Contemporary metabolism

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Contemporary metabolism

edited by Norbert Freinkel

Plenum Medical Book Co., c1979-

  • v. 1
  • v. 2

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Description and Table of Contents

Volume

v. 1 ISBN 9780306401275

Description

Despite a new title, Contemporary Metabolism, Volume 1 is actually the third volume in a continuing series and succeeds The Year in Metabolism 1975- 1976 and The Year in Metabolism 1977. As in the earlier volumes, the same internationally recognized authorities review the noteworthy recent devel- opments in their areas of expertise. In many instances they also address aspects that have not been considered previously. In this volume, Dr. J. Edwin Seegmiller again updates progress in understanding disorders of purine and pyrimidine metabolism. However, particular emphasis is placed on the emerging relationships with immune mechanisms. Dr. Charles S. Lieber is joined by Dr. Enrique Baraona in a continuing review of metabolic actions of ethanol. This chapter examines effects of ethanol on protein metabolism and selected features of lipid metabolism-two areas that were not included in the earlier volumes. Dr. DeWitt S. Goodman's review of disorders oflipid and lipoprotein metabo- lism builds on his previous chapters, but much additional attention is directed to a critical analysis of recent advances in epidemiology and lipoprotein structures. In collaboration with Dr. Brian L. G. Morgan, Dr. Myron Winick devotes his entire chapter to a detailed review of the impact of nutrition upon brain development-an overview that has now been rendered possible by the burgeoning recent developments in this area.

Table of Contents

  • 1 Disorders of Purine and Pyrimidine Metabolism.- 1.1. Introduction.- 1.2. Purine Metabolism.- 1.2.1. Hypoxanthine Reutilization as a Normal Regulator of Purine Synthesis de Novo.- 1.2.2. Drugs That Increase Purine Synthesis de Novo.- 1.2.3. Changes in Purine Metabolism with Cellular Proliferation.- 1.2.4. Role of the Purine Nucleotide Cycle.- 1.2.5. Role of the Purine Nucleotide Cycle in Transport Processes.- 1.2.6. Effect of Fructose.- 1.3. Adenosine Deaminase Deficiency Associated with Severe Combined Immunodeficiency Disease.- 1.3.1. Clinical Presentation.- 1.3.2. Frequency.- 1.3.3. Enzyme Abnormality.- 1.3.4. Screening Tests.- 1.3.5. Prenatal Diagnosis.- 1.3.6. Genetic Heterogeneity.- 1.3.7. Metabolic Studies.- 1.3.8. Model Systems of Adenosine Deaminase Deficiency.- 1.3.9. Treatment.- 1.4. Purine Nucleoside Phosphorylase Deficiency.- 1.4.1. Clinical Presentation.- 1.4.2. Enzyme Abnormalities.- 1.4.3. Purine Metabolites in Urine.- 1.4.4. Metabolic Studies.- 1.4.5. Treatment.- 1.4.6. Purine Nucleoside Phosphorylase Distribution in Human Tissues.- 1.5. Biochemical Basis of the Immunodeficiency in Adenosine Deaminase and Purkie Nucleoside Phosphorylase Deficiency.- 1.5.1. Ribonucleoside Accumulation.- 1.5.2. Pyrimidine Starvation.- 1.5.3. Possible Role of Cyclic AMP.- 1.5.4. Deoxyribonucleoside Accumulation.- 1.5.5. Implications for Therapy.- 1.6. Purine 5'-Nucleotidase Deficiency in Hypogammaglobulinemia.- 1.6.1. Clinical Categories with Low Purine 5'-Nucleotidase.- 1.6.2. Enzyme Characteristics.- 1.7. Adenine Phosphoribosyltransferase Deficiency.- 1.7.1. Clinical Presentation.- 1.7.2. Composition of Calculi.- 1.7.3. Purine Metabolites in the Urine and Plasma.- 1.7.4. Adenine Phosphoribosyltransferase Activity in Erythrocytes.- 1.7.5. Treatment.- 1.7.6. Metabolic Significance.- 1.7.7. Frequency.- 1.8. Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency.- 1.8.1. Genetic Heterogeneity.- 1.8.2. Enzyme Characteristics.- 1.8.3. Enzyme Assays.- 1.8.4. Genetic Transformation.- 1.8.5. Neurological Disorders.- 1.8.6. Attempts to Produce a Hypoxanthine-Guanine- Phosphoribosyltransferase-Deficient Mouse.- 1.8.7. Mechanism of Excessive Purine Synthesis.- 1.8.8. Other Metabolic Correlations.- 1.9. Increased Phosphoribosyl-1-Pyrophosphate Synthetase Activity.- 1.9.1. Enzyme Characteristics.- 1.9.2. Inheritance.- 1.9.3. Biochemical Studies.- 1.10. Xanthinuria.- 1.10.1. Conditions Associated with Hypouricemia.- 1.10.2. Clinical Presentation.- 1.11. Gouty Arthritis.- 1.11.1. Hyperuricemia.- 1.11.2. Diagnosis.- 1.11.3. Disorders Associated with Gout.- 1.11.4. The Kidney and Gout.- 1.11.5. Association of Hyperuricemia and Vascular Disease.- 1.11.6. Association of Hyperuricemia with Avascular Necrosis of the Femoral Head.- 1.11.7. Acute Attack of Gout.- 1.11.8. Treatment.- 1.11.9. Metabolic Factors That Contribute to Hyperuricemia.- 1.12. Decreased Adenylate Deaminase Activity.- 1.13. Abnormalities of Pyrimidine Metabolism.- 1.13.1. Ammonia and Pyrimidine Nucleotide Synthesis.- 1.13.2. Pyrimidine 5'-Nucleotidase Deficiency.- 1.13.3. Orotic Aciduria.- 1.14. Abnormalities of DNA Repair (Xeroderma Pigmentosum).- 1.15. Purine and Pyrimidine Compounds as Inhibitors of Viral and Cellular Proliferation.- 1.15.1. Effective Clinical Treatment of Herpes Encephalitis with Adenine Arabinoside.- 1.15.2. New Antiviral Agents.- References.- 2 Metabolic Actions of Ethanol.- 2.1. Effects of Ethanol on Protein Metabolism.- 2.1.1. Origin of the Increased Liver Protein.- 2.1.2. Type of Proteins That Accumulate after Chronic Alcohol Consumption.- 2.1.3. Mechanisms of the Alcohol-Induced Accumulation of Liver Protein.- 2.1.3.1. Effects of Ethanol on Protein Synthesis.- 2.1.3.2. Effects of Ethanol on Protein Secretion.- 2.1.3.3. Effects of Ethanol on Protein Catabolism.- 2.1.4. Summary of the Alcohol-Induced Alterations of Hepatic Protein Metabolism and Possible Consequences.- 2.2. Effects of Ethanol on Lipid Metabolism.- 2.2.1. Liver Upids.- 2.2.2. Alcohol-Induced Alterations in the Metabolism of Serum Lipoproteins.- 2.2.3. Alcohol, Coronary Heart Disease, and High-Density Lipoproteins.- 2.2.4. Conclusion.- References.- 3 Disorders of Lipid and Lipoprotein Metaboiism.- 3.1. Introduction.- 3.2. Lipoprotein Structure and Metabolism.- 3.2.1. General Review.- 3.2.2. Apolipoprotein C-II.- 3.2.3. High-Density Lipoproteins.- 3.2.4. The Lp(a) Lipoprotein.- 3.2.5. Lipoprotein-X and Liver Disease.- 3.3. Type III Hyperlipoproteinemia.- 3.3.1. Diagnosis.- 3.3.2. Apolipoprotein E.- 3.3.3. Pathophysiology
  • Treatment.- 3.4. Tangier Disease.- 3.5. High-Density Lipoprotein Levels and Coronary Heart Disease.- 3.5.1. Epidemiologic Studies.- 3.5.2. Alcohol, High-Density Lipoproteins, and Coronary Risk.- 3.5.3. Other Clinical Studies.- 3.5.4. Pathophysiology.- 3.5.5. Implications.- 3.6. Cholesterol Metabolism and Its Regulation.- 3.6.1. In Intact Humans.- 3.6.2. In Cultured Cells.- 3.7. Familial Hypercholesterolemia.- 3.7.1. Epidemiologic and Clinical Studies.- 3.7.2. Pathophysiology.- 3.7.3. Therapy.- 3.8. Chronic Renal Failure and Hyperlipidemia.- 3.8.1. Pathophysiology.- 3.8.2. Therapy.- 3.9. Hypertriglyceridemia.- 3.9.1. Pathophysiology.- 3.9.2. Diabetes Mellitus
  • Other Clinical Studies.- 3.9.3. Treatment Effects: Diet, Drugs, Exercise.- 3.10. Hyperlipidemia and Its Treatment.- 3.10.1. Epidemiologic Studies.- 3.10.2. Definition and Classification.- 3.10.3. Diet.- 3.10.4. Drugs.- 3.10.5. Prevention of Ischemic Heart Disease.- References.- 4 Nutrition and Cellular Growth of the Brain.- 4.1. Methods for Producing Early Malnutrition.- 4.2. Malnutrition and Brain Size.- 4.3. Malnutrition and Cellular Growth of the Brain.- 4.4. Malnutrition and Myelination.- 4.5. Other Effects of Malnutrition on the Growing Brain.- 4.6. Regional Changes Induced by Malnutrition.- 4.7. Malnutrition and Cellular Growth of the Peripheral Nerves.- 4.8. Malnutrition and Cellular Growth of the Human Brain.- References.- 5 Metabolic Aspects of Renal Stone Disease.- 5.1. Introduction.- 5.2. Renal Stone Disease Secondary to Increased Crystalloid Excretion.- 5.2.1. Hypercalciuria.- 5.2.2. Hyperuricosuria.- 5.2.3. Hyperoxaluria.- 5.3. Treatment of Renal Stone Disease.- References.- 6 Hormone Receptors, Cyclic Nucleotides, and Control of Cell Function.- 6.1. Introduction.- 6.2. Receptor Systems.- 6.2.1. Physiological Regulation of Receptors.- 6.2.2. Relationship of Receptors to Adenylate Cyclase.- 6.2.3. Opiate Receptors and Endorphins.- 6.2.4. Catecholamine Receptors.- 6.2.4.1. Adrenergic Receptors.- 6.2.4.2. a-Adrenergic Receptors.- 6.2.4.3. Dopamine.- 6.2.5. Hormone Receptors in the Kidney.- 6.2.6. Somatomedin Receptors, Multiplication- Stimulating Activity, and Other Growth Factors.- 6.2.7. Insulin Receptors.- 6.3. Regulation of Adenylate Cyclase.- 6.3.1. Guanine Nucleotide Control.- 6.3.2. Guanosine Triphosphatase.- 6.3.3. Guanine Nucleotides and Agonist Affinity.- 6.3.4. Cholera Toxin and Adenylate Cyclase.- 6.4. Protein Kinases.- 6.4.1. Cell Regulation by Occupied Cyclic AMP Receptors.- 6.5. Calcium Regulation of Cyclic Nucleotide Concentration.- 6.6. Cyclic Nucleotides in the Extracellular Fluids.- 6.6.1. Nephrogenous Cyclic AMP in Parathyroid and Related Disorders.- References.- 7 Diabetes Mellitus.- 7.1. Heterogeneity of Diabetes Mellitus.- 7.1.1. The Histocompatibility System (HLA) and Genetic Susceptibility to Diabetes Mellitus.- 7.1.2. Susceptibility to Viral Infection and Viral Infection in the Etiology of Diabetes Mellitus.- 7.1.5. Autoimmunity in Diabetes Mellitus.- 7.2. Insulin Secretion.- 7.2.1. Experimental Results in Animals: Hypothalamic Influences.- 7.2.2. Regulation in Man.- 7.2.2.1. Effects of Intraportal and Peripheral Infusions of Glucagon on Insulin Secretion.- 7.2.2.2. Effects of Secretin.- 7.2.2.3. Effects of Hypocalcemia and Theophylline.- 7.2.2.4. Plasma Insulin in Early Diabetes.- 7.2.2.5. Plasma Insulin in Diabetes.- 7.2.2.6. Measurement of Other Beta Cell Secretory Products: Proinsulin and C- Peptide.- 7.2.2.7. Effects of Control of Diabetes on Insulin Secretion.- 7.3. Insulin Resistance and Insulin Receptors.- 7.3.1. Insulin Resistance and Sensitivity.- 7.3.2. Insulin Receptors.- 7.3.2.1. Insulin Receptors and Insulin Resistance in Diabetes.- 7.3.2.2. Insulin-Binding in Other Clinical Conditions.- 7.3.3. Autoantibodies to Insulin Receptors.- 7.4. Diabetes and Exercise.- 7.4.1. Exercise and Diabetes Mellitus in Man.- 7.4.2. Effect of Exercise in Depancreatized Dogs.- 7.4.3. Effect of in Vitro Contracting Skeletal Muscle on Glucose Uptake.- 7.5. Diabetes and Pregnancy.- 7.5.1. Special Considerations.- 7.5.2. Management of Pregnancy in Diabetic Patients.- 7.6. Acidosis in Diabetes.- 7.6.1. Diabetic Ketoacidosis.- 7.6.1.1. Diabetic Ketoacidosis and Low-Dose Insulin Therapy.- 7.6.2. Lactic Acidosis.- 7.7. Long-Term Complications.- 7.7.1. Diabetic Neuropathy.- 7.7.1.1. Evidence of Genetic Heterogeneity.- 7.7.1.2. Radiculopathy.- 7.7.1.3. Peripheral Neuropathy.- 7.7.1.4. Diabetic Amyotrophy.- 7.7.1.5. Autonomic Neuropathy.- 7.7.1.6. Myoinositol Metabolism.- 7.7.1.7. Experimental Diabetes and Diabetic Neuropathy.- 7.7.2. Diabetic Microangiopathy.- 7.7.2.1. Muscle Capillary Basement Membrane Thickening.- 7.7.2.2. Diabetic Microangiopathy and Intravascular Factors.- 7.7.2.3. Diabetic Retinopathy.- 7.7.2.4. Renal Changes and Nephropathy.- 7.7.3. Bone Mass in Diabetes Mellitus.- 7.8. Treatment of Diabetes Mellitus.- 7.8.1. General Considerations.- 7.8.2. Glycosylated Hemoglobin and Diabetic Control.- 7.8.3. Diet.- 7.8.4. Insulin.- 7.8.4.1. Chronic Insulin Therapy.- 7.8.4.2. Insulin Antibodies.- 7.8.4.3. Lipoatrophy.- 7.8.4.4. Insulin Delivery Systems.- 7.8.5. Transplantation.- 7.8.6. Oral Hypoglycemic Agents.- References.- 8 Glucagon and Somatostatin.- 8.1. Anatomy of the Islets of Langerhans.- 8.1.1. Topographical Relationships of the Islet Cells.- 8.1.2. Vascular and Neural Relationships.- 8.1.3. "Paracrine" Relationships.- 8.1.4. Subcellular Specializations.- 8.1.4.1. Tight Junctions.- 8.1.4.2. Gap Junctions.- 8.2. Structure-Function Relationships of Glucagon.- 8.2.1. Biological Structure-Function Relationships.- 8.2.2. Immunologic Structure-Function Relationships.- 8.3. Pancreatic and Extrapancreatic Immunoreactive Glucagons.- 8.3.1. Immunoreactive Glucagon Fractions in Tissue Extracts.- 8.3.1.1. Pancreas.- 8.3.1.2. Stomach.- 8.3.1.3. Intestine.- 8.3.1.4. Salivary Gland.- 8.3.2. Biosynthesis of Pancreatic Glucagon.- 8.3.3. Extrapancreatic A Cells and Glucagon Secretion.- 8.3.3.1. A Cells.- 8.3.3.2. Glucagon.- 8.3.4. Immunoreactive Glucagon in Plasma.- 8.4. Glucagon Metabolism, Clearance, and Degradation.- 8.5. Actions of Glucagon.- 8.5.1. Mechanisms.- 8.5.1.1. Receptor Binding.- 8.5.1.2. Adenylate Cyclase Activation.- 8.5.1.3. Glycogenolysis.- 8.5.1.4. Gluconeogenesis.- 8.5.1.5. Ketogenesis.- 8.5.1.6. Effects on Lipids.- 8.5.2. Physiology.- 8.5.2.1. Glycogenolysis.- 8.5.2.2. Gluconeogenesis.- 8.6. Control of Glucagon Secretion.- 8.6.1. Control by Nutrients.- 8.6.1.1. Glucose.- 8.6.1.2. Amino Acids.- 8.6.1.3. Free Fatty Acids.- 8.6.2. Influence of Hormones.- 8.6.2.1. Gastrointestinal Hormones.- 8.6.2.2. Neurotensin and Substance P.- 8.6.2.3. Bombesin.- 8.6.2.4. Other Factors.- 8.6.3. Neural Control.- 8.6.3.1. Hypothalamic Influences.- 8.6.3.2. Adrenergic Stimulation-Stress and Exercise.- 8.6.3.3. Dopaminergic Influence.- 8.6.3.4. Serotonin.- 8.7. Glucagonlike Immunoreactivity (Enteroglucagon).- 8.8. Somatostatin.- 8.8.1. Distribution in Tissues.- 8.8.1.1. Central Nervous System.- 8.8.1.2. Gastrointestinal Tract.- 8.8.1.3. Pancreas.- 8.8.2. Pancreatic Somatostatin Release.- 8.8.3. Mechanism of Action.- 8.8.4. Abnormalities of Somatostatin.- 8.8.5. Somatostatin Degradation.- 8.8.6. Somatostatin Analogues.- 8.9. Glucagon in Clinical Medicine.- 8.9.1. Diabetes Mellitus.- 8.9.1.1. A-Cell Function in Diabetes.- 8.9.1.2. Effect of Insulin on A-Cell Function in Juvenile-Type Diabetes Mellitus.- 8.9.1.3. Effect of Insulin on Adult-Onset Diabetics.- 8.9.1.4. Pathophysiologic Importance of Glucagon in Insulin Deficiency.- 8.9.1.5. Controversy Concerning the Importance of Glucagon in Diabetes Mellitus.- 8.9.1.6. Controversy Concerning the Role of Glucagon in the Presence of Insulin.- 8.9.1.7. Mechanism of Somatostatin-Induced Amelioration of Diabetic Hyperglycemia.- 8.9.2. Glucagonoma.- 8.9.3. Nondiabetic Hyperglucagonemia.- 8.9.4. Glucagon Deficiency.- References.- 9 Recent Advances in Body Fuel Metabolism.- 9.1. Introduction.- 9.2. Glucose Metabolism.- 9.2.1. Is Glucagon Essential in Diabetes?.- 9.2.1.1. Somatostatin-Induced Hypoglucagonemia.- 9.2.1.2. Pancreatectomized Man.- 9.2.2. Effects of Hyperglucagonemia.- 9.2.2.1. Normal Man.- 9.2.2.2. Diabetes.- 9.2.2.3. Uremia.- 9.2.3. Glucose Production: Gluconeogenesis from Alanine.- 9.2.4. The Counterregulatory Response to Hypoglycemia.- 9.3. Ketone and Fatty Acid Metabolism.- 9.3.1. Hormonal Control of Ketogenesis.- 9.3.2. Role of Malonyl-Coenzyme A.- 9.3.3. Hypoketonemic Action of Alanine.- 9.4. Amino Acid Metabolism.- 9.4.1. Origin of Alanine Synthesized in Skeletal Muscle.- 9.4.2. Metabolic Fate of Glutamine Utilized by Intestine.- 9.5. Fuel Metabolism in Exercise.- 9.5.1. Influence of Glucose Ingestion before Exercise.- 9.5.2. Influence of Ethanol Ingestion.- 9.5.3. Glucose-Sparing Effect of Free Fatty Acids.- 9.5.4. Interaction of Exercise and Insulin in Diabetes 376.- References.- 10 What's New in Obesity: Current Understanding of Adipose Tissue Morphoiogy.- 10.1. Introduction.- 10.2. Techniques for Measuring Adipocyte Size and Number.- 10.2.1. Intact Tissue.- 10.2.2. Osmium-Fixed Tissue.- 10.2.3. Adipocyte Suspensions.- 10.2.4. Advantages and Disadvantages of Counting Techniques.- 10.3. Cellularity of Adipose Tissue in Man and Animals.- 10.3.1. Development of Adipose Cellularity in Man.- 10.3.2. Adipose Cellularity in Laboratory Rodents.- 10.3.3. Cellularity in Human Obesity.- 10.3.4. Cellularity in Animal Obesity.- 10.4. How Constant Is Adipocyte Number?.- 10.4.1. Stability of Cell Number.- 10.4.2. Changes in Cell Number.- 10.5. How Are New Adipocytes Formed?.- 10.6. Significance of Cell Size and Number in Energy Regulation.- References.- 11 Divalent Ion Metabolism.- 11.1. Introduction.- 11.2. Vitamin D.- 11.2.1. Introduction.- 11.2.2. Metabolism and Transport of 25-Hydroxy-Vitamin Dg.- 11.2.3. Regulation of 25-Hydroxy-Vitamin Dg-la- Hydroxylase and Generation of 1,25-Dihydroxy- Vitamin Dg.- 11.2.4. Measurement of Vitamin D Metabolites in Plasma.- 11.2.5. Actions of Vitamin D.- 11.2.5.1. Effects on Phosphate Homeostasis and Absorption.- 11.2.5.2. Actions of Vitamin D on the Kidney.- 11.2.5.3. Effect of Vitamin D on the Parathyroid Glands.- 11.2.6. Biological Actions of 24,25-Dihydroxy-Vitamin Dg..- 11.2.7. Metabolism and Degradation of Vitamin D.- 11.2.8. Intestinal Calcium Absorption and Mechanism of Adaptation to a Low-Calcium Diet.- 11.2.8.1. Methods of Assessing Calcium Absorption.- 11.3. Clinical Disorders That Involve Altered Vitamin D Metabolism.- 11.3.1. Abnormal Metabolism of 25-Hydroxy-Vitamin Dg.- 11.3.1.1. Liver Disease.- 11.3.1.2. Anticonvulsants.- 11.3.1.3. Nephrotic Syndrome.- 11.3.2. Defective Production of 1,25-Dihydroxy-Vitamin Dg.- 11.3.2.1. Renal Osteodystrophy.- 11.3.2.2. Diabetes MeUitus.- 11.3.2.3. Osteomalacia Related to Mesenchymal Tumor.- 11.3.2.4. Fanconi Syndrome.- 11.3.3. Other Disorders with Uncertain Relationship to Vitamin D.- 11.3.3.1. Neonatal Hypocalcemia.- 11.3.3.2. Familial Hypophosphatemic Vitamin-D- Resistant Rickets.- 11.3.3.3. "Itai-Itai" Disease.- 11.3.3.4. Metabolic Acidosis.- 11.3.3.5. Glucocorticoid Treatment.- 11.3.4. Endocrine Disorders with Altered Production of I, 25-Dihydroxy-Vitamin Dg.- 11. 3.4.1. Hypoparathyroidism.- 11.3.4.2. Pseudohypoparathyroidism.- 11.4. Phosphorus Metabolism.- 11.4.1. Regulation of Phosphorus by the Kidney.- 11.4.1.1. Effect of Restriction of Phosphorus Intake.- 11.4.1.2. Adaptation to High-Phosphorus Intake.- 11.4.1.3. Effect of Parathyroid Hormone.- 11.4.1.4. Effects of Estrogen on Phosphate Metabolism.- 11.4.1.5. Growth Hormone and Renal Phosphate Reabsorption.- 11.4.1.6. Other Factors That Affect Renal Handling of Phosphorus.- 11.4.2. Phosphate-Depletion Syndrome.- References.- 12 Metabolism of Amino Acids and Organic Acids.- 12.1. Pyruvate Metabolism and Its Disorders.- 12.2. Pyruvate Metabolism and Its Regulation.- 12.2.1. Pyruvate Kinase.- 12.2.2. The Pyruvate Dehydrogenase Complex.- 12.2.3. Pyruvate Carboxylase.- 12.2.4. Phosphoenolpyruvate Carboxykinase and the Malate Shutde.- 12.2.5. Metabolic Regulation of Pyruvate Metabolism.- 12.3. Specific Disorders of Pyruvate Metabolism.- 12.3.1. Erythrocyte Pyruvate Kinase Deficiency.- 12.3.2. Pyruvate Carboxylase Deficiency.- 12.3.3. Phosphoenolpyruvate Carboxykinase Deficiency.- 12.3.4. Pyruvate Dehydrogenase Complex Mutants.- 12.3.4.1. Pyruvate Decarboxylase Deficiency.- 12.3.4.2. Dihydrolipoyl Transacetylase Deficiency.- 12.3.4.3. Dihydrolipoyl Dehydrogenase Deficiency.- 12.3.5. Pyruvate Dehydrogenase Phosphatase Deficiency.- 12.3.6. Decreased Activity of Pyruvate Oxidation in Patients with Friedreich's Ataxia and OtherNeuromuscular Diseases.- References.
Volume

v. 2 ISBN 9780306409547

Description

It is abundantly clear that a number of subtle abnormalities in hypothalamic function are associated with human obesity. Some hormonal abnormalities-the diminished growth hormone responses, for example-are critically dependent on increased caloric intake and are quickly reversible with weight loss. Others, such as the blunted prolactin response to acute hypoglycemia, may persist in the reduced-obese state. Still others (e. g. , the blunted ACTH responses to insulin- induced hypoglycemia) may, in some patients, first appear in the reduced-obese state. It remains uncertain whether any of these abnormalities is ever antecedent to the presence of obesity. Obviously, it is difficult to plan experiments in which the amounts of stored triglyceride, the level of caloric intake, and the state or his- tory of obesity can all be individually evaluated. The issue is made even more complex by the fact that there may be subgroups of obese in whom hypothalamic function may be abnormal, whereas many obese may have nearly normal hypo- thalamic function. It should be remembered that for years clinicians and investigators, working with available research tools, have ruled out pituitary or hypothalamic abnor- malities as a cause of human obesity. These tools have oftentimes been no more sophisticated than skull roentgenograms and samples of excreted steroid hormones in 24-hr urine. The advent of radioimmunoassays for peptide hormones and the availability of synthetic releasing hormones have offered possibilities of studying hypothalamic function undreamed of just a few years ago.

Table of Contents

1 Diabetes Mellitus: Selected Aspects of Pathophysiology and Clinical Practice.- 1.1. Introduction.- 1.2. Insulin Secretion.- 1.2.1. Glucose Modulation of Nonglucose Beta Cell Secretagogues.- 1.2.2. Neural Factors in Islet Regulation.- 1.2.2.1. Central Nervous System Control.- 1.2.2.2. Cyclic Oscillations of Beta Cell function.- 1.2.2.3. Catecholamines.- 1.2.2.4. Prostaglandins.- 1.2.3. Non-Insulin-Dependent Diabetes Mellitus.- 1.2.3.1. Glucose Effects.- 1.2.3.2. Salicylates in NIDDM.- 1.2.3.3. Weight Reduction in NIDDM.- 1.3. Insulin Action.- 1.3.1. Physicochemical Characteristics of Insulin Binding.- 1.3.2. Insulin Binding in Human Disease.- 1.3.3. Insulin Receptor Structure.- 1.3.4. Postreceptor Mechanism of Insulin Action.- 1.4. Glucose Counterregulation after Insulin.- 1.4.1. Control of the Counterregulatory Response.- 1.4.2. Mechanism of Glucose Recovery.- 1.4.3. Hypoglycemia in Insulin-Dependent Diabetes.- 1.5. High-Purity Insulin.- 1.5.1. Immunologic Effects of Conventional Insulin.- 1.5.2. Clinical Studies of Hisrh-Purity Insulin.- 1.5.3. Role of High-Purity Insulin in Clinical Practice.- 1.6. Nonenzymatic Glycosylation of Proteins.- 1.6.1. The Glycosylated Hemoglobins.- 1.6.1.1. Chemistry and Biosynthesis of the Glycosylated Hemoglobins.- 1.6.1.2. Effects of Glycosylation on Hemoglobin function.- 1.6.1.3. Measurement of Glycosylated Hemoglobin.- 1.6.1.4. The Glycosylated Hemoglobins in Diabetes Mellitus.- 1.6.1.5. Clinical Pitfalls in Measurement and Interpretation of Glycosylated Hemoglobin.- 1.6.1.6. Utility of Glycosylated Hemoglobin Measurement.- 1.6.2. Glycosylation of Other Proteins.- 1.6.2.1. Plasma Proteins.- 1.6.2.2. Erythrocyte Membrane Proteins.- 1.6.2.3. Lens Crystallin Protein.- 1.7. Peripheral Neuropathy.- 1.7.1. Etiology.- 1.7.2. Glycemic Control and Peripheral Somatic/Sensory Neuropathy.- 1.7.3. Autonomic Neuropathy.- References.- 2 Glucagon: Secretion, Function, and Clinical Role.- 2.1. Anatomy of the Islets of Langerhans.- 2.1.1. Topographical Relationships of the Islet Cells.- 2.1.2. Vascular and Neural Relationships.- 2.1.3. Paracrine Relationships.- 2.1.4. Subcellular Specializations.- 2.1.4.1. Tight Junctions.- 2.1.4.2. Gap Junctions.- 2.2. Structure-Function Relationships of Glucagon.- 2.2.1. Biological Structure-Function Relationships.- 2.2.2. Immunologic Structure-Function Relationships.- 2.3. Pancreatic and Extrapancreatic Immunoreactive Glucagons.- 2.3.1. Immunoreactive Glucagon Fractions in Tissue Extracts.- 2.3.1.1. Pancreas.- 2.3.1.2. Stomach.- 2.3.1.3. Intestine and Colon.- 2.3.1.4. Salivary Gland.- 2.3.1.5. Brain.- 2.3.2. Biosynthesis of Pancreatic Glucagon.- 2.3.3. Extrapancreatic A Cells and Glucagon Secretion.- 2.3.3.1. A Cells.- 2.3.3.2. Gastric Glucagon Secretion.- 2.3.4. Immunoreactive Glucagon in Plasma.- 2.4. Glucagon Metabolism, Clearance, and Degradation.- 2.5. Actions of Glucagon.- 2.5.1. Mechanisms.- 2.5.1.1. Receptor Binding.- 2.5.1.2. Adenylate Cyclase Activation.- 2.5.1.3. Glycogenolysis.- 2.5.1.4. Gluconeogenesis.- 2.5.1.5. Ketogenesis.- 2.5.1.6. Effects on Lipids.- 2.5.2. Physiology.- 2.5.2.1. Glycogenolysis.- 2.5.2.2. Gluconeogenesis.- 2.6. Control of Glucagon Secretion.- 2.6.1. Control by Nutrients.- 2.6.1.1. Glucose.- 2.6.1.2. Amino Acids.- 2.6.1.3. Free Fatty Acids.- 2.6.2. Influence of Hormones.- 2.6.2.1. Gastrointestinal Hormones.- 2.6.2.2. Somatostatin.- 2.6.2.3. Neurotensin and Substance P.- 2.6.2.4. Pancreatic Polypeptide.- 2.6.2.5. Prostaglandins.- 2.6.2.6. Calcium.- 2.6.3. Neuroregulation.- 2.6.3.1. Hypothalamic Influences.- 2.6.3.2. Sympathetic Influences.- 2.6.3.3. Parasympathetic Influences.- 2.6.3.4. Dopamme and Serotonin.- 2.6.3.5. Opioid Influences.- 2.6.3.6. ?-Aminobutyric Acid.- 2.7. Glucagonlike Immunoreactivity (Enteroglucagon).- 2.8. Importance of Glucagon in Clinical Medicine.- 2.8.1. Diabetes Mellitus.- 2.8.1.1. A-Cell Function in Diabetes.- 2.8.1.2. Pathophysiological Importance of Glucagon in Diabetes.- 2.8.1.3. Etiology of Abnormal A-Cell Function in Diabetes.- 2.8.2. Glucagonoma.- 2.8.3. Glucagon Deficiency.- References.- 3 Hypothalamic-Pituitary Function in Obesity.- 3.1. Introduction.- 3.2. Obesity Syndromes with Known Hypothalamic Involvement.- 3.3. Involvement of the Hypothalamic-Pituitary Axis in Other Forms of Obesity.- 3.4. Hypothalamic-Pituitary Function in Idiopathic Human Obesity.- 3.5. Release of Growth Hormone in Obesity.- 3.6. Prolactin.- 3.7. Thyroid.- 3.8. ACTH and the Opioid Peptides.- 3.9. Summary.- References.- 4 Plasma Apolipoproteins and Lipoprotein Receptors: Role in the Metabolism of Lipoproteins.- 4.1. Introduction.- 4.2. Apolipoproteins.- 4.2.1. Apolipoproteins A-I, A-II, and A-IV.- 4.2.2. Apolipoprotein B.- 4.2.3. C Apoproteins.- 4.2.4. Apolipoprotein E.- 4.3. Cell Surface Receptors for Lipoproteins.- 4.3.1. Extrahepatic Receptors for Lipoproteins.- 4.3.2. Hepatic Receptors for Lipoproteins.- 4.4. Metabolism of Chylomicrons.- 4.4.1. Synthesis.- 4.4.2. Catabolism.- 4.5. Metabolism of Endogenous VLDL.- 4.6. Metabolism of LDL.- 4.6.1. Catabolism of LDL.- 4.7. Metabolism of HDL.- References.- 5 Alcohol, Amino Acids and Encephalopathy.- 5.1. The Role of Plasma Amino Acids in the Pathogenesis of Hepatic Encephalopathy.- 5.1.1. Ratio of Aromatic to Branched-Chain Amino Acids in Plasma.- 5.1.2. Plasma Tryptophan and Hepatic Encephalopathy.- 5.1.3. Plasma Tyrosine and Related Compounds.- 5.2. Depression of Plasma Branched-Chain Amino Acids in the Alcoholic.- 5.3. ?-Amino-n-Butyric Acid.- 5.3.1. Mechanism of Increased AANB after Chronic Alcohol Consumption.- 5.3.2. Usefulness of AANB as a Biochemical Marker of Chronic Alcohol Consumption.- References.- 6 GABA and Taurine: What Are Metabolites Like This Doing in Places Like That?.- 6.1. Introduction.- 6.2. GABA.- 6.2.1. Introduction.- 6.2.2. GABA in Brain.- 6.2.2.1. Glutamic Acid Decarboxylase-Dependent Synthesis.- 6.2.2.2. Other Mechanisms of GABA Synthesis.- 6.2.2.3. Mechanism of Neuroinhibition and Function of GABA in the Central Nervous System.- 6.2.2.4. Disposal of GABA in the Central Nervous System.- 6.2.3. GABA in Kidney.- 6.2.4. GABA in Pancreas.- 6.2.5. GABA in Ovary.- 6.2.6. GABA in Blood Vessels.- 6.2.7. Regulation of Glutamic Acid Decarboxylase.- 6.2.8. Measurement of GABA.- 6.3. Taurine.- 6.3.1. Introduction.- 6.3.2. Biosynthesis of Taurine.- 6.3.2.1. Taurine Biosynthesis in Man.- 6.3.3. Taurine Disposal.- 6.3.4. Taurine Peptides.- 6.3.5. Functional Role of Taurine.- 6.3.5.1. In Central Nervous System.- 6.3.5.2. In Retina.- 6.3.5.3. In Skeletal and Cardiac Muscle.- 6.3.5.4. In Endocrine Systems.- 6.3.5.5. In Radiation Exposure.- 6.3.5.6. In Volume Regulation.- 6.3.6. Measurement of Taurine.- 6.3.7. Homeostasis of Taurine Pools.- 6.3.7.1. Renal Handling of Taurine.- 6.4. Conclusion.- References.- 7 Nutrition and Aging.- 7.1. Introduction.- 7.2. Previous Nutrition and the Aging Process.- 7.2.1. Calories.- 7.2.2. Protein.- 7.2.3. Carbohydrate.- 7.2.4. Amino Acids.- 7.2.5. Free Choice.- 7.3. Protein Metabolism in the Elderly.- 7.3.1. Total Body Protein.- 7.3.2. Albumin Synthesis.- 7.3.3. Amino Acids.- References.- 8 Receptors and Second Messengers in Cell Function and Clinical Disorders.- 8.1. Introduction.- 8.2. Overview of Receptors, Second Messengers, and the Control of Cellular function.- 8.2.1. Identification of Cell Membrane Receptors.- 8.2.2. Regulation of Receptors.- 8.2.2.1. Receptor Regulation during the Activation of Adenylate Cyclase.- 8.2.2.2. Effects of Persistent Receptor Occupancy.- 8.2.2.3. Internalization.- 8.2.2.4. Other Types of Regulation of Receptors.- 8.2.3. Receptor Pathology.- 8.2.4. Future Directions in Receptor Research.- 8.3. Coupling of Receptor Function to Cell Regulation.- 8.3.1. Adenylate Cyclase.- 8.3.1.1. G Unit and Receptor Affinity.- 8.3.1.2. Role of Guanine Nucleotide Regulatory Unit in Fluoride and Hormone Activation of Adenylate Cyclase.- 8.3.1.3. Cholera Toxin and ADP-Ribosylation of the Guanine Nucleotide Regulatory Unit.- 8.3.1.4. Purification of the Regulatory Component.- 8.3.2. Calcium as a Cell Regulator.- 8.3.2.1. Determination of Cytosolic Calcium Concentration.- 8.3.2.2. The Regulation of Cytosolic Calcium.- 8.3.2.3. Calcium Antagonists and Ionophores.- 8.3.2.4. Hormonal Control of Calcium Transport.- 8.3.3. Insulin and Growth Factors.- 8.4. Second Messengers.- 8.4.1. Protein Kinases.- 8.4.1.1. Peptide Sequences within Kinase Substrates.- 8.4.1.2. Phosphoproteins and Ion Transport.- 8.4.1.3. Cell Regulation and Protein Kinase Activity.- 8.4.2. Calmodulin as an Intracellular Calcium Receptor.- 8.5. Model Systems with Genetic Defects in Hormone Regulation.- 8.6. Specific Receptors, Their Regulation, and Second Messengers.- 8.6.1 ?-Adrenergic Receptors.- 8.6.1.1. Regulation of ?-Adrenergic Receptors.- 8.6.1.2. Supersensitivity.- 8.6.1.3. Other Hormones.- 8.6.1.4. Nonhormonal Factors.- 8.6.1.5. Mediators of ?-Adrenergic Effects.- 8.6.2. ?-Adrenergic Receptors.- 8.6.2.1. Differentiation of ?1 and ?2 Receptors.- 8.6.2.2. Binding Studies of ?-Adrenergic Receptors.- 8.6.2.3. Regulation of ? Receptors.- 8.6.2.4. Supersensitivity.- 8.6.2.5. Other Hormones.- 8.6.2.6. Nonhormonal Factors.- 8.6.2.7. Mediators of ?-Adrenergic Effects.- 8.6.3. Dopamine Receptors.- 8.6.3.1. Differentiation of D-1 and D-2 Dopaminergic Receptors.- 8.6.3.2. Direct Binding Studies of Dopamine Receptors.- 8.6.3.3. Regulation of Dopamine Receptors.- 8.6.3.4. Clinical Utility of Dopaminergic Drugs.- 8.6.4. Insulin Receptors.- 8.7. Clinical Disorders and Adenylate Cyclase Systems.- 8.7.1. Pseudohypoparathyroidism.- 8.7.2. Cyclic Nucleotides in the Extracellular Fluids.- 8.7.3. Cancer and Hypercalcemia.- References.- 9 Stimulated Phosphatidylinositol Turnover: A Brief Appraisal.- 9.1. General Introduction.- 9.2. What is Stimulated PI Turnover?.- 9.2.1. Isotopic Labeling Artifacts.- 9.2.1.1. 32P Incorporation.- 9.2.1.2. Inositol Incorporation.- 9.2.1.3. Glycerol and Fatty Acid Incorporation.- 9.2.1.4. Pulse Chases and Direct Measurement of PI.- 9.2.2. Physiological Reality.- 9.3. Mechanism of PI Turnover.- 9.3.1. Reversal of the de Novo Synthesis Pathway.- 9.3.2. Phospholipase C (Phosphodiesterase).- 9.3.2.1. Lysosomal Enzyme.- 9.3.2.2. Cytoplasmic Enzyme.- 9.3.3 Deacylation of PI.- 9.4. Function of PI Turnover.- 9.4.1. Calcium Gating.- 9.4.1.1. Correlation of PI Turnover and Calcium Gating.- 9.4.1.2. Calcium Independence of PI Turnover.- 9.4.2. Membrane Fusion and Secretion.- 9.4.3. Cell Division.- 9.4.4. Protein Kinase Stimulation.- 9.4.5 Release of Arachidonic Acid for Prostaglandin Synthesis.- 9.5. Summary and Conclusions.- References.- 10 Disorders of Purine and Pyrimidine Metabolism: Basic and Clinical Considerations.- 10.1. Introduction.- 10.2. Purine Metabolism.- 10.2.1. New Developments and Progress.- 10.2.2. Assessment in Vivo.- 10.2.3. Hyperuricemia and Hypertension.- 10.3. Adenosine Deaminase Deficiency.- 10.3.1. Neurological Component of the Syndrome.- 10.3.2. Biochemical Mechanism of Immunodeficiency.- 10.3.3. Secondary Enzyme Abnormalities.- 10.3.4. Other Anticipated Defects.- 10.3.5. Enzymology.- 10.3.6. Radioimmunoassays.- 10.3.7. Screening Tests.- 10.3.8. Prenatal Diagnosis.- 10.3.9. Treatment.- 10.3.10. Promising New Therapeutic Approaches.- 10.4. Increased Adenosine Deaminase Activity.- 10.5. Purine Nucleoside Phosphorylase Deficiency.- 10.5.1. Clinical Presentation.- 10.5.2. Molecular Basis of PNP Deficiency.- 10.5.3. Genetics.- 10.5.4. Biochemical Mechanisms of Immunodeficiency in PNP Deficiency.- 10.5.5. Treatment.- 10.5.6. Model Systems.- 10.6. Lowered Purine 5?-Nucleotidase in Agammaglobulinemia.- 10.6.1. Human X-Linked Agammaglobulinemia.- 10.6.2. In Aging.- 10.7. Adenine Phosphoribosyltransferase Deficiency.- 10.7.1. Heterozygote.- 10.7.2. Homozygote.- 10.7.3. Genetics.- 10.7.4. Biochemical Features.- 10.7.5. Diagnosis.- 10.7.6. Treatment.- 10.8. Hypoxanthine Guanine Phosphoribosyltransferase Deficiency.- 10.8.1. Correlates with Clinical Expression.- 10.8.2. Mutation Rate.- 10.8.3. Biochemical Mechanisms of the Increased Rate of Purine Synthesis.- 10.8.4. Mechanism of Neurological and Behavioral Abnormality.- 10.8.5. Diagnosis and Heterozygote Detection.- 10.8.6. Preventive Control.- 10.8.7. Treatment.- 10.8.8. Genetic Transformation.- 10.9 Increased Phosphoribosylpyrophosphate Synthetase.- 10.9.1. Clinical Features.- 10.9.2. Inheritance.- 10.9.3. Mechanism of Excessive Purine Synthesis.- 10.9.4. Treatment.- 10.10. Xanthinuria.- 10.10.1. Clinical Presentation.- 10.10.2. Diagnosis.- 10.10.3. Treatment.- 10.11. Gout.- 10.11.1. Correlates of Hyperuricemia.- 10.11.2. Gout, Hyperuricemia, and Renal Damage.- 10.11.3. Associated Disease.- 10.11.4. Biochemical and Genetic Basis of Hyperuricemia and Gout.- 10.11.5. Enzyme Defects.- 10.11.6. Possible Additional Enzyme Defects.- 10.11.7. Renal Clearance of Uric Acid.- 10.11.8. Diagnostic Tests.- 10.11.9. Treatment.- 10.12. Decreased Adenylic Deaminase.- 10.13. Abnormalities of Pyrimidine Metabolism.- 10.13.1. Hereditary Orotic Aciduria.- 10.13.2. Orotic Aciduria of Hyperammonemia.- 10.13.3. Pyrimidine 5?-Nucleotidase Deficiency.- 10.14. Abnormal DNA Repair.- 10.15. Antineoplastic Drugs.- 10.15.1. Deoxycoformycin.- 10.16. Transcobalamin II Deficiency.- References.- 11 Metabolic Aspects of Urinary Stone Disease.- 11.1. Introduction.- 11.2. New Urinary Stone Diseases.- 11.2.1. 2,8-Dihydroxyadenine Stones.- 11.2.2. Oxipurinol Stones.- 11.2.3 Triamterene Stones.- 11.3. Cystine Stone Disease.- 11.4. Struvite Stone Disease.- 11.5. Calcium Stone Disease.- 11.5.1. Urinary Calcium.- 11.5.1.1. Hypercalciuria.- 11.5.1.2. Idiopathic Hypercalciuria.- 11.5.1.3. Primary Hyperparathyroidism.- 11.5.2. Urinary Oxalate.- 11.5.2.1. Relative Hyperoxaluria.- 11.5.2.2. Primary Hyperoxaluria.- 11.5.2.3. Enteric Hyperoxaluria.- 11.5.3. Urinary Uric Acid.- 11.5.3.1. Relative Hyperuricosuria.- 11.5.4. Inhibitors.- 11.5.5. Risk Factor Analysis.- 11.5.6. Treatment.- References.- 12 The Divalent Ions: Calcium, Phosphorus, and Magnesium and Vitamin D.- 12.1. Calcium Metabolism.- 12.1.1. Calcium and the Cell.- 12.1.2. Hypercalcemia.- 12.1.2.1. Physicochemical State of Calcium in Circulation.- 12.1.2.2. Pathophysiological Basis of Hypercalcemia.- 12.1.2.3. Causes of Hypercalcemia Encountered in Clinical Practice: Experience at the University of California, Los Angeles.- 12.1.2.4. Neoplasia.- 12.1.2.5. Hyperparathyroidism.- 12.1.2.6. Hypercalcemic Secondary Hyperparathyroidism.- 12.1.2.7. Vitamin D and Its Metabolites.- 12.1.2.8. The Treatment of Hypercalcemia.- 12.2. Vitamin D.- 12.2.1. Chemistry and Metabolism.- 12.2.1.1. Effects of Ultraviolet Radiation.- 12.2.1.2. Hepatic Hydroxylation.- 12.2.1.3. Effects of Drugs on Hepatic Hydroxylation.- 12.2.1.4. Renal Hydroxylation.- 12.2.1.5. Effects of Pituitary Hormones.- 12.2.1.6. Regulation by Parathyroid Hormone and Calcium.- 12.2.1.7. Effects of Age on 1,25-Dihydroxyvitamin D3 Hydroxylation.- 12.2.1.8. Lead and 1,25-Dihydroxyvitamin D3.- 12.2.1.9. 24,25-Dihydroxyvitamin D3.- 12.2.1.10. Enterohepatic Physiology of Vitamin D.- 12.2.1.11. Vitamin D and Parathyroid Hormone.- 12.2.1.12. Vitamin D and Corticosteroids.- 12.2.2. Actions of Vitamin D.- 12.2.2.1. Muscle.- 12.2.2.2. Bone.- 12.2.2.3. Intestine.- 12.2.3. Clinical Entities.- 12.2.3.1. Renal Osteodystrophy.- 12.2.3.2. Osteoporosis.- 12.2.3.3. Primary Hyperparathyroidism.- 12.2.3.4. Pseudohyperparathyroidism.- 12.2.3.5. Vitamin D-Dependent Rickets.- 12.2.3.6. Vitamin D Resistance.- 12.2.3.7. Vitamin D and Bone Disease of Total Parenteral Nutrition.- 12.2.3.8. Human Vitamin D Deficiency.- 12.2.3.9. Vitamin D and Sarcoidosis.- 12.3. Phosphate Metabolism.- 12.3.1. Regulation by the Kidney.- 12.3.1.1. Effects of Dietary Phosphate and Starvation.- 12.3.1.2. Effects of Parathyroid Hormone.- 12.3.1.3. Effects of Serum Calcium Levels.- 12.3.1.4. Actions of Vitamin D.- 12.3.1.5. Effects of Acid-Base Homeostasis.- 12.3.2. Phosphate Transport in the Renal Tubule: Brush Border Membrane Vesicles.- 12.3.3. Phosphate Depletion and Hypophosphatemia: Clinical Entities.- 12.3.3.1. Alcoholism.- 12.3.3.2. Diabetes Mellitus.- 12.3.3.3. Burn Injury.- 12.3.3.4. The Surgical Patient.- 12.3.3.5. Renal Transplantation Hypophosphatemia.- 12.3.3.6. Respiratory Alkalosis.- 12.3.4. Clinical and Biological Effects of Phosphate Deprivation or Depletion.- 12.3.4.1. Renal Responses.- 12.3.4.2. Acid-Base Balance Abnormalities.- 12.3.4.3. Abnormal Carbohydrate Metabolism.- 12.3.4.4 Impaired Cellular Membrane Integrity and Phospholipid Metabolism.- 12.3.5. Intestinal Absorption of Phosphate.- 12.3.6. Regulation of Body Phosphate by Supply and Requirement.- 12.4. Magnesium Metabolism.- 12.4.1. The Kidney in Magnesium Homeostasis.- 12.4.1.1. Interactions with Calcitonin.- 12.4.1.2. Interactions with Parathyroid Hormone.- 12.4.2. Magnesium Depletion.- 12.4.2.1. Effects of Magnesium Depletion on the Cardiovascular System.- 12.4.2.2. Effects of Magnesium Depletion on Skeletal Muscle.- 12.4.2.3. Magnesium Depletion and Bone.- 12.4.2.4. Magnesium Depletion Secondary to Aminoglycoside Therapy.- 12.4.2.5. Magnesium Depletion and Diuretic Therapy.- 12.4.3. Intestinal Tract in Magnesium Metabolism.- References.

by "Nielsen BookData"

Details

  • NCID
    BA18331056
  • ISBN
    • 0306401274
    • 0306409542
  • Country Code
    us
  • Title Language Code
    eng
  • Text Language Code
    eng
  • Place of Publication
    New York ; London
  • Pages/Volumes
    v.
  • Size
    24 cm
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