONS BY ALLELE-SPECIFIC electrophoresis, was confirmed. OLIGONUCLEOTIDE PROBES A gene A (normal) CCTG AGG Other techniques have been developed to detect mutations, because many muta- MstII site tions associated with genetic diseases do not occur within restriction enzyme recognition sites or cause detectable restriction fragment length differences gene S (sickle) CCTGTGG when digested with restriction enzymes. For example, oligonucleotide probes (no MstII site) (containing 15-20 nucleotides) can be synthesized that are complementary to a DNA sequence that includes a mutation. Different probes are produced for alle- B Restriction site absent in sickle-cell β–globin les that contain mutations and for those that have a normal DNA sequence. The gene β–globin region of the genome that contains the abnormal gene is amplified by PCR, and the samples of DNA are placed in narrow bands on nitrocellulose paper (“slot MstII MstII MstII blotting”).

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In liver cheap 180mg diltiazem visa medicine emoji, glu- cocorticoids stimulate gluconeogenesis and the synthesis of glycogen generic 180 mg diltiazem free shipping treatment lupus. The breakdown of liver glycogen is stimulated by epinephrine. CHAPTER 43 / ACTIONS OF HORMONES THAT REGULATE FUEL METABOLISM 795 glucose uptake by certain tissues), but taken together they promote survival in times Otto was now able to explain the of stress. For example, Otto knew the metabolic explana- the degradation of these macromolecules. In response to chronic stress, GCs act tion for the patient’s hyperglycemia. Some of to make fuels available, so that when the acute alarm sounds and epinephrine is Mr. Solemia’s muscle wasting and weakness released, the organism can fight or flee. When GCs are elevated, glucose uptake were caused by the catabolic effect of hyper- by the cells of many tissues is inhibited, lipolysis occurs in peripheral adipose cortisolemia on protein stores, such as those tissue, and proteolysis occurs in skin, lymphoid cells, and muscle. The fatty acids in skeletal muscle, to provide amino acids as that are released are oxidized by the liver for energy, and the glycerol and amino precursors for gluconeogenesis. This cata- acids serve in the liver as substrates for the production of glucose, which is con- bolic action also resulted in the degradation verted to glycogen and stored. The alarm signal of epinephrine stimulates liver of elastin, a major supportive protein of the glycogen breakdown, making glucose available as fuel to combat the acute skin, as well as an increased fragility of the stress. These changes resulted in the easy bruisability and the torn subcutaneous tis- to intracellular receptors, interaction of the steroid-receptor complex with GC sues of the lower abdomen, which resulted response elements on DNA, transcription of genes, and synthesis of specific pro- in red striae or stripes. The plethora (red- teins (see Chapter 16, section III. In some cases, the specific proteins respon- ness) of Mr. Solemia’s facial skin was also sible for the GC effect are known (e. In other cases, the proteins well as by a cortisol-induced increase in the responsible for the GC effect have not yet been identified. BIOCHEMISTRY If Corti Solemia’s problem had The secretory products of the thyroid acinar cells are tetraiodothyronine (thyroxine, been caused by a neoplasm of the T4) and triiodothyronine (T3). The basic adrenal cortex, what would his lev- steps in the synthesis of T3 and T4 in these cells involve the transport or trapping of els of blood ACTH and cortisol have been? Proteolytic cleavage of thyroglobulin releases free T3 and T4. The addi- The steps in thyroid hormone synthesis are stimulated by thyroid-stimulating hor- tional 22–25 g T “produced” 3 mone (TSH), a glycoprotein produced by the anterior pituitary. T3 is through an energy-requiring, iodide-trapping mechanism that is poorly defined but believed to be the predominant biologically may involve the Na ,K -ATPase coupled to a cotransporter for Na and iodide in active form of thyroid hormone in the body. The “central” deposition of fat in patients, such as Corti Solemia, with Cushing’s “disease” or syndrome is not readily explained because GCs actually cause I I lipolysis in adipose tissue. The increased appetite caused by an excess of GC HO O CH2 CH COOH and the lipogenic effects of the hyperinsulinemia that accompanies the GC-induced chronic increase in blood glucose levels have been suggested as possible causes. Why I I NH2 the fat is deposited centrally under these circumstances, however, is not understood. Simultaneously, there is a loss of adipose and muscle tissue below the elbows and knees, exaggerating the appearance of “central obesity” in Cushing’s “disease” or syndrome. HO O CH2 CH COOH I NH2 Approximately 35% of T4 is deiodinated at the 5 position to form T3, and 43% is deiodinated at the 5 position to form the inactive “reverse” T3. The cortisol I Colloid O OH would have acted on the CRH-producing Iodination I Coupling I+ cells of the hypothalamus and the ACTH- I I OH OH secreting cells of the anterior pituitary by a negative feedback mechanism to decrease I ACTH levels in the blood. Because his cortisol and ACTH levels were both high, Mr. Solemia’s tumor was most likely in the pituitary gland or possibly Exocytosis Pinocytosis Tgb in neoplastic extrapituitary tissue that was with T4 (+ T3) secreting ACTH “ectopically. Digestion Tgb Solemia’s tumor was in the anterior pituitary, by lysosomal with T4 not in an extrapituitary ACTH-producing site. The protein thyroglobulin (Tgb) is synthesized in thyroid follicular cells and secreted into the colloid.

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