Contemporary Metabolism
Kluwer Academic / Plenum Publishers (Verlag)
978-0-306-40954-7 (ISBN)
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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.
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.
| Erscheint lt. Verlag | 30.6.1982 |
|---|---|
| Zusatzinfo | 15 black & white illustrations, biography |
| Verlagsort | Dordrecht |
| Sprache | englisch |
| Gewicht | 931 g |
| Themenwelt | Studium ► 1. Studienabschnitt (Vorklinik) ► Biochemie / Molekularbiologie |
| ISBN-10 | 0-306-40954-2 / 0306409542 |
| ISBN-13 | 978-0-306-40954-7 / 9780306409547 |
| Zustand | Neuware |
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