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Obesity-induced inflammation and insulin resistance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194285 Year: Pages: 120 DOI: 10.3389/978-2-88919-428-5 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic disorder such as type 2 diabetes, fatty liver disease and cardiovascular disease. Insulin resistance is an underlying basis for the pathogenesis of these metabolic diseases. Overnutrition or obesity activates the innate immune system with subsequent recruitment of immune cells such as macrophages and T cells, which contributes to the development of insulin resistance. In particular, a significant advance in our understanding of obesity-associated inflammation and insulin resistance has been recognition of the critical role of adipose tissue macrophages (ATMs). ATMs are a prominent source of proinflammatory cytokines, such as TNF-a and IL-6, that can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signaling and cause systemic insulin resistance via endocrine signaling, providing a potential link between inflammation and insulin resistance. All articles in this topic highlight the interconnection between obesity, inflammation, and insulin resistance in all its diversity to the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of insulin resistance and diabetes.

Carotid Body: A New Target for Rescuing Neural Control of Cardiorespiratory Balance in Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199433 Year: Pages: 134 DOI: 10.3389/978-2-88919-943-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2016-01-19 14:05:46
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The carotid body (CB) is in charge of adjusting ventilatory and cardiovascular function during changes in arterial blood gases. Regardless this essential function, the CB has been implicated in the sensing of other physiological signals such as changes in blood flow and glucose levels. More important, malfunction of the CB chemoreceptors has been associated with the progression and deterioration of several disease states such as hypertension, heart failure, renal failure, insulin resistance, diabetes and sleep apnea. Although the mechanisms involved in the alterations of the CB function in pathophysiology are currently under intense research, the development of therapeutic approaches to restore normal CB chemoreflex function remains unsolved. Recent studies showing the effect of CB denervation in pathophysiology have unveiled a key role of these arterial chemoreceptors in the development of autonomic imbalance and respiratory disturbances, and suggest that targeting the CB could represent a novel strategy to improve disease outcome. Unfortunately, classical pharmacotherapy intended to normalize CB function may be hard to establish since several cellular pathways are involved in the CB dysfunction. Augmented levels of angiotensin II, endothelin-1, cytokines and free radicals along with decreases in nitric oxide had all been related to the CB dysfunction. Moreover, changes in expression of angiotensin receptors, nitric oxide synthases and cytokines that take place within the CB tissue in pathological states also contribute to the enhanced CB chemoreflex drive. It has been shown in heart failure, hypertension and obstructive sleep apnea that the CB becomes tonically hyper-reactive. During the progression of the disease this CB chemosensory facilitation process induces central nervous system plasticity. The altered autonomic-respiratory control leads to increased cardiorespiratory distress and the deterioration of the condition. The focus of this e-book will be to cover the role of the CB in pathophysiology and to provide new evidence of the pathways involved in the maladaptive potentiation of the CB chemoreflex function. In memory of Professor Mashiko Shirahata and Professor Constancio Gonzalez.

Obesity and Diabetes: Energy Regulation by Free Fatty Acid Receptors

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197477 Year: Pages: 45 DOI: 10.3389/978-2-88919-747-7 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Food intake regulates energy balance and its dysregulation leads to metabolic disorder, such as obesity and diabetes. During feeding, free fatty acids (FFAs) are not only essential nutrients but also act as signaling molecules in various cellular processes. Recently, several orphan G protein-coupled receptors (GPCRs) that act as FFA receptors (FFARs) have been identified; GPR40/FFAR1, GPR119, and GPR120 are activated by medium- and long-chain FFAs. GPR84 is activated by medium-chain FFAs. GPR41/FFAR3 and GPR43/FFAR2 are activated by short-chain FFAs. These FFARs have come to be regarded as new drug targets for metabolic disorder such as obesity and type 2 diabetes, because a number of pharmacological and physiological studies have shown that these receptors are primarily involved in the energy metabolism in various tissues; insulin secretion, gastrointestinal hormone secretion, adipokine secretion, regulation of inflammation, regulation of autonomic nervous system, relation to gut microbiota, and so on. This Research Topic provides a comprehensive overview of the energy regulation by free fatty acid receptors and a new prospect for treatment of metabolic disorder such as obesity and type 2 diabetes.

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