Produkt

KlappentextThe prevalence of obesity in developed countries is fast becoming a health issue on par with infectious diseases and malnutrition. Research in this area has grown substantially and includes the neurochemical pathways of the hypothalamus and its role in regulating energy expenditures in the body. This volume in the Progress in Brain Research series examines the emerging role of the hypothalamus as a crucial link between the sensing of nutrients and the control of insulin sensitivity, glucose uptake, and glucose production, the integrative role of the hypothalamus in thyroid and bone metabolism, the interaction between circadian information and energy metabolism, and the important interplay between the immune system and energy metabolism.

? All contributors are recognized experts in their respective specialities
? Provides expanded coverage of hypothalamic mechanisms involved in energy metabolism
? Includes many outstanding full-colour illustrations
? Contains special sections on circadian rhythms, immune system, thyroid and bone metabolism

Details

Weitere ISBN/GTIN9780080463483

ProduktartE-Book

EinbandartE-Book

FormatPDF

Format HinweisDRM Adobe

Verlag

Elsevier Science & Techn.

Erscheinungsjahr2006

Erscheinungsdatum21.08.2006

Seiten430 Seiten

SpracheEnglisch

Dateigrösse11541 Kbytes

Artikel-Nr.2739358

Rubriken

Genre9200

Inhalt/Kritik

Inhaltsverzeichnis

1;Cover;1
2;List of contributors;6
3;Preface;10
4;Acknowledgments;12
5;Contents;14
6;Section I: Hypothalamic Integration of Energy Metabolism;18
6.1;Chapter 1. The human hypothalamus in metabolic and episodic disorders;20
6.1.1;The hypothalamus in disorders of eating and metabolism;20
6.1.2;Disorders accompanied by disturbances in eating and metabolism;28
6.1.3;Development of the fetal hypothalamus, birth and programing of metabolism;45
6.1.4;Summary and conclusions;52
6.1.5;Acknowledgment;53
6.1.6;Appendix: The Dutch Famine 1944-1945;53
6.1.7;References;54
6.2;Chapter 2. Synaptic plasticity mediating leptin´s effect on metabolism;64
6.2.1;Introduction;64
6.2.2;Leptin is a key metabolic signal associated with the rapid rewiring of hypothalamic pathways;65
6.2.3;Leptin-deficient ob/ob animals have altered synaptology and electrophysiological properties in the arcuate nucleus;67
6.2.4;Leptin induces rapid rewiring of arcuate nucleus-feeding circuits in ob/ob mice;68
6.2.5;What is the mechanism of action of leptin in triggering synaptic plasticity?;68
6.2.6;Are the synaptic organization and electrophysiological properties of the hypothalamic POMC neurons altered in mice with diet-induced obesity?;70
6.2.7;Acknowledgment;70
6.2.8;References;70
6.3;Chapter 3. The hypothalamus, hormones, and hunger: alterations in human obesity and illness;74
6.3.1;Obesity;74
6.3.2;Gut hormones and appetite;75
6.3.3;Gut hormones and downstream pathways;76
6.3.4;Prader-Willi syndrome;78
6.3.5;Hypothalamic neuropeptides and human illness;79
6.3.6;Functional neuroimaging of appetite;79
6.3.7;Functional neuroimaging in obesity;82
6.3.8;Functional neuroimaging in PWS;83
6.3.9;Functional neuroimaging in the future;85
6.3.10;Acknowledgments;86
6.3.11;References;86
6.4;Chapter 4. Glucocorticoids, chronic stress, and obesity;92
6.4.1;Glucocorticoids and function in the HPA axis;93
6.4.2;The central stress response network;98
6.4.3;The downside of the chronic stress response;108
6.4.4;References;108
6.5;Chapter 5. Design and synthesis of (ant)-agonists that alter appetite and adiposity;124
6.5.1;Melanocortin receptors;124
6.5.2;Selective melanocortin receptor agonists;125
6.5.3;In vivo efficacy of melanocortin receptor agonists;126
6.5.4;Investigation of the site of anorectic action of melanocortin receptor agonists;126
6.5.5;Development of NPY antagonists and their anorectic effects;128
6.5.6;Y1 antagonists;128
6.5.7;Y5 antagonists;130
6.5.8;Y5 binding and receptor occupancy;131
6.5.9;Melanocortin receptor agonists interact with NPY receptor responsive neurons;132
6.5.10;Summary and conclusions;132
6.5.11;Acknowledgments;133
6.5.12;References;133
6.6;Chapter 6. Monogenic human obesity syndromes;136
6.6.1;Introduction;136
6.6.2;Congenital leptin deficiency;136
6.6.3;Response to leptin therapy;137
6.6.4;Is there a heterozygous phenotype?;138
6.6.5;Leptin receptor deficiency;139
6.6.6;POMC;139
6.6.7;Prohormone convertase 1 deficiency;139
6.6.8;Human MC4R deficiency;139
6.6.9;Summary;140
6.6.10;References;140
7;Section II: Hypothalamic Integration of Blood-borne Signals;144
7.1;Chapter 7. The selfish brain: competition for energy resources;146
7.1.1;Introduction;147
7.1.2;Maintenance of glucose fluxes to the brain;147
7.1.3;The role of the hippocampus/amygdala system in energy homeostasis;149
7.1.4;The balance between food intake and glucose allocation;151
7.1.5;Obesity and diabetes mellitus type 2 as a brain disease?;152
7.1.6;Future treatment strategies for obesity and diabetes mellitus type 2;153
7.1.7;Conclusions;155
7.1.8;References;155
7.2;Chapter 8. Integration of metabolic stimuli in the hypothalamic arcuate nucleus;158
7.2.1;Electrophysiological properties of ARC neurons;160
7.2.2;Modulation of synaptic inputs by active conductances;162
7.2.3;KATP channels and central integration of humoral factors;164
7.2.4;Future perspectives;167
7.2.5;Abbreviations;167
7.2.6;Acknowledgments;168
7.2.7;References;168
7.3;Chapter 9. Adipokines that link obesity and diabetes to the hypothalamus;172
7.3.1;Adipose tissue;172
7.3.2;Leptin;174
7.3.3;Conclusion;185
7.3.4;Acknowledgment;185
7.3.5;References;185
8;Section III: Hypothalamic Control of Bone and Thyroid Metabolism;192
8.1;Chapter 10. The circadian modulation of leptin-controlled bone formation;194
8.1.1;Introduction;194
8.1.2;High bone mass in circadian gene-mutant mice;195
8.1.3;Bone has a peripheral clock;195
8.1.4;Increased osteoblast proliferation contributes to HBM in (Per1-/-;Per2m/m) mice;196
8.1.5;The central control of bone formation;198
8.1.6;The peripheral clock is a target of sympathetic signaling in osteoblasts;200
8.1.7;Sympathetic signaling activates cell cycle clock via AP1 genes in osteoblasts;201
8.1.8;Leptin-dependent sympathetic signaling controls AP1 and clock genes in vivo;202
8.1.9;Discussion;203
8.1.10;Abbreviations;204
8.1.11;Acknowledgments;204
8.1.12;References;204
8.2;Chapter 11. Hypothalamic thyroid hormone feedback in health and disease;206
8.2.1;Introduction;207
8.2.2;Thyroid hormone feedback in the human hypothalamus;207
8.2.3;Major depression and glucocorticoid treatment;214
8.2.4;Hyperthyroidism;217
8.2.5;Nonthyroidal illness;220
8.2.6;Conclusion;221
8.2.7;Acknowlegdments;221
8.2.8;References;221
8.3;Chapter 12. The TRH neuron: a hypothalamic integrator of energy metabolism;226
8.3.1;Role of hypophysiotropic TRH neurons in energy homeostasis;227
8.3.2;Role of nonhypophysiotropic TRH neurons in energy homeostasis;240
8.3.3;Conclusions;244
8.3.4;References;244
9;Section IV: Rhythms, Sleep and Energy Metabolism;254
9.1;Chapter 13. The seventeenth C.U. Ariëns Kappers Lecture: an introduction;256
9.1.1;References;258
9.2;Chapter 14. Staying awake for dinner: hypothalamic integration of sleep, feeding, and circadian rhythms;260
9.2.1;Regulation of sleep and wakefulness: the flip-flop switch model;260
9.2.2;Role of the orexin neurons in behavioral state regulation;264
9.2.3;The hypothalamic integrator for circadian rhythms;265
9.2.4;References;267
9.3;Chapter 15. Circadian timing in health and disease;270
9.3.1;The suprachiasmatic nuclei as central pacemaker;270
9.3.2;Circadian clock genes;271
9.3.3;Entrainment of the SCN clock;274
9.3.4;Real-time imaging of molecular time-keeping in the SCN;275
9.3.5;Local circadian time-keeping in peripheral tissues underpins metabolic rhythms;277
9.3.6;Circadian timing in disease;279
9.3.7;Circadian timing and neurodegenerative disease;281
9.3.8;Acknowledgements;283
9.3.9;References;283
9.4;Chapter 16. Circadian time keeping: the daily ups and downs of genes, cells, and organisms;288
9.4.1;History of circadian rhythms: from hobby gardening to feedback loops in gene expression;288
9.4.2;A circadian clock in the test tube: protein kinases and phosphatases;290
9.4.3;Zeitgeber time, circadian time, and jet lag;291
9.4.4;The mammalian circadian timing system: a clock in every cell?;292
9.4.5;Human behaviour: larks and owls;294
9.4.6;Perspectives;297
9.4.7;Acknowledgments;297
9.4.8;References;297
9.5;Chapter 17. The hypothalamic clock and its control of glucose homeostasis;300
9.5.1;Introduction;300
9.5.2;A daily rhythm in plasma glucose concentrations;301
9.5.3;Circadian control of the autonomic nervous system;313
9.5.4;Clinical implications;315
9.5.5;Abbreviations;317
9.5.6;Acknowledgments;318
9.5.7;References;318
9.6;Chapter 18. Mechanisms and functions of coupling between sleep and temperature rhythms;326
9.6.1;Introduction;326
9.6.2;Description of the coupling between sleep and temperature rhythms;327
9.6.3;Possible sites of interaction in the circadian regulation of sleep and body temperature;330
9.6.4;A modulatory role of body temperature on sleep-regulating systems;331
9.6.5;The functional direction of coupling between sleep and increased skin temperature revisited;333
9.6.6;An alternative function for the increase in skin blood flow;335
9.6.7;Sleep deprivation;336
9.6.8;Acknowledgments;338
9.6.9;References;338
9.7;Chapter 19. What can we learn from seasonal animals about the regulation of energy balance?;342
9.7.1;Introduction;342
9.7.2;Seasonal strategies;343
9.7.3;A re-resetting of body weight set point;344
9.7.4;Body weight change by altered food intake or energy expenditure?;344
9.7.5;The role of compensatory energy balance systems;345
9.7.6;The leptin paradox;346
9.7.7;In search of novel systems of control;347
9.7.8;Gene expression changes are linked to photoperiod not secondary events;348
9.7.9;Temporal changes in gene expression;349
9.7.10;A hypothetical model of interaction between H3R and VGF;350
9.7.11;Perspective;351
9.7.12;Acknowledgment;352
9.7.13;References;352
10;Section V: Hypothalamic Integration of Sensory´´ Information;356
10.1;Chapter 20. Organization of circadian functions: interaction with the body;358
10.1.1;Introduction;359
10.1.2;Circadian rhythm of SCN neurons and their anatomical organization;359
10.1.3;Hypothalamic projections of the SCN;361
10.1.4;SCN prepares the body for changes in activity;364
10.1.5;Autonomic control of our organs;366
10.1.6;An unbalanced autonomic output; leading to disease?;368
10.1.7;Input to the biological clock;370
10.1.8;Transmission of metabolic information to the SCN;372
10.1.9;Conclusions;373
10.1.10;References;373
10.2;Chapter 21. Hypoglycemia in diabetes: pathophysiological mechanisms and diurnal variation;378
10.2.1;Introduction;379
10.2.2;Hypoglycemia-associated autonomic failure;379
10.2.3;Mechanisms of HAAF;379
10.2.4;Diverse causes of HAAF;381
10.2.5;Acknowledgments;381
10.2.6;References;381
10.3;Chapter 22. Hypothalamic integration of immune function and metabolism;384
10.3.1;Introduction;385
10.3.2;Summary of afferent signals;396
10.3.3;Arcuate nucleus;398
10.3.4;Paraventricular nucleus;400
10.3.5;Ventromedial hypothalamus;403
10.3.6;Lateral hypothalamic area;404
10.3.7;Supraoptic nucleus;405
10.3.8;Abbreviations;414
10.3.9;Acknowledgment;414
10.3.10;References;414
11;Subject Index;424mehr

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