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Clinical Approach to Sodium Homeostasis Disorders in Children with Pituitary-Suprasellar Tumors.
Tuli, G, Matarazzo, P, de Sanctis, L
Neuroendocrinology. 2020;(3-4):161-171
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Abstract
Children with pituitary-suprasellar tumors are at high risk of developing sodium metabolism disorders since the tumoral mass itself or surgical and medical treatment can damage AVP release circuits. Additional risk factors are represented by the use of hypotonic fluids, the young age, total parenteral nutrition, and obstructive hydrocephalus secondary to tumor pathology. The most frequent hyponatremic disorders related to AVP in these patients are the syndrome of inappropriate ADH secretion and the cerebral/renal salt wasting syndrome, while hypernatremic conditions include central diabetes insipidus (CDI) and adipsic CDI. The main challenge in the management of these patients is to promptly distinguish the AVP release disorder at the base of the sodium imbalance and treat it correctly by avoiding rapid sodium fluctuations. These disorders can coexist or follow each other in a few hours or days; therefore, careful clinical and biochemical monitoring is necessary, especially during surgery, the use of chemotherapeutic agents, or radiotherapy. This monitoring should be performed by experienced healthcare professionals and should be multidisciplinary, including pediatric endocrinologists, neurosurgeons, and oncologists since maintaining sodium homeostasis also plays a prognostic role in terms of disease survival, therapeutic response, hospitalization rate, and mortality. In this review, we analyze the management of sodium homeostasis disorders in children with pituitary-suprasellar tumors and discuss the main challenges in the diagnosis and treatment of these conditions based on literature data and over 30 years of clinical experience at our Department of Pediatric Endocrinology.
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Gut Dysbiosis Dysregulates Central and Systemic Homeostasis via Suboptimal Mitochondrial Function: Assessment, Treatment and Classification Implications.
Anderson, G, Maes, M
Current topics in medicinal chemistry. 2020;(7):524-539
Abstract
The gut and mitochondria have emerged as two important hubs at the cutting edge of research across a diverse array of medical conditions, including most psychiatric conditions. This article highlights the interaction of the gut and mitochondria over the course of development, with an emphasis on the consequences for transdiagnostic processes across psychiatry, but with relevance to wider medical conditions. As well as raised levels of circulating lipopolysaccharide (LPS) arising from increased gut permeability, the loss of the short-chain fatty acid, butyrate, is an important mediator of how gut dysbiosis modulates mitochondrial function. Reactive cells, central glia and systemic immune cells are also modulated by the gut, in part via impacts on mitochondrial function in these cells. Gut-driven alterations in the activity of reactive cells over the course of development are proposed to be an important determinant of the transdiagnostic influence of glia and the immune system. Stress, including prenatal stress, also acts via the gut. The suppression of butyrate, coupled to raised LPS, drives oxidative and nitrosative stress signalling that culminates in the activation of acidic sphingomyelinase-induced ceramide. Raised ceramide levels negatively regulate mitochondrial function, both directly and via its negative impact on daytime, arousal-promoting orexin and night-time sleep-promoting pineal gland-derived melatonin. Both orexin and melatonin positively regulate mitochondria oxidative phosphorylation. Consequently, gut-mediated increases in ceramide have impacts on the circadian rhythm and the circadian regulation of mitochondrial function. Butyrate, orexin and melatonin can positively regulate mitochondria via the disinhibition of the pyruvate dehydrogenase complex, leading to increased conversion of pyruvate to acetyl- CoA. Acetyl-CoA is a necessary co-substrate for the initiation of the melatonergic pathway in mitochondria and therefore the beneficial effects of mitochondria melatonin synthesis on mitochondrial function. This has a number of treatment implications across psychiatric and wider medical conditions, including the utilization of sodium butyrate and melatonin. Overall, gut dysbiosis and increased gut permeability have significant impacts on central and systemic homeostasis via the regulation of mitochondrial function, especially in central glia and systemic immune cells.
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A State-of-the-Science Review of Arsenic's Effects on Glucose Homeostasis in Experimental Models.
Castriota, F, Rieswijk, L, Dahlberg, S, La Merrill, MA, Steinmaus, C, Smith, MT, Wang, JC
Environmental health perspectives. 2020;(1):16001
Abstract
BACKGROUND The prevalence of type 2 diabetes (T2D) has more than doubled since 1980. Poor nutrition, sedentary lifestyle, and obesity are among the primary risk factors. While an estimated 70% of cases are attributed to excess adiposity, there is an increased interest in understanding the contribution of environmental agents to diabetes causation and severity. Arsenic is one of these environmental chemicals, with multiple epidemiology studies supporting its association with T2D. Despite extensive research, the molecular mechanism by which arsenic exerts its diabetogenic effects remains unclear. OBJECTIVES We conducted a literature search focused on arsenite exposure in vivo and in vitro, using relevant end points to elucidate potential mechanisms of oral arsenic exposure and diabetes development. METHODS We explored experimental results for potential mechanisms and elucidated the distinct effects that occur at high vs. low exposure. We also performed network analyses relying on publicly available data, which supported our key findings. RESULTS While several mechanisms may be involved, our findings support that arsenite has effects on whole-body glucose homeostasis, insulin-stimulated glucose uptake, glucose-stimulated insulin secretion, hepatic glucose metabolism, and both adipose and pancreatic β-cell dysfunction. DISCUSSION This review applies state-of-the-science approaches to identify the current knowledge gaps in our understanding of arsenite on diabetes development. https://doi.org/10.1289/EHP4517.
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Bacterial manganese sensing and homeostasis.
Waters, LS
Current opinion in chemical biology. 2020;:96-102
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Abstract
Manganese (Mn) plays a complex role in the survival of pathogenic and symbiotic bacteria in eukaryotic hosts and is also important for free-living bacteria to thrive in stressful environments. This review summarizes new aspects of regulatory strategies to control intracellular Mn levels and gives an overview of several newly identified families of bacterial Mn transporters. Recent illustrative examples of advances in quantification of intracellular Mn pools and characterization of the effects of Mn perturbations are highlighted. These discoveries help define mechanisms of Mn selectivity and toxicity and could enable new strategies to combat pathogenic bacteria and promote growth of desirable bacteria.
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Sulfur Homeostasis in Plants.
Li, Q, Gao, Y, Yang, A
International journal of molecular sciences. 2020;(23)
Abstract
Sulfur (S) is an essential macronutrient for plant growth and development. S is majorly absorbed as sulfate from soil, and is then translocated to plastids in leaves, where it is assimilated into organic products. Cysteine (Cys) is the first organic product generated from S, and it is used as a precursor to synthesize many S-containing metabolites with important biological functions, such as glutathione (GSH) and methionine (Met). The reduction of sulfate takes place in a two-step reaction involving a variety of enzymes. Sulfate transporters (SULTRs) are responsible for the absorption of SO42- from the soil and the transport of SO42- in plants. There are 12-16 members in the S transporter family, which is divided into five categories based on coding sequence homology and biochemical functions. When exposed to S deficiency, plants will alter a series of morphological and physiological processes. Adaptive strategies, including cis-acting elements, transcription factors, non-coding microRNAs, and phytohormones, have evolved in plants to respond to S deficiency. In addition, there is crosstalk between S and other nutrients in plants. In this review, we summarize the recent progress in understanding the mechanisms underlying S homeostasis in plants.
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Transcription factors and transporters in zinc homeostasis: lessons learned from fungi.
Eide, DJ
Critical reviews in biochemistry and molecular biology. 2020;(1):88-110
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Abstract
Zinc is an essential nutrient for all organisms because this metal serves as a critical structural or catalytic cofactor for many proteins. These zinc-dependent proteins are abundant in the cytosol as well as within organelles of eukaryotic cells such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and storage compartments such as the fungal vacuole. Therefore, cells need zinc transporters so that they can efficiently take up the metal and move it around within cells. In addition, because zinc levels in the environment can vary drastically, the activity of many of these transporters and other components of zinc homeostasis is regulated at the level of transcription by zinc-responsive transcription factors. Mechanisms of post-transcriptional control are also important for zinc homeostasis. In this review, the focus will be on our current knowledge of zinc transporters and their regulation by zinc-responsive transcription factors and other mechanisms in fungi because these organisms have served as useful paradigms of zinc homeostasis in all organisms. With this foundation, extension to other organisms will be made where warranted.
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Thiol-disulfide homeostasis: an integrated approach with biochemical and clinical aspects.
Erel, Ö, Erdoğan, S
Turkish journal of medical sciences. 2020;(SI-2):1728-1738
Abstract
Dynamic thiol-disulfide homeostasis (TDH) is a new area has begun to attract more scrutiny. Dynamic TDH is reversal of thiol oxidation in proteins and represents the status of thiols (-SH) and disulfides (-S-S-). Organic compounds containing the sulfhydryl group is called thiol, composed of sulfur and hydrogen atoms. Disulfides are the most important class of dynamic, redox responsive covalent bonds build in between two thiol groups. For many years, thiol levels were analyzed by several methods. During last years, measurements of disulfide levels have been analyzed by a novel automated method, developed by Erel and Neselioglu. In this method, addition to thiol (termed as native thiol) levels, disulfide levels were also measured and sum of native thiol and disulfide levels were termed as total thiol. Therefore, TDH was begun to be understood in organism. In healthy humans, TDH is maintained within a certain range. Dysregulated dynamic TDH has been implicated several disorders with unknown etiology. A growing body of evidence has demonstrated that the thiol-disulfide homeostasis is involved in variety diseases, such as diabetes mellitus, hypertension, nonsmall cell lung cancer, familial Mediterranean fever (FMF), inflammatory bowel diseases, occupational diseases, gestational diabetes mellitus and preeclampsia. These results may elucidate some pathogenic mechanism or may be a predictor indicating diagnostic clue, prognostic marker or therapeutic sign. In conclusion, protection of the thiol-disulfide homeostasis is of great importance for the human being. Evidence achieved so far has proposed that thiol-disulfide homeostasis is an important issue needs to elucidate wholly.
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Immunoregulatory Sensory Circuits in Group 3 Innate Lymphoid Cell (ILC3) Function and Tissue Homeostasis.
Domingues, RG, Hepworth, MR
Frontiers in immunology. 2020;:116
Abstract
Recent years have seen a revolution in our understanding of how cells of the immune system are modulated and regulated not only via complex interactions with other immune cells, but also through a range of potent inputs derived from diverse and varied biological systems. Within complex tissue environments, such as the gastrointestinal tract and lung, these systems act to orchestrate and temporally align immune responses, regulate cellular function, and ensure tissue homeostasis and protective immunity. Group 3 Innate Lymphoid Cells (ILC3s) are key sentinels of barrier tissue homeostasis and critical regulators of host-commensal mutualism-and respond rapidly to damage, inflammation and infection to restore tissue health. Recent findings place ILC3s as strategic integrators of environmental signals. As a consequence, ILC3s are ideally positioned to detect perturbations in cues derived from the environment-such as the diet and microbiota-as well as signals produced by the host nervous, endocrine and circadian systems. Together these cues act in concert to induce ILC3 effector function, and form critical sensory circuits that continually function to reinforce tissue homeostasis. In this review we will take a holistic, organismal view of ILC3 biology and explore the tissue sensory circuits that regulate ILC3 function and align ILC3 responses with changes within the intestinal environment.
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Regulation of Iron Homeostasis and Use in Chloroplasts.
Kroh, GE, Pilon, M
International journal of molecular sciences. 2020;(9)
Abstract
Iron (Fe) is essential for life because of its role in protein cofactors. Photosynthesis, in particular photosynthetic electron transport, has a very high demand for Fe cofactors. Fe is commonly limiting in the environment, and therefore photosynthetic organisms must acclimate to Fe availability and avoid stress associated with Fe deficiency. In plants, adjustment of metabolism, of Fe utilization, and gene expression, is especially important in the chloroplasts during Fe limitation. In this review, we discuss Fe use, Fe transport, and mechanisms of acclimation to Fe limitation in photosynthetic lineages with a focus on the photosynthetic electron transport chain. We compare Fe homeostasis in Cyanobacteria, the evolutionary ancestors of chloroplasts, with Fe homeostasis in green algae and in land plants in order to provide a deeper understanding of how chloroplasts and photosynthesis may cope with Fe limitation.
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The Implication of Gut Hormones in the Regulation of Energy Homeostasis and Their Role in the Pathophysiology of Obesity.
Koliaki, C, Liatis, S, Dalamaga, M, Kokkinos, A
Current obesity reports. 2020;(3):255-271
Abstract
PURPOSE OF REVIEW This review provides an update on the role of gut hormones and their interactions in the regulation of energy homeostasis, describes gut hormone adaptations in obesity and in response to weight loss, and summarizes the current evidence on the role of gut hormone-based therapies for obesity treatment. RECENT FINDINGS Gut hormones play a key role in regulating eating behaviour, energy and glucose homeostasis. Dysregulated gut hormone responses have been proposed to be pathogenetically involved in the development and perpetuation of obesity. Summarizing the major gut hormone changes in obesity, obese individuals are characterized by blunted postprandial ghrelin suppression, loss of premeal ghrelin peaks, impaired diurnal ghrelin variability and reduced fasting and postprandial levels of anorexigenic peptides. Adaptive alterations of gut hormone levels are implicated in weight regain, thus complicating hypocaloric dietary interventions, and can further explain the profound weight loss and metabolic improvement following bariatric surgery. A plethora of compounds mimicking gut hormone changes after bariatric surgery are currently under investigation, introducing a new era in the pharmacotherapy of obesity. The current trend is to combine different gut hormone receptor agonists and target multiple systems simultaneously, in order to replicate as closely as possible the gut hormone milieu after bariatric surgery and circumvent the counter-regulatory adaptive changes associated with dietary energy restriction. An increasing number of preclinical and early-phase clinical trials reveal the additive benefits obtained with dual or triple gut peptide receptor agonists in reducing body weight and improving glycaemia. Gut hormones act as potent regulators of energy and glucose homeostasis. Therapeutic strategies targeting their levels or receptors emerge as a promising approach to treat patients with obesity and hyperglycaemia.