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Author: Qingchun Tong
Publisher: CRC Press
ISBN: 100036691X
Category : Medical
Languages : en
Pages : 330
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Book Description
This book focuses on neuron signaling in the regulation of metabolism and body weight, and especially on methods used in these studies. Obesity and related metabolic syndromes have reached epidemic status, but still are no effective strategies for prevention and treatment. Body weight homeostasis is maintained by balanced food intake and energy expenditure, both of which are under the control of brain neurons. In the recent years, significant progress has been made in identifying specific neurons, neural pathways, and non-neuron cells in feeding regulation, as well as in delineating autonomic nervous systems targeting peripheral metabolic tissues in the regulation of energy expenditure and metabolism. This book reviews recent progress on important neuron signaling for body weight and metabolic regulation and the state-of-the-art methods that has been applied in this field, ranging from animal models with neuron-specific manipulations, pharmacology, optogenetics, in vivo Ca2+ imaging, and viral tracing. Readers will be exposed to latest research frontiers on neuron regulation of metabolism. Key Features Explores the role signaling between neurons plays with respect to metabolism Documents how neurotransmitters affect the regulation of feeding Describes various methods and technologies used to study the neuronal control of metabolism Includes contributions from an international team of leading researchers. Related Titles Lim, W. & B. Mayer. Cell Signaling: Principles and Mechanisms (ISBN 978-0-8153-4244-1) Feltz, A. Physiology of Neurons (ISBN 978-0-8153-4600-5) Zempleni, J. & K. Dakshinamurti, eds. Nutrients and Cell Signaling (ISBN 978-0367-39307-6)
Author: Qingchun Tong
Publisher: CRC Press
ISBN: 100036691X
Category : Medical
Languages : en
Pages : 330
Get Book Here
Book Description
This book focuses on neuron signaling in the regulation of metabolism and body weight, and especially on methods used in these studies. Obesity and related metabolic syndromes have reached epidemic status, but still are no effective strategies for prevention and treatment. Body weight homeostasis is maintained by balanced food intake and energy expenditure, both of which are under the control of brain neurons. In the recent years, significant progress has been made in identifying specific neurons, neural pathways, and non-neuron cells in feeding regulation, as well as in delineating autonomic nervous systems targeting peripheral metabolic tissues in the regulation of energy expenditure and metabolism. This book reviews recent progress on important neuron signaling for body weight and metabolic regulation and the state-of-the-art methods that has been applied in this field, ranging from animal models with neuron-specific manipulations, pharmacology, optogenetics, in vivo Ca2+ imaging, and viral tracing. Readers will be exposed to latest research frontiers on neuron regulation of metabolism. Key Features Explores the role signaling between neurons plays with respect to metabolism Documents how neurotransmitters affect the regulation of feeding Describes various methods and technologies used to study the neuronal control of metabolism Includes contributions from an international team of leading researchers. Related Titles Lim, W. & B. Mayer. Cell Signaling: Principles and Mechanisms (ISBN 978-0-8153-4244-1) Feltz, A. Physiology of Neurons (ISBN 978-0-8153-4600-5) Zempleni, J. & K. Dakshinamurti, eds. Nutrients and Cell Signaling (ISBN 978-0367-39307-6)
Author: Qi Wu
Publisher: Springer
ISBN: 9811312869
Category : Medical
Languages : en
Pages : 233
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Book Description
This book systemically describes the mechanisms underlying the neural regulation of metabolism. Metabolic diseases, including obesity and its associated conditions, currently affect more than 500 million people worldwide. Recent research has shown that the neural regulation of metabolism is a central mechanism that controls metabolic status physiologically and pathophysiologically. The book first introduces the latest studies on the neural and cellular mechanisms of hypothalamic neurons, hypothalamic glial cells, neural circuitries, cellular signaling pathways, and synaptic plasticity in the control of appetite, body weight, feeding-related behaviors and metabolic disorders. It then summarizes the humoral mechanisms by which critical adipocyte-derived hormones and lipoprotein lipase regulate lipid and glucose metabolism, and examines the role of the hypothalamus-sympathetic nerve, a critical nerve pathway from CNS to peripheral nervous system (PNS), in the regulation of metabolism in multiple tissues/organs. Furthermore, the book discusses the functions of adipose tissue in energy metabolism. Lastly, it explores dietary interventions to treat neural diseases and some of the emerging technologies used to study the neural regulation of metabolism. Presenting cutting-edge developments in the neural regulation of metabolism, the book is a valuable reference resource for graduate students and researchers in the field of neuroscience and metabolism.
Author: Qingchun Tong
Publisher: CRC Press
ISBN: 1000366901
Category : Medical
Languages : en
Pages : 336
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Book Description
This book focuses on neuron signaling in the regulation of metabolism and body weight, and especially on methods used in these studies. Obesity and related metabolic syndromes have reached epidemic status, but still are no effective strategies for prevention and treatment. Body weight homeostasis is maintained by balanced food intake and energy expenditure, both of which are under the control of brain neurons. In the recent years, significant progress has been made in identifying specific neurons, neural pathways, and non-neuron cells in feeding regulation, as well as in delineating autonomic nervous systems targeting peripheral metabolic tissues in the regulation of energy expenditure and metabolism. This book reviews recent progress on important neuron signaling for body weight and metabolic regulation and the state-of-the-art methods that has been applied in this field, ranging from animal models with neuron-specific manipulations, pharmacology, optogenetics, in vivo Ca2+ imaging, and viral tracing. Readers will be exposed to latest research frontiers on neuron regulation of metabolism. Key Features Explores the role signaling between neurons plays with respect to metabolism Documents how neurotransmitters affect the regulation of feeding Describes various methods and technologies used to study the neuronal control of metabolism Includes contributions from an international team of leading researchers. Related Titles Lim, W. & B. Mayer. Cell Signaling: Principles and Mechanisms (ISBN 978-0-8153-4244-1) Feltz, A. Physiology of Neurons (ISBN 978-0-8153-4600-5) Zempleni, J. & K. Dakshinamurti, eds. Nutrients and Cell Signaling (ISBN 978-0367-39307-6)
Author: E. I. Sokolov
Publisher: VSP
ISBN: 9789067642125
Category : Medical
Languages : en
Pages : 338
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Book Description
This book is the result of the study of metabolic and hormonal disorders in patients suffering obesity and diabetes mellitus, focusing on mechanisms of formation of atherosclerotic changes in the myocardium and vessels in diabetes mellitus patient.
Author: Johannes Hirrlinger
Publisher: Humana Press
ISBN: 9781493910588
Category : Medical
Languages : en
Pages : 0
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Book Description
Brain Energy Metabolism addresses its challenging subject by presenting diverse technologies allowing for the investigation of brain energy metabolism on different levels of complexity. Model systems are discussed, starting from the reductionist approach like primary cell cultures which allow assessing of the properties and functions of a single brain cell type with many different types of analysis, however, at the expense of neglecting the interaction between cell types in the brain. On the other end, analysis in animals and humans in vivo is discussed, maintaining the full complexity of the tissue and the organism but making high demands on the methods of analysis. Written for the popular Neuromethods series, chapters include the kind of detailed description and key implementation advice that aims to support reproducible results in the lab. Meticulous and authoritative, Brain Energy Metabolism provides an ideal guide for researchers interested in brain energy metabolism with the hope of stimulating more research in this exciting and very important field.
Author: Rashid John Darbandi
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Book Description
Using the biochemically tractable Xenopus oocyte model system, we have previously characterized a novel metabolic regulation of cell death. We found that glucose-6-phosphate (G6P) via the pentose phosphate pathway leads to increased nicotinamide adenine dinucleotide phosphate (NADPH) levels, a subsequent increase in cytosolic acetyl-coenzyme A and activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). We recently identified coenzyme A (CoA), derived from the breakdown of acetyl-CoA, as the key metabolic signal that mediates a novel mechanism of calmodulindependent activation of CaMKII. CoA binds directly to the calmodulin (CaM) binding domain (CaMBD) of CaMKII resulting in its activation and downstream inhibitory phosphorylation of caspase-2, suppressing apoptosis. In this dissertation, we questioned whether there are other CaMBD containing proteins metabolically regulated by CoA. In an unbiased approach, CaM binding proteins were first isolated from Xenopus extract using a CaM-Sepharose column. Purified CaM binding proteins were then incubated with CoA-Sepharose in a second purification step and resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and silver staining. The results indicate the presence of numerous CaM-binding proteins that also bind CoA and are thus potentially metabolically regulated. In a targeted approach, we tested the ability of aberrant glucose signaling to regulate the CaM-binding protein PI3K. We found that addition of G6P, mimicking aberrant glucose metabolism, or CoA to X. laevis egg extracts activated Akt in a phosphatidylinositol 3-kinase (PI3K), phosphoinositidedependent protein kinase 1(PDPK1)-dependent manner. Additionally, we show that CoA binds directly to and activates PI3K. These findings uncover a novel mechanism of PI3K activation by aberrant glucose metabolism and suggest a potentially unknown constitutive activation pathway of PI3K/Akt by aberrant glucose signaling.
Author: Jeffrey G. Tasker
Publisher:
ISBN: 9783030623845
Category :
Languages : en
Pages : 0
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Book Description
This volume discusses current research on glial-neuronal interactions in several neuroendocrine systems. Glial-neuronal bidirectional transmission represents one of the fastest-growing areas of investigation in neuroscience today. Unraveling the interactions and signaling synergy between glial cells and neurons is critical to advancing our understanding of brain function. Consequently, this book summarizes the latest findings on the roles of astrocytes, microglia and tanycytes in the control of synaptic transmission, synaptic plasticity, blood-brain signaling, neuroinflammation and immune signaling. In addition, leading experts in the field discuss how reproductive function, the stress response and energy homeostasis are regulated by glial-neuronal communication. Given its scope, the book is essential reading for undergraduate and graduate students in the neurosciences, as well as postdoctoral fellows and established researchers who are looking for a comprehensive overview of glial-neuronal crosstalk in neuroendocrine systems. This is the eleventh volume in the International Neuroendocrine Federation (INF) Masterclass in Neuroendocrinology series (Volumes 1-7 published by Wiley), which aims to illustrate the highest standards and highlight the latest technologies in basic and clinical research, and aspires to provide inspiration for further exploration into the exciting field of neuroendocrinology.
Author: Santiago Ramón y Cajal
Publisher: History of Neuroscience
ISBN: 0195065166
Category : Nervous system
Languages : en
Pages : 977
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Book Description
This book is a reprint of an English translation of Cajal's original work, with abundant notes and commentaries by the editor. This text describes Cajal's fundamental contributions to neuroscience, which continue to be important today. It accurately details Cajal's ideas and data, and providesreaders with the opportunity to learn what Cajal thought about his research career and the significance of his observations. Excerpts from Tello's memorial lectures also provide a contemporary view of Cajal's work.
Author: Harry T. Lawless
Publisher: Springer Science & Business Media
ISBN: 1441964886
Category : Technology & Engineering
Languages : en
Pages : 603
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Book Description
The ?eld of sensory science has grown exponentially since the publication of the p- vious version of this work. Fifteen years ago the journal Food Quality and Preference was fairly new. Now it holds an eminent position as a venue for research on sensory test methods (among many other topics). Hundreds of articles relevant to sensory testing have appeared in that and in other journals such as the Journal of Sensory Studies. Knowledge of the intricate cellular processes in chemoreception, as well as their genetic basis, has undergone nothing less than a revolution, culminating in the award of the Nobel Prize to Buck and Axel in 2004 for their discovery of the olfactory receptor gene super family. Advances in statistical methodology have accelerated as well. Sensometrics meetings are now vigorous and well-attended annual events. Ideas like Thurstonian modeling were not widely embraced 15 years ago, but now seem to be part of the everyday thought process of many sensory scientists. And yet, some things stay the same. Sensory testing will always involve human participants. Humans are tough measuring instruments to work with. They come with varying degrees of acumen, training, experiences, differing genetic equipment, sensory capabilities, and of course, different preferences. Human foibles and their associated error variance will continue to place a limitation on sensory tests and actionable results. Reducing, controlling, partitioning, and explaining error variance are all at the heart of good test methods and practices.
Author: Mengjie Wang
Publisher:
ISBN:
Category :
Languages : en
Pages : 181
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Book Description
Insulin-like growth factor 1 (IGF-1) and insulin exert biological effects through highly homologous tyrosine kinase receptors, which are ubiquitously expressed in rodents. During the last two decades, substantial progress has been made in understanding the role of IGF-1 and insulin signaling in the brain. Major progress has been made in identifying differences of IGF-1 and insulin signaling in the brain and understanding the phenotypic discrepancies of disruptions of the IGF-1 receptors (IGF1Rs) and insulin receptors (IRs) in the brain. Metabolic diseases such as obesity and diabetes are global public health crises. Moreover, perturbations of metabolism cause various reproductive diseases such as abnormal puberty onset, irregular estrus cycle, altered ovarian function, infertility and reproductive system cancers. Thus, understanding and deciphering brain IGF1R and IR signaling are crucial to current research and crucial for potential therapeutic interventions for metabolic and reproductive diseases. Neurons are the fundamental units of the brain and carry out distinct functions, which raises another challenge -- understanding the role of a given subset of neurons. Two subsets of neurons-leptin receptor (LepRb) neuron and kisspeptin (Kiss1) neuron have drawn my attention due to their distinct activities in metabolism and reproduction respectively. Current technique Cre/loxP system enables conditional suppression of gene expression in distinct subsets of neurons of interest. We used this technique to generate transgenic mice to study the role of IGF1R and IR signaling in LepRb neurons and Kiss1 neurons. Chapter 1 gives a review of metabolic and reproductive function of IGF1R and IR, and a central control of metabolism and reproduction by LepRb neurons and Kiss1 neurons. By characterizing reproductive and metabolic phenotype of mice lacking IGF1Rs and/or IRs exclusively in LepRb neurons (IGF1RLepRb mice and IGF1R/IRLepRb mice), we found that IGF1RLepRb and IGF1R/IRLepRb mice experienced growth retardation, delayed puberty and impaired fertility. Male mice had decreased gonadotropin and testosterone levels, impaired testicular histology, suggesting direct disruptions of hypothalamic-pituitary-gonadal axis. Interestingly, female reproductive hormones were normal at 4 weeks of age, while IGF1R/IRLepRb showed elevated gonadotropin and decreased follicle counts compared to female IGF1RLepRb or control mice. The decreased serum growth hormone (GH) and IGF-1 levels in male IGF1RLepRb mice demonstrates communication between LepRb neurons and the GH/IGF-1 axis. Our findings highlight the importance of IGF1R in LepRb neurons in the regulation of body growth, puberty and fertility (Chapter 2). In Chapter 3, we found female IGF1RLepRb mice had decreased body weight and food intake accompanied by increased VO2, physical activity, and thermogenic gene expression in brown adipose tissue (BAT). These effects were sexually dimorphic; IGF1R signaling was not critical in regulating body weight, food intake or glucose homeostasis in male mice. Interestingly, IGF1R/IRLepRb mice showed dramatically increased fat mass percentage and insulin insensitivity compared to either IGF1RLepRb or control mice. In sum, loss of IGF1R in LepRb neurons confers resistance to obesity due to increased energy expenditure (EE), showing IGF1R signaling is obesogenic. These effects diminished in IGF1R/IRLepRb mice due to decreased EE and physical activity and increased lipid storage in BAT, suggesting IR signaling in LepRb neurons has an overall protective effect against obesity. Thus, our findings provide novel evidence that IGF1R and IR signaling in LepRb neurons interact and provide counterbalancing effects on the regulation of body composition and insulin sensitivity. Kiss1 neurons express LepRbs; however, we have shown that leptin's effects on puberty in mice do not require Kiss1 neurons. But we do not know whether the effects of IGF1R and IR signaling require Kiss1 neurons. To answer this question, we have now generated transgenic mice lacking IGF1Rs and/or IRs exclusively in Kiss1 neurons (IGF1RKiss1 mice and IGFR/IRKiss1 mice) (Chapter 4). We found that IGF1RKiss1 mice experienced decreased body weight, body length, delayed pubertal development and decreased litter size. Surprisingly, these parameters were comparable between the IGF1RKiss1 and IGF1R/IRKiss1 mice. These results indicate IGF1R signaling in Kiss1 neurons is the major driver of effects on body weight, body length and adult fertility. Notably, IGF1R/IRKiss1 mice had significantly increased fat mass, decreased physical activity and disrupted glucose homeostasis, which suggest IGF1R and IR may have compensatory effects in the regulation of fat mass, physical activity and glucose homeostasis. In summary, IGF1R and IR signaling in Kiss1 neurons have unique and cooperative roles in regulating metabolic and reproductive functions. The reproductive axis is linked to nutritional status. Previous chapters demonstrated that undernutrition (decreased food intake and body weight) was associated with reproductive dysfunctions, in Chapter 5 we discussed the role of overnutrition in reproduction. Recent work shows that gut microbial dysbiosis contributes to the risk of obesity in children whose mothers consume a high fat diet during both gestation and lactation or gestation alone. Obesity predisposes children to developing early puberty. However, to date, no study has examined how maternal high-fat-diet (MHFD) during lactation regulates pubertal timing, and fertility of children. Here, we found MHFD during lactation markedly altered the gut microbiota of dams and offspring. This outcome was associated with juvenile obesity, early puberty, and irregular estrous cycles. We also found that MHFD induced early puberty may be mediated by increased IGF-1 signaling. Moreover, MHFD during lactation disrupted glucose and energy homeostasis. Remarkably, permitting coprophagia between MHFD and maternal normal chow offspring successfully reversed early puberty and insulin insensitivity. Our data suggest that microbial reconstitution may prevent or treat early puberty and insulin insensitivity. In summary, this dissertation 1) dissected the crucial role of IGF1R and IR signaling in metabolism and reproduction in distinct subsets of neurons; 2) demonstrated IGF1R signaling in both LepRb and Kiss1 neurons plays a dominant role in the regulation of puberty, fertility and growth; 4) IGF1R and IR signaling in both LepRb neurons and Kiss1 neurons have compensatory roles in the regulation of body composition and glucose homeostasis; 5) finally, demonstrated MHFD during lactation is crucial to metabolic and reproductive health of offspring, which is mediated via modulation of gut microbiota.
