ß-cell Stimulus-secretion Coupling [microform] : a Role for Uncoupling Protein 2 PDF Download
Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download ß-cell Stimulus-secretion Coupling [microform] : a Role for Uncoupling Protein 2 PDF full book. Access full book title ß-cell Stimulus-secretion Coupling [microform] : a Role for Uncoupling Protein 2 by Jamie W. (Jamie William) Joseph. Download full books in PDF and EPUB format.
Author: Jamie W. (Jamie William) Joseph Publisher: Library and Archives Canada = Bibliothèque et Archives Canada ISBN: 9780612944947 Category : Languages : en Pages : 560
Book Description
A key event in insulin secretion from the pancreatic P-cell is glucose-stimulated mitochondrial production of adenosine triphosphate (ATP). Uncoupling protein-2 (UCP2) is localized to the inner mitochondrial membrane and plays a role as a "typical" uncoupler that modulates the efficiency of ATP production by catalyzing the translocation of protons across the mitochondrial membrane. This uncoupling reduces the protonmotive force that drives ATP synthase activity and thus reduces the ability of the beta-cell to increase ATP levels in response to glucose. The work presented here focuses on the role of UCP2 in the pancreatic beta-cell and the involvement of UCP2 in free fatty acid (FFA) induced beta-cell defects leading to type 2 diabetes. UCP2 was found to negatively regulate glucose-stimulated insulin secretion (GSIS). UCP2 expression is increased by FFAs suggesting a possible causal link between UCP2 and beta-cell defects associated with elevated FFA. Mice fed a high fat diet (HFD) have elevated UCP2 protein levels and blunted GSIS with no compensatory increase in beta-cell mass. Mice lacking UCP2 are resistant to the effects of a HFD on beta-cell function. HFD fed UCP2 ( -/- ) mice show no loss in GSIS and have an increase beta-cell mass. In order to assess the mechanism of enhanced beta-cell insulin secretion in mice lacking UCP2 an in vitro model was developed where isolated islets were exposed to 0.4 mM palmitate for 48 hours. The most proximal consequence of palmitate induced UCP2 levels appears to decrease glucose-stimulated changes in the mitochondrial membrane potential and this diminishes the downstream glucose-stimulated increase in both the ATP/ADP ratio and cytosolic Ca 2+. This leads to an attenuation of GSIS. UCP2 ( -/- ) mice have no loss in beta-cell glucose-stimulated hyperpolarization of the mitochondrial membrane potential and maintain their ability to secrete insulin in a glucose-dependent fashion. Therefore HFD fed mice or palmitate exposed islets lose their glucose sensitivity by a mechanism that likely involves increased UCP2. In addition, UCP2 may also modulate the oscillatory pattern of ATP production and thus oscillations in KATP channel activity, plasma membrane potential and insulin secretion. UCP2 is an important regulator of glucose sensing in the pancreatic beta-cell and upregulation of UCP2 in the pre-diabetic state could contribute to the loss of glucose responsiveness observed in obesity-related type 2 diabetes.
Author: Jamie W. (Jamie William) Joseph Publisher: Library and Archives Canada = Bibliothèque et Archives Canada ISBN: 9780612944947 Category : Languages : en Pages : 560
Book Description
A key event in insulin secretion from the pancreatic P-cell is glucose-stimulated mitochondrial production of adenosine triphosphate (ATP). Uncoupling protein-2 (UCP2) is localized to the inner mitochondrial membrane and plays a role as a "typical" uncoupler that modulates the efficiency of ATP production by catalyzing the translocation of protons across the mitochondrial membrane. This uncoupling reduces the protonmotive force that drives ATP synthase activity and thus reduces the ability of the beta-cell to increase ATP levels in response to glucose. The work presented here focuses on the role of UCP2 in the pancreatic beta-cell and the involvement of UCP2 in free fatty acid (FFA) induced beta-cell defects leading to type 2 diabetes. UCP2 was found to negatively regulate glucose-stimulated insulin secretion (GSIS). UCP2 expression is increased by FFAs suggesting a possible causal link between UCP2 and beta-cell defects associated with elevated FFA. Mice fed a high fat diet (HFD) have elevated UCP2 protein levels and blunted GSIS with no compensatory increase in beta-cell mass. Mice lacking UCP2 are resistant to the effects of a HFD on beta-cell function. HFD fed UCP2 ( -/- ) mice show no loss in GSIS and have an increase beta-cell mass. In order to assess the mechanism of enhanced beta-cell insulin secretion in mice lacking UCP2 an in vitro model was developed where isolated islets were exposed to 0.4 mM palmitate for 48 hours. The most proximal consequence of palmitate induced UCP2 levels appears to decrease glucose-stimulated changes in the mitochondrial membrane potential and this diminishes the downstream glucose-stimulated increase in both the ATP/ADP ratio and cytosolic Ca 2+. This leads to an attenuation of GSIS. UCP2 ( -/- ) mice have no loss in beta-cell glucose-stimulated hyperpolarization of the mitochondrial membrane potential and maintain their ability to secrete insulin in a glucose-dependent fashion. Therefore HFD fed mice or palmitate exposed islets lose their glucose sensitivity by a mechanism that likely involves increased UCP2. In addition, UCP2 may also modulate the oscillatory pattern of ATP production and thus oscillations in KATP channel activity, plasma membrane potential and insulin secretion. UCP2 is an important regulator of glucose sensing in the pancreatic beta-cell and upregulation of UCP2 in the pre-diabetic state could contribute to the loss of glucose responsiveness observed in obesity-related type 2 diabetes.
Author: Tso-Pang Yao Publisher: Springer Science & Business Media ISBN: 3642216315 Category : Medical Languages : en Pages : 269
Book Description
The book highlights work from many different labs that taught us abnormal HDACs potentially contribute to the development or progression of many human diseases including immune dysfunctions, heart disease, cancer, memory impairment, aging, and metabolic disorders.
Author: Alexander G. Volkov Publisher: Springer Science & Business Media ISBN: 354037843X Category : Science Languages : en Pages : 513
Book Description
This book compiles new findings in plant electrophysiology from the work of internationally renowned experts in the fields of electrophysiology, bio-electrochemistry, biophysics, signal transduction, phloem transport, tropisms, ion channels, plant electrochemistry, and membrane transport. Opening with a historical introduction, the book reviews methods in plant electrophysiology, introducing such topics as measuring membrane potentials and ion fluxes, path-clamp technique, and electrochemical sensors. The coverage includes experimental results and their theoretical interpretation.
Author: Lorenzo Lamattina Publisher: Springer Science & Business Media ISBN: 3540451315 Category : Science Languages : en Pages : 291
Book Description
This book presents recent advances in the study of nitric oxide (NO) biology, biochemistry, molecular biology, and physiology in plants. It provides an overview of current understanding of the NO actions involved in adaptive responses of plant fitness to environmental constraints. Coverage places special emphasis on NO-dependent signaling, molecular adjustments, and targets as key elements in plant growth, development, and stress physiology.
Author: Roland Benz Publisher: Wiley-VCH Verlag GmbH ISBN: 9783527307753 Category : Eukaryotic Cells Languages : en Pages : 0
Book Description
For the first time, current knowledge on this important of proteins is now available in a single resource. This first book on porins in prokaryotes and eukaryotes relates the known physiological functions of porins to their molecular structure and mechanism. It brings together biophysical evidence with studies performed in a cellular context, presenting a unified picture of the fundamental importance of porins for cellular function. From the contents: Structure of Prokaryotic Porins Functional Reconstitution of Porins Regulation of Bacterial Porin Function Role of Porins in Antibiotic Susceptibility Drug Efflux and Protein Export through Porins Structure and Function of Mitochondrial Porins VDAC Function in Intracellular Signalling and Apoptosis With 16 contributions by an interdisciplinary team of leading porin researchers, this reference is essential reading for every molecular or structural biologist with an interest in this important protein family.
Author: Lutz Hein Publisher: Springer Science & Business Media ISBN: 9783540001096 Category : Medical Languages : en Pages : 692
Book Description
Up-to-date information on animal models generated by transgenic or gene targeting techniques. Naturally, the focus is on the mouse system. Each chapter has been written by leading experts in the field and gives an overview on existing animal models. This is facilitated by tables, which list the most important genetically engineered animal models and their phenotypes. This book aims at illustrating the impact of transgenic animal models in the field of Experimental Pharmacology and Toxicology, which includes their role in the understanding of basic cellular mechanisms, the evaluation of potential drug targets or the testing for drug effects.
Author: S.S. Guraya Publisher: New Age International ISBN: 8122419682 Category : Languages : en Pages : 23
Book Description
Summarizes and integrates the results obtained on the study ovarian components with the techniques like electron microscopy and histochemistry in order to provide an insight into the basic subcellular, and molecular aspects of human primordial follicles, oogenesis (oocyte growth and maturation), ovulation, fertilization and early embryogenesis.
Author: Gerhard Heldmaier Publisher: Springer Science & Business Media ISBN: 9783540674108 Category : Medical Languages : en Pages : 568
Book Description
This book gives an up-to-date account of the current knowledge of cold adaptation in animals, including phenomena like hibernation, daily torpor, thermoregulation and thermogenesis, metabolic regulation, freeze tolerance, anaerobiosis, metabolic depression and related processes. For the next four years - until the 12th International Hibernation Symposium - it will serve as a state-of-the-art reference source for every scientist and graduate student working in these areas of physiology and zoology.
Author: Mogens L. Glass Publisher: Springer Science & Business Media ISBN: 3540939857 Category : Science Languages : en Pages : 543
Book Description
Hopefully, this book will be taken off of the shelf frequently to be studied carefully over many years. More than 40 researchers were involved in this project, which examines respiration, circulation, and metabolism from ?sh to the land vertebrates, including human beings. A breathable and stable atmosphere ?rst appeared about 500 million years ago. Oxygen levels are not stable in aquatic environments and exclusively water-breathing ?sh must still cope with the ever-changing levels of O 2 and with large temperature changes. This is re?ected in their sophisticated count- current systems, with high O extraction and internal and external O receptors. 2 2 The conquest for the terrestrial environment took place in the late Devonian period (355–359 million years ago), and recent discoveries portray the gradual transitional evolution of land vertebrates. The oxygen-rich and relatively stable atmospheric conditionsimpliedthatoxygen-sensingmechanismswererelativelysimpleandl- gain compared with acid–base regulation. Recently, physiology has expanded into related ?elds such as biochemistry, molecular biology, morphology and anatomy. In the light of the work in these ?elds, the introduction of DNA-based cladograms, which can be used to evaluate the likelihood of land vertebrates and lung?sh as a sister group, could explain why their cardio-respiratory control systems are similar. The diffusing capacity of a duck lung is 40 times higher than that of a toad or lung?sh. Certainly, some animals have evolved to rich high-performance levels.
Author: J. Michael Lord Publisher: Springer Science & Business Media ISBN: 3642121764 Category : Science Languages : en Pages : 275
Book Description
Many plants produce enzymes collectively known as ribosome-inactivating proteins (RIPs). RIPs catalyze the removal of an adenine residue from a conserved loop in the large ribosomal RNA. The adenine residue removed by this depurination is crucial for the binding of elongation factors. Ribosomes modified in this way are no longer able to carry out protein synthesis. Most RIPs exist as single polypeptides (Type 1 RIPs) which are largely non-toxic to mammalian cells because they are unable to enter them and thus cannot reach their ribosomal substrate. In some instances, however, the RIP forms part of a heterodimer where its partner polypeptide is a lectin (Type 2 RIPs). These heterodimeric RIPs are able to bind to and enter mammalian cells. Their ability to reach and modify ribosomes in target cells means these proteins are some of the most potently cytotoxic poisons found in nature, and are widely assumed to play a protective role as part of the host plant’s defenses. RIPs are able to further damage target cells by inducing apoptosis. In addition, certain plants produce lectins lacking an RIP component but which are also cytotoxic. This book focuses on the structure/function and some potential applications of these toxic plant proteins.
![ß-cell Stimulus-secretion Coupling [microform] : a Role for Uncoupling Protein 2 PDF](https://books.google.com/books/content/images/frontcover/R4aFAAAACAAJ?fife=w150-h200)
Author: Jamie W. (Jamie William) Joseph![ß-cell Stimulus-secretion Coupling [microform] : a Role for Uncoupling Protein 2 PDF](https://books.google.com/books/content/images/frontcover/R4aFAAAACAAJ?fife=w80-h100)
Author: Jamie W. (Jamie William) Joseph
Author: Tso-Pang Yao
Author: Alexander G. Volkov
Author: Lorenzo Lamattina
Author: Roland Benz
Author: Lutz Hein
Author: S.S. Guraya
Author: Gerhard Heldmaier
Author: Mogens L. Glass
Author: J. Michael Lord