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Treatment Options for Chemical Sensitivity
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
A second example in metabolic coupling with the core clock originated with the finding that the mammalian ortholog of the yeast sirtuin deacetylases (for silent information regulator), proteins that activate or silence chromatin according to availability of fuel, comprises part of an additional feedback loop with the core clock.97,98 Sirtuins are present in transcription complexes with the clock, and in turn modulate activity of clock transcription factors. CLOCK-BMAL1 activates the major pathway for mammalian NAD+ synthesis, involving its regeneration from nicotinamide mediated by nicotinamide phosphoribosyltransferase (NAMPT).99,100 NAD+ concentration in cells varies across the light–dark cycle, consistent with a role for NAD+ as an oscillating metabolite linking metabolic cycles with the clock. Both NAMPT and SIRT1, similar to the NHRs and AMPK, are regulated not only by the clock but also by the nutritional status of the organism. For example, fasting increases NAMPT expression in an AMPK-dependent manner in skeletal muscle, whereas fasting and caloric restriction increase SIRT1 activity across multiple tissues. Thus, regulation of the clock by NAD+ and SIRT1 allows for fine-tuning and synchronization of the core molecular clock with the environment. Because NAD+-dependent deacetylases regulate gluconeogenesis and many other pathways,101 it will be important to further delineate the role of clock in NAD+-driven metabolism. A second NAD+-regulated pathway has recently been linked to circadian feeding cycles: PARP-1 activity is circadian in the liver and interacts with the CLOCK protein to poly-ADP-ribosylate it. Since PARP-1 is regulated by NAD+, this provides yet another pathway for metabolic signals to regulate the core clock pathway.102 Collectively, these findings identify incoming (AMPK and PARP-1) and outgoing (NAD+/Sirtuin) sensors that couple nutrient availability, metabolism, and the clock.
Visfatin gene expression and oxidative stress in pregnancy induced hypertension
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Hanan M.A. El-Taweel, Nevein A. Salah, Amal K. Selem, A.A. El-Refaeey, A.F. Abdel-Aziz
Adipokines play an important role in some process including inflammation, organization of food intake, and arrangement of body weight homeostasis, proliferation, insulin sensitivity, immunity and vascular homeostasis [10]. In obesity and type 2 diabetes mellitus have an alteration in adipokine production. Also, there is imbalance in adipokine production at the onset of insulin resistance, adipose tissue inflammation, chronic systemic inflammation, cardiovascular disease and endothelial dysfunction [11]. Fukuhara et al. [12] are the first one that characterize visfatin as an adipokine and show that insulin mimetic properties in mice with binding to and promoting the insulin receptor. Visfatin was found identical to pre-B cell colony enhancing factor (PBEF). It is a highly conserved 52 kDa cytokine-like protein. It increases the maturation of B cell precursors in relation to interleukin-7 and stem cell factor [11] and also suppresses the apoptosis of neutrophils [13]. Rongvaux et al. [14] reported that visfatin displays intrinsic enzymatic activity as a nicotinamide phosphoribosyl transferase (Nampt). However, the physiological connection of NAMPT stay argumentative [15], Revollo et al. [16] showed that the critical role of NAMPT in the monitoring of glucose metabolism through the NAD biosynthetic activity.