Academic literature on the topic 'Vitamin D acts'
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Journal articles on the topic "Vitamin D acts"
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Brown, Alex J., Adriana Dusso, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 277, no. 2 (August 1, 1999): F157—F175. http://dx.doi.org/10.1152/ajprenal.1999.277.2.f157.
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The vitamin D endocrine systems plays a critical role in calcium and phosphate homeostasis. The active form of vitamin D, 1,25-dihydroxyvitamin D3[1,25(OH)2D3], binds with high affinity to a specific cellular receptor that acts as a ligand-activated transcription factor. The activated vitamin D receptor (VDR) dimerizes with another nuclear receptor, the retinoid X receptor (RXR), and the heterodimer binds to specific DNA motifs (vitamin D response elements, VDREs) in the promoter region of target genes. This heterodimer recruits nuclear coactivators and components of the transcriptional preinitiation complex to alter the rate of gene transcription. 1,25(OH)2D3also binds to a cell-surface receptor that mediates the activation of second messenger pathways, some of which may modulate the activity of the VDR. Recent studies with VDR-ablated mice confirm that the most critical role of 1,25(OH)2D3is the activation of genes that control intestinal calcium transport. However, 1,25(OH)2D3can control the expression of many genes involved in a plethora of biological actions. Many of these nonclassic responses have suggested a number of therapeutic applications for 1,25(OH)2D3and its analogs.
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Haryana, Nila Reswari, Qonita Rachmah, Mahmud Aditya Rifqi, Rian Diana, Dominikus Raditya Atmaka, Stefania Widya Setyaningtyas, Aliffah Nurria Nastiti, and Asri Meidyah Agustin. "Roles of Vitamins in Immunity and COVID-19: A Literature Review." Media Gizi Indonesia 17, no. 3 (September 30, 2022): 224–33. http://dx.doi.org/10.20473/mgi.v17i3.224-233.
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SARS-CoV-2 is a severe acute respiratory virus that causes Coronavirus Disease-19 (COVID-19). Even before the COVID-19 pandemic, diet was undeniably important in immunity. In order to be more resilient during and after the pandemic, understanding the role of vitamins is crucial. This review aims to explore the role of vitamins in supporting the immune system and its correlation to COVID-19. The article search was done using five electronic databases (i.e., Google Scholar, Semantic Scholar, ScienceDirect, PubMed, and PMC). Some of the keywords utilized in the literature search were “vitamin A and immunity” OR “vitamin B and immunity” OR “vitamin C and immunity” OR “vitamin D and immunity” OR “vitamin E and immunity”. A total of 51 articles was assessed in this literature review. Research finds vitamin A plays a role in both innate immune system cell function and humoral immunity by regulating, differentiating, and maturing immune system cells. Vitamin B complex primarily reduces inflammation by lowering serum C-reactive protein levels (CRP), while vitamin C strengthens epithelial barriers, phagocytes, T and B lymphocytes, and inflammatory mediators, to improve the immune system. Vitamin D acts as a mediator in the vitamin D receptor (VDR), an inner immune system component that regulates the humoral and adaptive immune systems through unique genetic transcriptions. Finally, vitamin E acts as an antioxidant, lowering the production of reactive oxygen and nitrogen species (ROS and RNS). In conclusion, all vitamins are essential in improving individual’s immune system that prevent from infectious diseases including COVID-19.
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Carlberg, Carsten. "Vitamin D: A Micronutrient Regulating Genes." Current Pharmaceutical Design 25, no. 15 (August 19, 2019): 1740–46. http://dx.doi.org/10.2174/1381612825666190705193227.
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Background:At sufficient sun exposure, humans can synthesize vitamin D3 endogenously in their skin, but today’s lifestyle makes the secosteroid a true vitamin that needs to be taken up by diet or supplementation with pills. The vitamin D3 metabolite 1α,25-dihydroxyvitamin D3 acts as a nuclear hormone activating the transcription factor vitamin D receptor (VDR).Methods:This review discusses the biological effects of micronutrient vitamin D ranging from calcium homeostasis and bone formation to the modulation of innate and adaptive immunity.Results:Since normal human diet is sufficient in vitamin D, the need for efficient vitamin D3 synthesis in the skin acts as an evolutionary driver for its lightening during the migration out of Africa towards North. Via activating the VDR, vitamin D has direct effects on the epigenome and the expression of more than 1000 genes in most human tissues and cell types.Conclusion:The pleiotropic action of vitamin D in health and disease prevention is explained through complex gene regulatory events of the transcription factor VDR.
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Kaminsky, O. V. "Vitamin D dosage." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 17, no. 5 (January 4, 2022): 435–42. http://dx.doi.org/10.22141/2224-0721.17.5.2021.241524.
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Despite its historical name, vitamin D is not a vitamin at all but a hormone that, when activated, is a metabolically active steroid fat-soluble hormone that acts on cellular receptors. Vitamin D hormone is synthesized endogenously and then metabolized in the body, provi-ding that there are the necessary precursors and some factors — the effects of ultraviolet light on the skin. At the same time, vitamins themselves are nutrients, co-factors of biochemical reactions that are not synthesized in the body and cannot interact with receptors, consumed with food, so the hormone D is not a vitamin. Disputes about its use and dosage continue throughout the study period of vitamin D hormone. Most reputable experts in Europe and the USA support the need to replenish and maintain a normal level of vitamin D, believing it to be completely safe and useful. In 2011, the US Endocrine Society issued clinical practice guidelines for vitamin D, indicating that the desired serum concentration of 25(OH)D is > 75 nmol/l (> 30 ng/ml) to achieve the maximum effect of this vitamin on calcium metabolism, bone, and muscle metabolism. According to them, for a consistent increase in serum 25(OH)D above 75 nmol/l (30 ng/ml), adults may require at least 1,500-2,000 IU/day of additional vitamin D, at least 1,000 IU/day in children and adolescents. The most common form of thyroid dysfunction is secondary hyperparathyroidism, which develops due to vitamin D defect/deficiency (80–90 %). Non-optimal serum concentrations of 25(OH)D lead to secondary hyperparathyroidism, potentially leading to decreased bone mineralization and, ultimately, to an increased risk of osteopenia, osteoporosis and fractures, cardiac arrhythmia, and increased blood pressure. Vitamin D is most commonly used at a star-ting dose of 5,000 IU daily for 2–3 months, then transferring patients to maintenance doses of 2,000–4,000 IU/day daily that are consi-dered safe. However, it should be noted that some patients will need constant administration of 5,000 IU of vitamin D per day for a long time (years) to maintain the target optimal level of 25(OH)D in the blood, especially in patients with normocalcemic forms of secondary hyperparathyroidism.
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Berridge, Michael J. "Vitamin D deficiency and diabetes." Biochemical Journal 474, no. 8 (March 24, 2017): 1321–32. http://dx.doi.org/10.1042/bcj20170042.
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Vitamin D deficiency has been linked to the onset of diabetes. This review summarizes the role of Vitamin D in maintaining the normal release of insulin by the pancreatic beta cells (β-cells). Diabetes is initiated by the onset of insulin resistance. The β-cells can overcome this resistance by releasing more insulin, thus preventing hyperglycaemia. However, as this hyperactivity increases, the β-cells experience excessive Ca2+ and reactive oxygen species (ROS) signalling that results in cell death and the onset of diabetes. Vitamin D deficiency contributes to both the initial insulin resistance and the subsequent onset of diabetes caused by β-cell death. Vitamin D acts to reduce inflammation, which is a major process in inducing insulin resistance. Vitamin D maintains the normal resting levels of both Ca2+ and ROS that are elevated in the β-cells during diabetes. Vitamin D also has a very significant role in maintaining the epigenome. Epigenetic alterations are a feature of diabetes by which many diabetes-related genes are inactivated by hypermethylation. Vitamin D acts to prevent such hypermethylation by increasing the expression of the DNA demethylases that prevent hypermethylation of multiple gene promoter regions of many diabetes-related genes. What is remarkable is just how many cellular processes are maintained by Vitamin D. When Vitamin D is deficient, many of these processes begin to decline and this sets the stage for the onset of diseases such as diabetes.
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Shivakumar, Ashwini Tumkur, Sowmya Halasabalu Kalgeri, and Prasanna K. Santhekadur. "Vitamin D Target Genes in Dental Health." Open Access Macedonian Journal of Medical Sciences 10, F (September 2, 2022): 571–77. http://dx.doi.org/10.3889/oamjms.2022.9962.
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INTRODUCTION: Vitamin D is an important molecule which plays pivotal role in overall human health and metabolism. This vitamin acts as both vitamin as well as hormone, and thus, dual nature of this vitamin makes it as one of the important chemicals required for the overall health, harmonious growth, and development. Recently, this vitamin is gaining large attention in dentistry, and it is becoming master regulator of dental health. It is well studied that vitamin D plays major role in calcium absorption for bone and teeth mineralisation, it acts as odontogenic inducer of differentiation of human dental pulp cells and in tooth development. STUDY SELECTION, DATA, AND SOURCES: Vitamin D regulates various signalling pathways in dental network and plays a beneficial role. Synthesis of vitamin D takes place in multiple steps in human body. The natural form of vitamin D is fat soluble in nature and is produced in the skin from 7-dehydrocholesterol molecules. Natural Sunlight through its ultraviolet B (UVB) energy converts the precursor7-dehydrocholesterol molecules to vitamin D3. Advanced and unhealthy lifestyle of modern times has led to the deficiency of vitamin D and metabolic syndrome. CONCLUSIONS: Deficiency of vitamin D also leads to various dental problems including dental caries, gingivitis, and periodontal disease. In this short review, we are discussing the role of vitamin D and importance of its target genes in dental health. CLINICAL RELEVANCE: Vitamin D has a major role in managing the oral health this article updates the clinician with the different genes which are responsible for the regulation of vitamin D in different tissues.
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Takeyama, Ken-Ichi, Yoshikazu Masuhiro, Hiroaki Fuse, Hideki Endoh, Akiko Murayama, Sachiko Kitanaka, Miyuki Suzawa, Junn Yanagisawa, and Shigeaki Kato. "Selective Interaction of Vitamin D Receptor with Transcriptional Coactivators by a Vitamin D Analog." Molecular and Cellular Biology 19, no. 2 (February 1, 1999): 1049–55. http://dx.doi.org/10.1128/mcb.19.2.1049.
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ABSTRACT The nuclear vitamin D receptor (VDR) is a member of a nuclear receptor superfamily and acts as a ligand-dependent transcription factor. A family of cotranscriptional activators (SRC-1, TIF2, and AIB-1) interacts with and activates the transactivation function of nuclear receptors in a ligand-dependent way. We examined interaction of VDR with these coactivators that was induced by several vitamin D analogs, since they exert differential subsets of the biological action of vitamin D through unknown mechanisms. Unlike other vitamin D analogs tested, OCT (22-oxa-1α,25-dihydroxyvitamin D3) induced interaction of VDR with TIF2 but not with SRC-1 or AIB-1. Consistent with these interactions, only TIF2 was able to potentiate the transactivation function of VDR bound to OCT. Thus, the present findings suggest that the structure of VDR is altered in a vitamin D analog-specific way, resulting in selective interactions of VDR with coactivators. Such selective interaction of coactivators with VDR may specify the array of biological actions of a vitamin D analog like OCT, possibly through activating a particular set of target gene promoters.
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Mele, Chiara, Marina Caputo, Alessandro Bisceglia, Maria Teresa Samà, Marco Zavattaro, Gianluca Aimaretti, Loredana Pagano, Flavia Prodam, and Paolo Marzullo. "Immunomodulatory Effects of Vitamin D in Thyroid Diseases." Nutrients 12, no. 5 (May 16, 2020): 1444. http://dx.doi.org/10.3390/nu12051444.
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Vitamin D is a secosteroid with a pleiotropic role in multiple physiological processes. Besides the well-known activity on bone homeostasis, recent studies suggested a peculiar role of vitamin D in different non-skeletal pathways, including a key role in the modulation of immune responses. Recent evidences demonstrated that vitamin D acts on innate and adaptative immunity and seems to exert an immunomodulating action on autoimmune diseases and cancers. Several studies demonstrated a relationship between vitamin D deficiency, autoimmune thyroid disorders, and thyroid cancer. This review aims to summarize the evidences on the immunomodulatory effect of vitamin D on thyroid diseases.
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Duda-Wiewiórka, Magdalena, and Kazimierz Pityński. "VITAMIN D IN NORMAL AND PATHOLOGICALLY CHANGED ENDOMETRIUM." Wiadomości Lekarskie 72, no. 3 (2019): 452–56. http://dx.doi.org/10.36740/wlek201903125.
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More and more evidence from research confirms the significance of vitamin D (VD) in the development of endometrial pathologies. Apart from the well known role of VD in regulation of calcium levels, VD acts as modulator to many genes involved in cell growth, immunological functions and protein synthesis. The newest research shows that VD acts multidirectionally and its common deficiency has a causal link to the pathogenesis of many gynecological and cancerous conditions. It is postulated that VD affects the endometrium via various mechanisms. The discovery that most tissues have VD receptors was ground-breaking in understanding its role in various medical conditions, including the neoplasmal development mechanism, but the degree, to which the VD metabolism in the eutopic endometrium during pathological conditions is impaired, has not yet been explained.
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Jena, Sarita, Wai-Ping Lee, Declan Doherty, and Paul D. Thompson. "PIAS4 represses vitamin D receptor-mediated signaling and acts as an E3-SUMO ligase towards vitamin D receptor." Journal of Steroid Biochemistry and Molecular Biology 132, no. 1-2 (October 2012): 24–31. http://dx.doi.org/10.1016/j.jsbmb.2012.04.006.
Full textBooks on the topic "Vitamin D acts"
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H, Glorieux Francis, ed. Rickets. Vevey, Switzerland: Nestlé Nutrition, 1991.
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H, Morii, ed. Calcium-regulating hormones. Basel: Karger, 1991.
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Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.
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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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Turney, Ben, and John Reynard. Kidney stones. Edited by John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0013.
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The composition of kidney stones is variable and the predisposing factors multifactorial. Consequently, a detailed evaluation of the patient’s lifestyle, diet, fluid intake, medical history, drug history, urinary tract anatomy, blood, and urine biochemistry and stone composition is required determine predisposing factors for stone formation in an individual patient. Combinatorial subtle variants in biochemistry may act synergistically to increase risk of stone formation/recurrence. Many medications may alter blood and/or urine biochemistry and predispose to stone formation. Corticosteroids increase absorption of calcium from the gut and cause hypercalciuria. Topirimate (for seizures or migraines), sulphasalazine (for rheumatoid arthritis), diuretics containing triamterene, acetazolamide (for myotonia), antacids containing trisilicate, calcium supplements, vitamin D supplements, vitamin C in high doses, indinavir (for HIV), and some herbal medicines (containing ephedrine) all increase stone risk.
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Segaert, Siegfried. The Role of 1a,25-Dihydroxyvitamin D3 and the Vitamin D Receptor in the Control of Proliferation and Differentiation of the Epidermal Keratinocyte (Acta Biomedica Lovaniensia 196). Leuven Univ Pr, 1999.
Find full textBook chapters on the topic "Vitamin D acts"
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"1,25-DIHYDROXYVITAMIN D3 ACTS DIRECTLY ON HUMAN LYMPHOCYTES AND INTERFERES WITH THE CELLULAR RESPONSE TO INTERLEUKIN-2." In Vitamin D, 354–55. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.354.
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Singh Chauhan, Vikram. "Vitamin D and the Immune System." In Vitamin D. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97300.
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In the past few decades, various novel actions of vitamin D have been discovered. The mechanism of action of calcitriol or vitamin D is mediated by the Vitamin D receptor (VDR), a subfamily of nuclear receptors, which acts as a transcription factor in the target cells after formation of a heterodimer with the retinoid X receptor (RXR). As the VDR has been found in virtually all cell types, vitamin D exerts multiple actions on different tissues. Vitamin D has important immunomodulatory actions, which includes enhancement of the innate immune system and inhibition of the adaptative immune responses. These actions are associated with an increase in production of interleukin (IL)-4 by T helper (Th)-2 lymphocytes and the up-regulation of regulatory T lymphocytes. Vitamin D can regulate the immune responses in secondary lymphoid organs as well as in target organs through a number of mechanisms. Vitamin D inhibits the expression of APC cytokines, such as interleukin-1 (IL-1), IL-6, IL-12, and tissue necrosis factor- α (TNF-α) and decreases the expression of a set of major histocompatibility complex (MCH) class II cell surface proteins in macrophages. Vitamin D also inhibits B cell differentiation and antibody production. These actions reflect an important role of Vitamin D in balancing the immune system.
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Brody, David L. "Fatigue." In Concussion Care Manual, 71–72. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199383863.003.0015.
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A systematic approach to fatigue: figure out how bad it is; rule out the complaint of concussion-related fatigue as an excuse to get out of school, work, or unpleasant chores at home by asking the collateral source about how fatigued the patient acts in everyday life; rule out depression; rule out a primary sleep disorder; rule out alcohol, sedating medications, and other drugs; rule out withdrawal from stimulants; rule out a systemic cause such as hypotension, hypoxemia, renal failure, liver failure, anemia, hyponatremia, hypothyroidism, vitamin D deficiency, or chronic urinary tract infection. If these are not present or fatigue persists after treatment, consider prescribing one or more of the following: a very gradually progressive exercise program, bright light treatment, complete alcohol cessation, a diet that is low in refined sugar, a stimulant, amantadine, and modafinil.
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Brody, David L. "Fatigue." In Concussion Care Manual, edited by David L. Brody, 107–10. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190054793.003.0016.
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A systematic approach to fatigue: Figure out how bad it is; rule out the complaint of concussion-related fatigue as an excuse to get out of school, work, or unpleasant chores at home by asking the collateral source how fatigued the patient acts in everyday life; rule out depression; rule out a primary sleep disorder; rule out alcohol, sedating medications, and other drugs; rule out withdrawal from stimulants; rule out a systemic cause such as hypotension, hypoxemia, renal failure, liver failure, anemia, hyponatremia, hypothyroidism, vitamin D deficiency, and chronic urinary tract infection. If these are not present or fatigue persists after treatment, consider prescribing one or more of the following: a very gradually progressive exercise program, bright light treatment, complete alcohol cessation, a diet that is low in refined sugar, a stimulant, amantadine, and modafinil. Consider using a quantitative measure, such as The Fatigue Severity Scale.
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Frey, Perry A., and Adrian D. Hegeman. "Coenzymes I: Organic Coenzymes." In Enzymatic Reaction Mechanisms. Oxford University Press, 2007. http://dx.doi.org/10.1093/oso/9780195122589.003.0007.
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Most enzymatic reactions proceed with chemical changes that cannot be brought about by the side chains of amino acid residues. These enzymes function in cooperation with coenzymes and cofactors, which lend physicochemical potentialities not found in amino acids. Many coenzymes are organic molecules incorporating functional groups with chemical properties that enable them to facilitate reactions of certain types. These molecules bind to active sites tailored for them through evolution and equipped to assist in their coenzymatic functions. Many of these coenzymes were derived from vitamins, and in early biochemistry investigations, vitamins and coenzymes were often regarded as closely linked and even synonymous. However, vitamins such as vitamin D are more akin to hormones than to coenzymes, and in modern biochemistry, the newly discovered coenzymes are not related to vitamins and have identities independent of any nutritional origin. More than 25 biological molecules may be regarded as coenzymatic in nature. In this book, the most common coenzymes and their functions are described in two chapters, the organic coenzymes in this chapter, and the metallo-coenzymes in chapter 4. Each coenzyme and cognate enzyme form a union that allows them to act as a single catalytic entity functioning in concert to bring about a difficult chemical transformation. Each coenzyme provides the chemistry required for a class of enzymatic processes, and the mechanisms of enzymatic catalysis are often revealed through the actions of the participating coenzymes. Nicotinamide adenine dinucleotide (NAD+) is the coenzymatic form of the vitamin niacin (vitamin B1). The structural formula for NAD+ is shown in fig. 3-1 along with the biochemically reactive bonds and their importance in metabolism. NADH is the reduced form of NAD+ and is produced in the dehydrogenation of substrates. The closely related forms NADP+ and NADPH are phosphorylated at the 2′-hydroxyl group of the adenosyl moiety. NADP+ and NADPH generally participate in biosynthesis (anabolism), whereas NAD+ and NADH generally participate in biodegradative metabolism (catabolism). NAD+ and NADH were formerly known as DPN+ and DPNH, for diphosphopyridine nucleotide, and TPN+ and TPNH, for triphosphopyridine nucleotide. The most frequent function of NAD+ is as an acceptor of a hydrogen atom and two electrons, a hydride equivalent, in reactions of oxidoreductases, commonly known as dehydrogenases.
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Fowkes, Rob, V. Krishna Chatterjee, and Mark Gurnell. "Principles of hormone action." In Oxford Textbook of Medicine, edited by Mark Gurnell, 2245–57. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0243.
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Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include: peptides (e.g. hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic substances (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly.
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Gurnell, Mark, Jacky Burrin, and V. Krishna Chatterjee. "Principles of hormone action." In Oxford Textbook of Medicine, 1787–98. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.1301_update_001.
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Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include (1) peptides (e.g hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; (2) steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic substances (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly....
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M. Jasim, Adnan, and Mohammed J. Jawad. "Pharmaceutical Applications of Vitamin E TPGS." In Vitamin E in Health and Disease - Interactions, Diseases and Health Aspects [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97474.
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D-tocopheryl polyethylene glycol succinate (Vitamin E TPGS) has been approved as a safe pharmaceutical adjuvant by FDA, and several drug delivery systems (DDS) based on TPGS have been developed. TPGS properties as a P-gp inhibitor, solubilizer/absorption and permeation enhancer in drug delivery and TPGS-related formulations such as nanocrystals, nanosuspensions, tablets/solid dispersions, vaccine system adjuvant, nutritional supplement, film plasticizer, anticancer reagent, and so on, are discussed in this review. Consequenly, TPGS can inhibit ATP-dependent P-glycoprotein activity and act as a potent excipient that promotes the efficiency of delivery and the therapeutic effect of drugs. Inhibition of P-gp occurs through mitochondria-dependent inhibition of the P-gp pump. Many of the latest studies address the use of TPGS for many poorly water-soluble or permeable drugs in the manufacture of nanodrugs or other formulations. In addition, it has been reported that TPGS shows a robust improvement in chylomicron secretion at low concentrations and improves intestinal lymphatic transport, which would also boost the potential of drug absorption. It also indicates that there are still many problems facing clinical translation of TPGS-based nanomedicines, requiring a more deep evaluation of TPGS properties and a future-based delivery method.
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Brown, Todd, Michelle Kendall, and Grace McComsey. "Vitamin D, OPG/RANKL, and Inflammation with Alendronate Treatment in HIV-Infected Patients with Reduced Bone Mineral Density: A Secondary Analysis of AIDS Clinical Trial Group (ACTG) A5163." In CLINICAL - Metabolic Bone Disease: Clinical Trials, OR29–6—OR29–6. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.or10.or29-6.
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