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Most of glycogen synthesis occurs through the lengthening of the polysaccharide UDP–Glucose glycogen synthase chains of a preexisting glycogen molecule (a glycogen primer) in which the reducing UDP end of the glycogen is attached to the protein glycogenin discount 10 mg glucotrol xl visa diabetes symptoms 9 days. To lengthen the glycogen chains purchase glucotrol xl 10 mg line diabetes mellitus latin, glucosyl residues are added from UDP-glucose to the nonreducing ends of the chain by glycogen synthase. The anomeric carbon of each glucosyl residue is attached Glycogen core in an -1,4 bond to the hydroxyl on carbon 4 of the terminal glucosyl residue. When the chain reaches 11 residues in length, a 6- to 8-residue piece is cleaved by amylo-4:6- 6 UDP–Glucose transferase and reattached to a glucosyl unit by an -1,6 bond. Both chains continue to glycogen synthase 6 UDP lengthen until they are long enough to produce two new branches. This process contin- ues, producing highly branched molecules. Glycogen synthase, the enzyme that attaches the glucosyl residues in 1,4-bonds, is the regulated step in the pathway. The synthesis of new glycogen primer molecules also occurs. Glycogenin, the Glycogen core protein to which glycogen is attached, glycosylates itself (autoglycosylation) by 4:6 transferase attaching the glucosyl residue of UDP-glucose to the hydroxyl side chain of a ser- (branching enzyme) ine residue in the protein. The protein then extends the carbohydrate chain (using UDP-glucose as the substrate) until the glucosyl chain is long enough to serve as a substrate for glycogen synthase. Degradation of Glycogen Glycogen is degraded by two enzymes, glycogen phosphorylase and the debrancher Continue with glycogen synthesis enzyme (Fig. The enzyme glycogen phosphorylase starts at the end of a chain at all non-reducing ends and successively cleaves glucosyl residues by adding phosphate to the terminal gly- Fig. See text for cosidic bond, thereby releasing glucose 1-phosphate. The debrancher enzyme, which catalyzes the removal of major roles; increased sites for the four residues closest to the branchpoint, has two catalytic activities: it acts as a synthesis and degradation, and transferase and as an 1,6-glucosidase. As a transferase, the debrancher first enhancing the solubility of the molecule. The one glucosyl residue remaining at the 1,6-branch is hydrolyzed by the amylo-1,6-glucosidase activity of the debrancher, resulting in the release of free glucose. Thus, one glucose and approximately 7 to 9 glucose 1-phos- phate residues are released for every branchpoint. A lysosomal glucosidase hydrolyzes this glycogen to glucose. REGULATION OF GLYCOGEN SYNTHESIS disrupt the function of liver and muscle cells. AND DEGRADATION Children with this disease usually die of heart failure at a few months of age. The regulation of glycogen synthesis in different tissues matches the function of glycogen in each tissue. Liver glycogen serves principally for the support of Glucose residue Glucose residue blood glucose during fasting or during extreme need (e. Glycogen Storage Diseases Type Enzyme Affected Primary Organ Involved Manifestationsa Glycogen core O Glycogen synthase Liver Hypoglycemia, hyperke- 8 Pi b tonemia, FTT early death glycogen phosphorylase c I Glucose 6-phosphatase Liver Enlarged liver and kidney, 8 Glucose–1–P ( ) (Von Gierke’s disease) growth failure, fasting hypoglycemia, acidosis, lipemia, thrombocyte dys- function. II Lysosomal - All organs with lysosomes Infantile form: early-onset glucosidase progressive muscle hypo- Glycogen core tonia, cardiac failure,death before 2 years; juvenile α–1,6–glucosidase form: later-onset myopa- thy with variable cardiac 1 Glucose ( ) involvement, adultform: limb-girdle muscular dys- Glycogen core trophy-like features. Glyco- gen deposits accumulate glycogen phosphorylase in lysosomes. Degradation continues III Amylo-1,6-glucosidase Liver, skeletal muscle, Fasting hypoglycemia; (debrancher) heart hepatomegaly in infancy in some. IV Amylo-4,6-glucosidase Liver Hepatosplenomegaly; (branching enzyme) symptoms may arise from a hepatic reaction to the presence of a foreign body (glycogen with long outer branches). V Muscle glycogen phos- Skeletal muscle Exercise-induced muscular phorylase (McArdle’s pain, cramps, and pro- disease) gressive weakness, sometimes with A series of inborn errors of metab- myoglobinuria olism, the glycogen storage dis- VI Liver glycogen Liver Hepatomegaly, mild hypo- phosphorylase glycemia, good eases, result from deficiencies in prognosis the enzymes of glycogenolysis (see Table VII Phosphofructokinase-I Muscle, red blood cells As in type V, in addition, 28. Muscle glycogen phosphorylase, the enzymopathic hemolysis key regulatory enzyme of glycogen degrada- IXd Phosphorylase kinase Liver As in VI. Why Reproduced with permission, from Annu Rev Nutr 1993; 13:85. Therefore, there are deficiency of liver glycogen phosphorylase several subtypes of this disease, corresponding to defects in the different subunits. CHAPTER 28 / FORMATION AND DEGRADATION OF GLYCOGEN 517 Table 28.
This makes the strength examination somewhat more subjective and focuses on the importance of the examiner having ex- tensive pediatric experience purchase glucotrol xl 10 mg without prescription blood sugar range after eating. Muscle Tone Muscle tone is another important aspect in monitoring the assessment of gait impairments purchase glucotrol xl 10mg without a prescription diabetic diet needs. In routine clinical evaluations, gastrocnemius and rectus spasticity provides a general overview. Also, subjective comments about the relative importance of the spasticity and the children’s support, as well as problems that the spasticity is causing, should be noted. For more detailed assessments, the major motor groups in the lower extremities should have numerical assessment of spasticity. The modified Ashworth scale is pre- ferred because it provides more options and allows notation of hypotonia (Table 7. Passive Range-of-Motion Assessment Muscle contractures are monitored by routinely recording specific measures made in the same fashion. These measures often include specific joint range of motion as accurately as the clinician can determine. Notation should also be made with regard to the source of the contracture, especially if it is be- lieved to be a muscle contracture or a fixed joint-based contracture. Bone deformities and length should be noted as well. The specific joint examina- tion should include a back examination with comments of scoliosis as de- termined by the forward bend test, significant lordosis, or kyphosis present in standing or sitting. At the hip, knee, ankle, and foot, standard joint ranges of motion are recorded. A videotape of these children should be made in an open area with a predetermined format. The format requires that the children be undressed to only thin underwear or swimming suits. The videotape is made with a frontal and a rear view, then with both right and left lateral views. The videotape should include gait with bare feet, with the shoes and orthotics that are typ- ically worn, and the children should be asked to run. Also, different assistive devices are included as appropriate. Usually, the videotape is 1 to 2 minutes long and is seldom more than 3 minutes long. A storage and retrieval system for the videotapes must be available so they can be retrieved for each clinic visit. At each visit, the video is reviewed as the children’s gait is observed. On routine evaluations, a videotape is always made at the first evaluation, and a new videotape is added as changes are noted with each examination. When children are under age 3 years, a new videotape is typically made every 6 months. From 3 to 12 years of age, a new videotape is made every 12 months, and over 12 years of age, approximately every 2 to 3 years. This time table is individualized to each child and a new videotape is made only when some change is noted based on a subjective clinical evaluation of the child and of previous videotapes. Kinematics During kinematic evaluations, the motion of each joint is measured as the children walk. These measurements are used to provide additional informa- tion to help make major interventional decisions, such as surgery or difficult orthotic decisions. Also, the kinematic evaluation is important as a measure Figure 7. The most common gait meas- of children’s response to treatment. Kinematic evaluations are performed urement system requires that the individual only as part of a full gait analysis. The modern interest in measurements of being measured is instrumented with retro- human motion started in the first half of the 1900s with the use of stop-frame reflective markers that are imaged by multiple video pictures from which each angle could be drawn to assign measures video cameras.
Results Textbooks Many physicians use textbooks to guide their clinical practice discount glucotrol xl 10mg otc diabetes causes signs symptoms and treatment. Of the 45 textbooks buy 10mg glucotrol xl amex diabetes diet best fruits, there was no specific guidance on the duration, frequency or length of ice treatment in 17. There was advice on the length of treatment in 28 texts but the recommendations varied with the type of injury, its location and severity, and the type of ice therapy recommended. There was advice given on the frequency of treatment in 21 texts and 22 advised on the optimum duration of treatment. It was clear from this small study, which is open to many possible criticisms, that there is little consensus among textbooks on one of the most common treatments in soft tissue injury management. If there is little agreement in textbooks, answer may be found in the original research. This was searched and organised into a number of key areas, looking first at the effect on skin temperature. As expected, the drop in skin temperature was proportional to the temperature and duration of application. Direct application of a wet ice pack for 5 minutes reduced skin temperature to 7⋅6ºC, and, after 10 minutes, the skin temperature was 5ºC. Ice may be applied using various modalities and in one study comparing wet ice, dry ice and cryogen packs, the mean skin temperatures were 12ºC, 9⋅9ºC and 7⋅3ºC respectively after 15 minutes. Other studies confirmed these general findings, and using a standard ice pack (1kg ice in a plastic bag) the initial skin temperature of 19ºC dropped to 14ºC at 30 minutes. Animal studies Researchers have used animal models to examine the effect of cold on muscle physiology. There are, of course, limitations to this research and temperature effect cannot always be generalised to humans. A number of studies confirm the effect of ice in reducing muscle temperature and, in a study of ice application for 20 minutes in sheep,21 intramuscular temperature reduction did not return to pretreatment levels after two hours. When ice was applied a second time, intramuscular temperature continued to fall. Higher temperatures were recorded in the traumatised limb. In a study of cold applied to the skin of the mouse, increased blood vessel permeability with fluid extravasation and oedema occurred with temperatures below 15ºC. In a study of the effect of ice on injured rat muscle, however, cryotherapy did not reduce microvascular diameters or decrease microvascular perfusion. Human studies Animal studies can help us understand the physiological effect of temperature reduction but the key to clinical care is to understand the therapeutic effect in clinical practice. A number of researchers have examined the effect of tissue temperature reduction, but it is difficult to compare the results of the different studies because of variation in research methods and measurements. The temperature reduction at tissue level is illustrated in one study where ice was applied continuously for 85 minutes27 and the temperature dropped by 5ºC, 9ºC and 7ºC at depths of 7 cm, 6 cm and 4 cm. Compression may also enhance temperature reduction28 with the changes at 1 cm below the fat layer and at 2 cm below the fat layer being greater with compression at 12⋅8ºC and 10⋅1ºC. Subcutaneous fat, being an insulating material, inhibits the cooling effect and while significant cooling occurs with 10 minutes of ice application to a depth of 2 cm in those with less than 1 cm of fat,29 athletes with more than 2 cm of fat, required 20–30 minutes. There is an inverse relationship between adipose tissue and temperature decrease so that subcutaneous fat may mean that short duration ice application may be ineffective in cooling deeper tissue levels. The above paragraphs highlight only some of the studies on ice application. The consensus from studies of ice application, for periods varying from five minutes to 85 minutes, is that the temperature is reduced in the first 10 minutes with little further reduction from 10 to 20 minutes. The temperature drop is determined by the area of contact between the ice and the skin, the temperature difference and tissue conductivity but most published studies do not measure the area of ice application, subcutaneous fat, nor use comparable methods of calculating depth, or measuring temperature. Where temperature is 48 The role of ice in soft tissue injury management measured, in human and animal studies, there is wide variation in the temperature recorded at different depths in different studies with wide standard deviations.