Contemporary Metabolism: Volume 2

ISBN-13: 9781468441895 / Angielski / Miękka / 2012 / 564 str.

Norbert Freinkel

Opis

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."

Spis treści

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.