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Geomagnetic Field Effects on Living Systems
Published in Shoogo Ueno, Tsukasa Shigemitsu, Bioelectromagnetism, 2022
Furthermore, in N. lugens, Wan et al. (2020b) found that appetite-related regulatory pathways (neuropeptide signaling) and phenotypic outcomes (glucose levels and phloem ingestion) can be influenced by changes in the GMF intensity, which is suggested to finally result in decreases in adult body weight. The physiological and behavioral responses of N. lugens to strong changes in the GMF intensity highlight the GMF’s role in the complicated system of maintaining animal energy homeostasis via appetite regulation (Wan et al., 2020b). Energy homeostasis is also critical for migratory animals that can undergo large-scale spatial displacements in a short time (Chapman et al., 2015). Previous works on fueling behavior of several migratory birds (Fransson et al., 2001; Kullberg et al., 2007; Henshaw et al., 2008) all suggested that a difference in the GMF intensity between the emigration and immigration areas could be important environmental cues for the regulation of biological processes during migration. Thus, the weight loss suggests an adaptive response of migratory N. lugens to the changes in the GMF intensity during S-N migration or N-S remigration (Wan et al., 2020b).
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
These findings raise the possibility that disruption of nuclear hormone receptor (NHR) cycles may perturb the clock, and conversely, that delay, advance or reduced amplitude of circadian oscillations may impair NHR function. Knock-in mice of the NHR co-repressor NCor display increased energy expenditure, and a shift in the oscillation in the abundance of RNAs encoding oxidative, glycolytic, and respiratory genes, indicating that disruption of the phase of expression of NHRs contributes to metabolic deregulation.79 Mistiming of gene expression rhythms as a cause of metabolic deregulation has also been suggested by studies in Rev-erbα mutant animals, in which a phase shift in oscillating rhythms of metabolic gene transcription, rather than changes in total abundance of RNA, correspond with altered energy balance.80 Misalignment between gene transcription cycles within metabolic tissues and the behavioral cycle (of fasting and feeding) may be sufficient to alter energy homeostasis. For instance, high fat feeding provided at the incorrect circadian time leads to greater weight gain in mice than isocaloric feeding at the normal circadian time.81
Associations between Genetic Polymorphisms and Heart Rate Variability
Published in Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker, ECG Time Series Variability Analysis, 2017
Anne Voigt, Jasha W. Trompf, Mikhail Tamayo, Ethan Ng, Yuling Zhou, Yaxin Lu, Slade Matthews, Brett D. Hambly, Herbert F. Jelinek
TCF7L2 is a DNA-binding transcription factor that plays an important role in canonical Wnt signaling by binding β-catenin. Wnt signaling has defined roles in determining cell fate, survival, proliferation, and movement, and has a recognized function in embryonic development as well as carcinogenesis (Savic et al. 2011). Furthermore, and with particular importance to diabetes, Wnt signaling attenuates the synthesis of GLP-1 by intestinal L cells. GLP-1 is insulinotropic and also mimics insulin in glucose regulation, energy homeostasis, and food intake. Consequently, it is proposed that TCF7L2 gene variants may predispose individuals to T2DM by indirectly altering GLP-1 levels. Indeed, TCF7L2 polymorphisms are correlated with impaired GLP-1-induced insulin secretion and pancreatic β-cell function (Loos et al. 2007; Boccardi et al. 2010). However, direct links between HRV and this gene polymorphism have not yet been reported.
Implications of estrogen receptor alpha (ERa) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Thomas J. Degroat, Kristie M. Conde, Troy A. Roepke
This study represents new insight into the role of ERα in OPFR-initiated disruption of ingestive behaviors and energy homeostasis. Dysregulation of energy homeostasis might result in metabolic disorders such as obesity, diabetes, and metabolic syndrome. Therefore, it is important to understand the underlying toxicological mechanisms involved following OPFR exposure that may be pre-disposing human populations to such conditions. Future studies should use these data as a foundation with which to build upon by the addition of further mechanistic examinations of metabolism and energy expenditure. OPFR disruption of electrophysiological activity of NPY and POMC neurons has been previously demonstrated (Vail and Roepke 2020), and future use of selective ERα knockout in these neuronal populations might provide valuable insight into how OPFR exposure interacts with estrogenic regulation of neuronal homeostatic hubs.