Read Books Online and Download eBooks, EPub, PDF, Mobi, Kindle, Text Full Free.
Lipid Metabolism In The Liver Adipose And Muscle With Glucocorticoids And How These Organs Can Regulate Each Other
Download Lipid Metabolism In The Liver Adipose And Muscle With Glucocorticoids And How These Organs Can Regulate Each Other full books in PDF, epub, and Kindle. Read online Lipid Metabolism In The Liver Adipose And Muscle With Glucocorticoids And How These Organs Can Regulate Each Other ebook anywhere anytime directly on your device. Fast Download speed and no annoying ads. We cannot guarantee that every ebooks is available!
Book Synopsis Lipid Metabolism in the Liver, Adipose, and Muscle with Glucocorticoids and how These Organs Can Regulate Each Other by : Wangkuk Son
Download or read book Lipid Metabolism in the Liver, Adipose, and Muscle with Glucocorticoids and how These Organs Can Regulate Each Other written by Wangkuk Son and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Background: The Western diet is characterized by a high amount of n-6 PUFA and low n-3 PUFA. Due to the structural difference of composing fatty acid, Omega-3 PUFAs have beneficial effects while omega-6 PUFAs elicit adverse effects on lipid metabolism, building the foundation of metabolic syndrome and various diseases. Objective: Determine whether fat composition in an HFD affects GC-induced alterations in lipid handling by the liver, adipose tissue, and skeletal muscle. Methods: Male wild-type C57BL/6 mice were randomized into two groups: n-6 (45% fat 177.5 g lard) and n-3 (45% fat 177.5 g Menhaden oil). After 4 weeks on their diets, groups were divided to receive either daily injections of dexamethasone (3 mg/kg/day) or sterile PBS for 1 week while continuing diets. Results: Omega-3 HFD diet ameliorates adipocyte hypertrophy and hepatic fatty accumulation by involving associated lipid metabolism markers (CD36 and FABP). Conclusion: The present study's result demonstrated that the change of fat composition in HFD could beneficially alter the fatty acid accumulation, adipocyte size, and associated lipid metabolism markers..
Book Synopsis Regulation of Lipid Metabolism in Adipose Tissue and Skeletal Muscle by : Zhihao Jia
Download or read book Regulation of Lipid Metabolism in Adipose Tissue and Skeletal Muscle written by Zhihao Jia and published by Frontiers Media SA. This book was released on 2022-11-29 with total page 135 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Glucocorticoid Signaling by : Jen-Chywan Wang
Download or read book Glucocorticoid Signaling written by Jen-Chywan Wang and published by Springer. This book was released on 2015-07-27 with total page 387 pages. Available in PDF, EPUB and Kindle. Book excerpt: This timely volume provides a comprehensive overview of glucocorticoids and their role in regulating many aspects of physiology and their use in the treatment of disease. The book is broken into four sections that begin by giving a general introduction to glucocorticoids and a brief history of the field. The second section will discuss the effects of glucocorticoids on metabolism, while the third section will cover the effects of glucocorticoids on key tissues. The final section will discuss general topics, such as animal models in glucocorticoid research and clinical implications of glucocorticoid research. Featuring chapters from leaders in the field, this volume will be of interest to both researchers and clinicians.
Book Synopsis Hypothalamic Glucocorticoid Action Regulates Lipid Metabolism by : Miguel Cardoso
Download or read book Hypothalamic Glucocorticoid Action Regulates Lipid Metabolism written by Miguel Cardoso and published by . This book was released on 2022 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Background: In metabolic disease statues, such as diabetes and obesity, dyslipidemia is characterized by a dysregulation of lipid homeostasis, due in part to elevated triglyceride (TG)-rich very low-density lipoprotein (VLDL-TG) production and secretion by the liver. Further, these metabolic diseases are associated with excessive levels and/or actions of glucocorticoids (GCs), which may contribute to dyslipidemia. The dysregulation of VLDL-TG secretion, and particularly its hypersecretion in metabolic disease states, remains largely unknown. The brain, including the medial basal hypothalamus (MBH), senses circulating nutrients and hormones to regulate lipid metabolism and VLDL-TG secretion. Whereas the peripheral effects of GCs are well known, including the direct effect of GCs to stimulate hepatic VLDL-TG secretion, the central effects of GCs acting in the MBH to regulate lipid metabolism is unknown. Given the link between GCs and metabolic disease states, that GCs act in the periphery to effect lipid metabolism, and the fact that the brain is a hormone-responsive liporegulatory site, the aim of this study was to explore if GCs can act directly in the MBH to regulate liver VLDL-TG secretion to better understand mechanisms by which blood lipid levels may be lowered in those with dyslipidemia. Hypothesis: (1) GCs act via the glucocorticoid receptors (GRs) in the MBH to modulate liver lipid homeostasis by increasing plasma TG and hepatic VLDL-TG secretion; (2) inhibition of MBH GC action (by blocking MBH GRs or downstream mediators of GC-GR action specifically within the MBH), will improve liver lipid metabolism in diet-induced hyperlipidemic rats. Methods: Male Sprague Dawley rats underwent stereotaxic MBH bilateral cannulation and vascular catheterization to enable direct-continuous MBH infusion, intravenous infusion, and arterial blood sampling. Following MBH cannulation, a subset of rats received either a MBH specific injection of a lentivirus containing a GRshRNA, to act as a GR knockdown, a heat shock protein 90 sh RNA (Hsp90 shRNA), to act as an Hsp90 knockdown, or a mismatch (MM) sequence to act as a control. A subset of rats were subjected to a 3-day high fat diet (HFD), as an acute model of diet-induced obesity. Following a 10-hour fast, free-moving, conscious rats were subjected to a direct, and continuous MBH infusion of a specific brain treatment (dexamethasone (DEX), as a synthetic GC, mifepristone, as a GR inhibitor, or a Hsp90 inhibitor) or saline paired with an intravenous poloxamer injection to inhibit lipoprotein lipase. Plasma samples were collected and TGs, glucose, and free fatty acids (FFAs) were quantified. Following experimentation rats were euthanized and brain and liver samples were collected for gene expression and protein level analysis. Results: Direct MBH GC infusion, in the form of DEX, increased plasma VLDL-TG secretion compared to MBH vehicle-infused controls, and this effect was negated via the inhibition of the MBH GR. These changes occurred independent of changes in plasma apolipoprotein B (apoB)- 48, apoB-100, glucose, FFAs, hepatic expression of Srebf1c, Scd1, Dgat1/2, Fasn, Lpin2, Cideb, Nr1h3, Nr1h2, Arf1, Cpt1a, Ppara, or hepatic protein levels of MTP, P-ACC/ACC, DGAT1, Arf1, or FAS relative to controls. In HFD-fed rats, which are characterized by elevated basal plasma GC and TGs, the chronic (13-day) inhibition of the GR via GRshRNA or the inhibition of Hsp90, in the MBH, significantly decreased plasma TGs and TG-rich lipoprotein secretion. The chronic (13-day) inhibition of Hsp90 in the MBH, using Hsp90 shRNA, in the 3-day HFD fed rats was associated with lower basal plasma FFAs, and lower plasma TG:apoB-100 ratio following experimentation compared to HFD controls. Conclusion: The results of these studies provide evidence that MBH GC action alters fasting lipid metabolism, by increasing TG-rich lipoprotein secretion. Further, we show for the first time that inhibition of GRs in the MBH negates diet-induced hypertriglyceridemia. The significance of this data is that it suggests that GC action in the hypothalamus may contribute to TG-rich lipoprotein overproduction and dysregulation of lipid homeostasis in diet-induced hypertriglyeridemia.
Book Synopsis The Hypothalamus-Pituitary-Adrenal Axis by :
Download or read book The Hypothalamus-Pituitary-Adrenal Axis written by and published by Elsevier. This book was released on 2008-09-12 with total page 413 pages. Available in PDF, EPUB and Kindle. Book excerpt: The hypothalamic-pituitary-adrenal axis controls reactions to stress and regulates various body processes such as digestion, the immune system, mood and sexuality, and energy usage. This volume focuses on the role it plays in the immune system and provides substantive experimental and clinical data to support current understanding in the field, and potential applications of this knowledge in the treatment of disease. Evidence presented in this book suggests that the nervous, endocrine, and immune systems form the Neuroendoimmune Supersystem, which integrates all the biological functions of higher organisms both in health and disease for their entire life cycle Contributors include both the scientists who initiated the work on the HPA axis and on the autonomic nervous system, and those who joined the field later
Book Synopsis Adipose Tissue Lipolysis and the Regulation of Hepatic Lipid Metabolism by : Sicheng Zhang
Download or read book Adipose Tissue Lipolysis and the Regulation of Hepatic Lipid Metabolism written by Sicheng Zhang and published by . This book was released on 2023 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: The communication between adipocytes and liver plays a crucial role in the physiological regulation of metabolism and understanding the basis of this dynamic inter-organ communication has the potential to advance clinical therapies. This is particularly important for conditions like obesity, fatty liver disease, and type 2 diabetes, which have emerged as global metabolic disorders. Consequently, the investigation of the communication between the liver and adipose tissue has been a hot point in metabolic research for many years (Azzu, Vacca et al. 2020).Numerous studies have investigated adipose tissue and its secretome composition, however, a comprehensive global analysis of the lipidome was still absent. In this study, we used the beta-3-adrenergic receptor agonist, CL-316,243 (CL), to stimulate adipose tissue lipolysis in both in vivo and in vitro settings (Zhang, Williams et al. 2023). A single dose of CL treatment was deemed an appropriate model to mimic acute adipose tissue lipolysis. Additionally, we conducted a time course analysis to investigate the dynamic changes in the adipose tissue lipolysis lipidome and its impact on hepatic lipidome, considering the lipid flux originating from adipose tissue lipolysis. We also utilized ATGL adipose tissue-specific knockout mice as a model to underscore the significance of adipose tissue lipolysis in hepatic lipid remodeling (Kim, Tang et al. 2016). Our study provides a comprehensive perspective on how adipose tissue lipolysis remodels the hepatic lipidome. Furthermore, we identified specific lipid alterations of interest, including the accumulation of linoleic acid and the release of odd-chain free fatty acids. Another pivotal aspect of the study on the interaction between adipose tissue and the liver is how the liver responds to adipose tissue lipolysis. In this investigation, we applied RNA-seq and subsequent bioinformatic analysis to detect novel hepatic regulators. In addition to the well-established regulators such as PPARa, HNF4a, and SREBP1c, we identified hepatic glucocorticoid receptor (GR) as another critical transcription factor involved in this process, which is activated by the hypothalamic-pituitary adrenal (HPA) axis. Furthermore, it appears that hepatic GR plays a crucial role in regulating ketogenesis and triglyceride accumulation during adipose tissue lipolysis. Notably, our research revealed that Plin5 serves as a downstream target whose expression is controlled by hepatic GR directly. And absence of hepatic Plin5 also impedes ketogenesis. This suggests that the Adipose-HPA-GR-PLIN5 axis may represent an important regulatory pathway in ketogenesis. In addition to RNA-seq, we employed Assay of Transposase-Accessible Chromatin ATAC-seq as an additional tool to investigate hepatic regulators. Our findings suggest that a novel transcription factor, Elk4, may potentially have a role in hepatic metabolism, specifically in glucose metabolism and pyruvate metabolism. However, given the limited knowledge available about Elk4, further research is warranted to understand more about its functions and mechanisms.
Book Synopsis Mechanisms of Insulin Action by : Alan R. Saltiel
Download or read book Mechanisms of Insulin Action written by Alan R. Saltiel and published by Springer Science & Business Media. This book was released on 2007-10-05 with total page 223 pages. Available in PDF, EPUB and Kindle. Book excerpt: More than 18 million people in the United States have diabetes mellitus, and about 90% of these have the type 2 form of the disease. This book attempts to dissect the complexity of the molecular mechanisms of insulin action with a special emphasis on those features of the system that are subject to alteration in type 2 diabetes and other insulin resistant states. It explores insulin action at the most basic levels, through complex systems.
Book Synopsis Adipose Tissue in Health and Disease by : Todd Leff
Download or read book Adipose Tissue in Health and Disease written by Todd Leff and published by John Wiley & Sons. This book was released on 2010-03-19 with total page 530 pages. Available in PDF, EPUB and Kindle. Book excerpt: This timely and most comprehensive reference available on the topic covers all the different aspects vital in the fight against the global obesity epidemic. Following a look at adipose tissue development and morphology, the authors go on to examine its metabolic and endocrine functions and its role in disease. The final section deals with comparative and evolutionary aspects of the tissue. The result is an essential resource for cell and molecular biologists, physiologists, biochemists, pharmacologists, and those working in the pharmaceutical industry.
Book Synopsis Comparative Physiology of Fasting, Starvation, and Food Limitation by : Marshall D. McCue
Download or read book Comparative Physiology of Fasting, Starvation, and Food Limitation written by Marshall D. McCue and published by Springer Science & Business Media. This book was released on 2012-05-17 with total page 431 pages. Available in PDF, EPUB and Kindle. Book excerpt: All animals face the possibility of food limitation and ultimately starvation-induced mortality. This book summarizes state of the art of starvation biology from the ecological causes of food limitation to the physiological and evolutionary consequences of prolonged fasting. It is written for an audience with an understanding of general principles in animal physiology, yet offers a level of analysis and interpretation that will engage seasoned scientists. Each chapter is written by active researchers in the field of comparative physiology and draws on the primary literature of starvation both in nature and the laboratory. The chapters are organized among broad taxonomic categories, such as protists, arthropods, fishes, reptiles, birds, and flying, aquatic, and terrestrial mammals including humans; particularly well-studied animal models, e.g. endotherms are further organized by experimental approaches, such as analyses of blood metabolites, stable isotopes, thermobiology, and modeling of body composition.
Book Synopsis The Role of Angiopoietin-like 4 in Lipid Homeostasis by : Nora Gray
Download or read book The Role of Angiopoietin-like 4 in Lipid Homeostasis written by Nora Gray and published by . This book was released on 2012 with total page 174 pages. Available in PDF, EPUB and Kindle. Book excerpt: Abstract The Role of Angiopoietin-like 4 in Lipid Homeostasis by Nora Elizabeth Forbes Gray Doctor of Philosophy in Molecular and Biochemical Nutrition University of California, Berkeley Professor Jen-Chywan Wang, Chair Alterations in the regulation of lipid homeostasis are major causes of metabolic diseases like obesity, insulin resistance and the metabolic syndrome. These diseases affect millions of people and therefore constitute a pressing public health concern. The mobilization of lipids is a key regulatory step in lipid homeostasis and the proteins that mobilize lipids from adipocytes to other tissues are therefore potential targets for therapeutic interventions. One such protein is angiopoietin-like 4 (Angptl4), a secreted protein induced by fasting and glucocorticoid treatment that inhibits lipoprotein lipase (LPL) and induces intracellular adipocyte lipolysis. These studies seek to characterize the role of Angptl4 in modulating lipid homeostasis. We found that Angptl4 is involved in the lipolytic response to fasting, glucocorticoids and catecholamines and in each case it modulates intracellular cAMP levels. We further discovered that purified Angptl4 can directly increase cAMP and lipolysis in adipocytes in a dose-dependent manner. We were also able to dissociate ability of Angptl4 to inhibit LPL from its ability to induce lipolysis by determining that just the C-terminal domain, which cannot inhibit LPL, can induce adipocyte lipolysis. Initial attempts to uncover the mechanism by which Angptl4 modulates cAMP showed that soluble adenylate cyclase is important for the lipolytic response to Angptl4. Additionally, Angptl4 treatment increases activation of focal adhesion kinase (FAK) and inhibition of FAK attenuates the lipolytic response to Angptl4, suggesting the potential involvement of integrins in Angptl4 signaling in adipocytes although more research is needed to confirm this possibility. In addition to its expression in white adipose tissue, Angptl4 levels are also high in the liver where its expression is regulated by glucocorticoids. Because mice lacking Angptl4 are protected from glucocorticoid-induced fatty liver and hyperlipidemia we wanted to investigate the lipogenic role of Angptl4 in the liver. Using stable isotope labeling and gene expression analysis we found that glucocorticoids increase the rate of triglyceride synthesis as well as de novo lipogenesis but this effect is blunted in mice that lack Angptl4. There was also differential hepatic expression of genes involved in lipogenesis in the mice without Angptl4. Treatment of hepatocytes with purified Angptl4 revealed that the increase in triglyceride synthesis is not a direct effect of the protein, nor are the alterations in the expression of most lipogenic genes. Two notable exceptions, however, are Agpat1 and Agpat2, the expression of which was induced by Angptl4 treatment. This is a previously undescribed role of Angptl4 and further research is necessary to understand the mechanism by which it could be modulating transcription. A third tissue with high expression of Angptl4 is brown adipose tissue. Because of its role in lipolysis and the fact that lipolysis is critical for adaptive thermogenesis, we investigated the how Angptl4 might be involved in thermoregulation. We found that mice lacking Angptl4 maintained a consistently lower body temperature during cold exposure. We further determined that lipolysis in brown adipose tissue was impaired in these mice and the induction of thermogenic genes was compromised relative to wild types. We also found that mice without Angptl4 maintain a lower body temperature during fasting than WT mice. These results indicate a potential role of Angptl4 in thermogenesis, which could have important implications for obesity. These studies confirm that Angptl4 is important for the regulation of lipid homeostasis. A more complete understanding of its mechanism, including the identification of a receptor that can mediate its intracellular effects, will be crucial for evaluating the potential of Angptl4 as a therapeutic target for diseases of deregulated lipid metabolism.
Book Synopsis Thyroid Hormone Metabolism by : Georg Hennemann
Download or read book Thyroid Hormone Metabolism written by Georg Hennemann and published by Marcel Dekker. This book was released on 1986 with total page 656 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Investigating Diet and Exercise Modifications on Delta-6 Desaturase and Ghrelin Regulation of Skeletal Muscle and White Adipose Tissue Lipid Metabolism by : Barbora Hucik-Worndl
Download or read book Investigating Diet and Exercise Modifications on Delta-6 Desaturase and Ghrelin Regulation of Skeletal Muscle and White Adipose Tissue Lipid Metabolism written by Barbora Hucik-Worndl and published by . This book was released on 2021 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Evidence supports a role for delta-6 desaturase (D6D) and ghrelin in regulating white adipose tissue (WAT) and skeletal muscle metabolism, particularly in the context of lifestyle modifications such as dietary fat consumption and exercise training. Changes in D6D activity, an enzyme involved in omega-3 polyunsaturated fatty acid (n-3 PUFA) metabolism, are associated with ¬¬¬altered whole-body glucose metabolism and increased risk of developing metabolic diseases such as Type 2 diabetes (T2D). In addition to signaling hunger and stimulating growth hormone (GH) release, ghrelin contributes to the control of WAT lipolysis. Studies have shown that circulating ghrelin levels change with high-fat diet (HFD) consumption and exercise. However, it is unknown how D6D and ghrelin regulate adipose and skeletal muscle metabolism in the context of different lifestyle modifications. In the first part of the thesis, reduced D6D activity partially protected Fads2+/- mice from high-fat diet (HFD)-induced impairments in glucose tolerance. We also investigated the impact of different n-3 PUFA using a Fads2-/- mice. Mice were fed either a flaxseed (contains alpha-linolenic acid) or menhaden (eicosapentaenoic and docosahexaenoic acid) oil diet. Flax-fed Fads2-/- mice had increased insulin sensitivity and decreased body weight compared to menhaden-fed Fads2-/- mice. However, neither of these studies showed changes in whole-body energy expenditure, skeletal muscle lipid species content and composition, or other protein markers of glucose or fatty acid uptake, storage or oxidation. To our knowledge, these novel studies are the first to investigate the effect of D6D activity on skeletal muscle glucose and lipid metabolism. These findings suggest that dietary fat consumption (regardless of quantity or composition) does not influence the effects of D6D activity at the level of skeletal muscle. The last part of this thesis investigated the role of ghrelin in modulating B-adrenergic-stimulated WAT lipolysis. Although the acylated isoform (AG) blunted WAT lipolysis in LFD-fed rats, 5 days and 6 weeks of HFD consumption both impaired ghrelin's anti-lipolytic effect, which was not restored with exercise training. This study showed that HFD-feeding impairs ghrelin's ability to regulate WAT lipolysis. Collectively, this thesis demonstrates that D6D and ghrelin regulation of peripheral tissue metabolism is dependent on dietary fat content and composition.
Book Synopsis Mechanisms and Significance of Adipose Inflammatory Recruitment by : Fahrettin Haczeyni
Download or read book Mechanisms and Significance of Adipose Inflammatory Recruitment written by Fahrettin Haczeyni and published by . This book was released on 2015 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Adipose tissue has significant roles in whole body energy homeostasis, systemic insulin sensitivity, and lipid metabolism. Increased food intake, physical inactivity, and genetic predisposition lead to over-expansion of adipose tissues. Under constant energy surplus, adipocytes become hypertrophic and adipose tissues undergo hyperplasia. These tissue modifications lead to recruitment of preadipocytes and preadipocyte progenitors (mesenchymal stem cells) into adipogenic lineage, thereby increases the lipid storage capacity of adipose tissues. This keeps circulating blood glucose and fatty acids below toxic levels; however, adipocytes have a saturation point where they cannot store more lipids; when adipocytes are completely engorged with lipids, they start expressing stress signals to recruit inflammation into the tissue. While the mechanisms involved in recruitment of adipose inflammation remain largely unknown, some findings point to "extensive adiposity" as the responsible factor. This thesis focuses on persistent adipose inflammation and its relationship with metabolic comorbidities such as insulin resistance, type 2 diabetes, and particularly, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). A theme of this research is that adipose tissue is not inert, but as closely linked functional "mini endocrine organs" distributed throughout the body. The current literature regarding structural and functional differences in different adipose tissues is reviewed with a focus on morphometric changes (under energy surplus), and systemic effects of adipose inflammation and dysfunction (development of insulin resistance, NAFLD, etc.). The contributions of muscle activity in bodily energy homeostasis and the close interaction between muscle, adipose, liver and insulin metabolism are discussed, and the implications of "adipose failure: for lipid partitioning into the liver, a key pathway to pathogenesis of NAFLD/NASH is highlighted. The low yield of cellular material and the excessive lipid contamination make it harder to work with adipose compared to liver. The candidate developed experimental protocols for this study, which were optimised, including adipose morphometric analysis, that were used to describe the development and progression of adipose tissue inflammation and fatty liver disease in a mouse model of NASH. We examined the effects of feeding an atherogenic diet (23% fat, 45% carbohydrate, 0.19% cholesterol) on adipose morphometry and the recruitment of inflammatory cells. We studied Alms1 mutant foz/foz mice, which have a profound disturbance of hypothalamic appetite regulation. foz/foz mice fed an atherogenic diet developed adipocyte hypertrophy, adipose inflammation, hyperglycemia, and evidence of NASH. Wildtype (WT) mice fed the same diet developed milder metabolic phenotype compared to foz/foz mice. The phenotypic switch towards a proinflammatory phenotype in enlarged adipocytes, this increasing cellular stress causes recruitment of macrophage crown-like structures (CLSs) into adipose tissue and a higher rate of adipocyte injury/necrosis. Toll-like receptors (TLRs) are innate immune system receptors activated by danger-associated molecular patterns (DAMPs). Necrotic cellular debris contains DAMPs which can stimulate TLR9 signalling. Activation of TLR9, particularly in macrophages, exacerbates adipose inflammation. Other works support a role for TLR4 in adipose inflammation, but the roles of other pattern recognizing receptors are less clear. In this study, we used Tlr9-/- mouse to investigate the contribution of TLR9 signalling, if any, to adipose inflammatory recruitment. Increased calorie intake with atherogenic feeding for 24 weeks, led to inflammation in adipose tissue. TLR9 deletion abolished this effect. Correspondingly, NASH prevalence was much less in Tlr9-/- mice. The farnesoid X receptor (FXR) agonist obeticholic acid (6-ECDCA) improves steatosis in patients with NASH, but protective mechanisms remain unresolved. We therefore investigated the effects of 6-ECDCA (1mg/kg/day) on glucose metabolism, multiple adipose compartments and liver in atherogenic diet-fed foz/foz and WT mice. 6-ECDCA reduced body weight, liver mass and hepatic lipid partitioning with striking improvement of glucose tolerance in WT but not foz/foz mice, in which it had no effect on liver histology. 6-ECDCA limited expansion of adipose tissues in atherogenic diet-fed WT but not foz/foz mice. In addition, 6-ECDCA treatment altered macrophage polarization towards a more anti-inflammatory phenotype in WT mouse adipose compartments but not foz/foz mice. To conclude, 6-ECDCA improves glucose metabolism, adiposity and adipose inflammation in animals with a milder metabolic phenotype. Conversely, 6-ECDCA fails to improve adipose inflammation or hepatic lipid partitioning in profoundly obese mice, and there is no reversal of NASH. These results help explain why 6-ECDCA treatment against human NASH improves steatosis but fails to reverse NASH pathology. Physical inactivity contributes to adverse effects of overnutrition. We studied the effects of an exercise intervention on adipose and liver pathology. From weaning, mice were provided with an in-cage exercise wheel, in which they were calculated to run over 4 km/day. In this study, voluntary exercise protected mice against the metabolic effects of high calorie intake and atherogenic dietary feeding by reducing adipose inflammation and maintaining systemic insulin sensitivity, the latter principally with its effects on muscle. Improvements in fatty liver pathology appear to be one of the benefits conferred by exercise. In the final chapter, the most important findings of earlier experiments are discussed in relation to and how they extend the knowledge in the field. Dysfunction of adipose tissue related to stress and inflammation is of pathologic importance. Limited lipid storage capacity and pro-inflammatory factors released from adipose depots can disrupt normal functioning of other organs. Circulating lipids increase when adipose is inflamed and leading to adverse effects on other tissues, primarily the liver. Meanwhile, inflammation in adipose tissue becomes persistent. Obesity-associated NAFLD/NASH, type 2 diabetes and metabolic syndrome are closely linked to persistent adipose inflammation.
Book Synopsis Principles of Endocrinology and Hormone Action by : Antonino Belfiore
Download or read book Principles of Endocrinology and Hormone Action written by Antonino Belfiore and published by Springer. This book was released on 2018-02-08 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: This volume provides comprehensive coverage of the current knowledge of the physiology of the endocrine system and hormone synthesis and release, transport, and action at the molecular and cellular levels. It presents essential as well as in-depth information of value to both medical students and specialists in Endocrinology, Gynecology, Pediatrics, and Internal Medicine. Although it is well established that the endocrine system regulates essential functions involved in growth, reproduction, and homeostasis, it is increasingly being recognized that this complex regulatory system comprises not only hormones secreted by the classic endocrine glands but also hormones and regulatory factors produced by many organs, and involves extensive crosstalk with the neural and immune system. At the same time, our knowledge of the molecular basis of hormone action has greatly improved. Understanding this complexity of endocrine physiology is crucial to prevent endocrine disorders, to improve the sensitivity of our diagnostic tools, and to provide the rationale for pharmacological, immunological, or genetic interventions. It is such understanding that this book is designed to foster.
Book Synopsis Lipid Metabolism in Skeletal Muscle: the Role of Perilipin 5 and Adipose Triglyceride Lipase in Regulating Metabolism in Skeletal Muscle by : Rachael Ruth Mason
Download or read book Lipid Metabolism in Skeletal Muscle: the Role of Perilipin 5 and Adipose Triglyceride Lipase in Regulating Metabolism in Skeletal Muscle written by Rachael Ruth Mason and published by . This book was released on 2014 with total page 245 pages. Available in PDF, EPUB and Kindle. Book excerpt: Our understanding of the importance of limiting fats in our diet has grown exponentially, especially with today's diet and health-food obsessed world. However, the numbers of people who are not only overweight, but obese, grows daily. With this ever increasing problem, our understanding of lipid metabolism has rapidly progressed in the last 30 years. The identification of key proteins, namely perilipin 1 (PLIN1), hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) has provided great insight into the regulation of lipolysis, the process of lipid breakdown. While the primary focus of much lipid metabolism research was in tissue specifically designed for storing lipids, namely adipose tissue, more recently skeletal muscle has been recognised as having a major role in lipid storage and metabolism to provide energy. However, our understandings of the exact mechanisms that regulate skeletal muscle lipolysis remain largely undetermined. The identification of the protein super-family, the Perilipins (PLIN), with at least five members, has seen a resurgence of research in lipid metabolism. It has been hypothesised that each member may have a unique tissue distribution and unique function. As members of the PLIN family exist in skeletal muscle, their function in skeletal muscle is the primary focus of this thesis. Identification of the PLIN family increased the focus of lipid metabolism research in non-adipose tissue. In skeletal muscle, PLIN5 is the most abundant member of the PLIN family. The aim of this thesis was to investigate the role of PLIN5 and ATGL in regulating lipid metabolism in skeletal muscle. Firstly, we used the PLIN5 null mouse to show the role PLIN5 has on maintaining skeletal muscle insulin action and coordinating skeletal muscle triacylglycerol metabolism. Secondly, we showed that PLIN5 null mice were not resistant to diet-induced obesity and had impaired whole body insulin sensitivity similar to that of the low fat diet PLIN5 null mouse. Together, these studies highlight the importance of PLIN5 in skeletal muscle lipid and glucose metabolism. The third aspect of the thesis was to examine the role PLIN5 has in lipid droplets in circumstances of perturbed lipid metabolism. Furthermore, its interaction with other major lipolytic proteins in these situations was also investigated. The rationale behind this approach was previous observations that have shown that PLIN5 associates with lipid droplets and ATGL and CGI-58 in cell culture systems. We demonstrated that PLIN5 was highly colocalised with ATGL and CGI-58 at rest, though acute exercise did not affect this relationship. Lastly, we identified that serine phosphorylation of ATGL site 404 is not increased in skeletal muscle during moderate intensity exercise and that AMPK does not appear to be the activating kinase of the ATGL Ser404 in skeletal muscle. The work in this thesis extends our understanding of the physiological mechanisms of lipid metabolism and the effect it has on glucose metabolism and insulin sensitivity in skeletal muscle.
Book Synopsis The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease by : Eliza B. Geer
Download or read book The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease written by Eliza B. Geer and published by Springer. This book was released on 2016-12-01 with total page 323 pages. Available in PDF, EPUB and Kindle. Book excerpt: Cushing ́s syndrome is a rare disorder that is associated with many co-morbidities such as systemic hypertension, diabetes, osteoporosis, impaired immune function, and psychiatric disease, all of which severely reduce quality of life and life expectancy. This book reviews the role of cortisol in the human body, focusing on the effects of excess cortisol due to Cushing’s syndrome as well as the role of the HPA axis in metabolism, inflammation, and neuropsychiatric function. The volume will cover basic mechanistic data, clinical outcomes data, and novel therapies. Also discussed are everything from abnormalities of the HPA axis, to the role of the HPA axis in the development of neuropsychiatric disorders and metabolic disorders, to new definitions of Cushing’s remission and recurrence. The Hypothalamic Pituitary Adrenal Axis in Health and Disease will provide a comprehensive and multi-disciplinary review of the pathophysiology and outcomes of excess cortisol in the human body and brain as well as the role of the HPA axis in other disease states.
Download or read book Stress Resilience written by Alon Chen and published by Academic Press. This book was released on 2019-11 with total page 390 pages. Available in PDF, EPUB and Kindle. Book excerpt: Stress Resilience: Molecular and Behavioral Aspects presents the first reference available on the full-breadth of cutting-edge research being carried out in this field. It includes a wide range of basic molecular knowledge on the potential associations between resilience phenomenon and biochemical balance, but also focuses on the molecular and cellular mechanisms underlying stress resilience. World-renowned experts provide chapters that cover everything from the neural circuits of resilience, the effects of early-life adversity, and the transgenerational inheritance of resilience. This unique and timely book will be a go-to resource for neuroscientists and biological psychiatrists who want to improve their understanding of the consequences of stress and on how some people are able to avoid it. Approaches resilience as a process rather than as a static trait Provides basic molecular knowledge on the potential associations between resilience phenomenon and biochemical balance Presents thorough coverage of both the genetic and environmental factors that contribute to resilience
