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Geomagnetic Field Effects on Living Systems
Published in Shoogo Ueno, Tsukasa Shigemitsu, Bioelectromagnetism, 2022
Carter et al. (2020) demonstrated a quantum biological phenomenon whereby a combination of 3 mT SMF and 7 kV/m EF ameliorated hyperglycemia and enhance insulin sensitivity in three different mouse models of type 2 diabetes: Bardet-Biedl syndrome, leptin receptor-deficient, and high-fat diet (HFD) mice. Surprisingly, all mice have a 30% or greater reduction in blood glucose and these effects appeared rapidly, within 3 days of exposure (continuously 24 hours/day for 3 days, or for 7 hours/day for a total of 3 days), without adverse effects (Carter et al., 2020). However, the glucose levels were returned to the pre-exposure levels when the daily exposure was stopped (Carter et al., 2020). Interestingly, both exposures to SMF and EF were required simultaneously, and exposure to SMF alone exacerbated diabetes through unknown mechanisms (Carter et al., 2020). In addition, human liver cells treated with both SMF and EF for 6 hours demonstrated an increase in glycogen, a surrogate marker for insulin sensitivity, indicating a similar effect with mice. This enhancement of insulin sensitivity occurred due to altered redox homeostasis, mediated primarily by the hepatic mitochondrial superoxide O2− (Carter et al., 2020). That is, both exposures to SMF and EF promoted activation of the antioxidant enzyme SOD2 in hepatic mitochondria and enhanced superoxide scavenging activity (Carter et al., 2020). Furthermore, it was found that non-cyclooxygenase-derived prostanoids (F2-isoprostanes), which are a biomarker of oxidative stress, decreased by about 40%, and the master transcription factor NRF2 in redox signaling was elevated by both exposures (Carter et al., 2020). Thus, both exposures to SMF and EF enhanced the redox reaction by increasing the release of glutathione into the blood via the NRF2, and reduced oxidative stress to improve insulin resistance (Carter et al., 2020).
Novel Microbial Compounds as a Boon in Health Management
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Shubha Rani Sharma, Rajani Sharma, Debasish Kar
A vast number of research works have proved that a high-fat diet can destroy the bacteria present in the gut thus leading to profuse weight gain. Several functions of the microbes in the gut have been recognized like digestion, altering hunger, etc. Thus, several scientists are involved in the investigation of various microbiomes present in obese people, as well as underweight people, and what is the role of these microbes in maintaining body weight? They have established that the food that we eat directly affects the presence of microbes in our gut. Some of the food items promote the growth of the bacteria that increase the bodyweight of the person while some support the growth of those bacteria which decrease the body weight. Now it is a matter of ponderance as to which of the fats serve to increase the microbial flora instrumental in promoting obesity. The common bad fats which increase the bodyweight are refined omega 6 vegetable oils like soybean oil. The polyunsaturated fats obtained from soybean, canola, and other seed oils cause inflammation and need to be avoided. Though we are actually misguided by the personals involved in marketing in the food industry that these types of vegetable fats are good for our health and do not cause any harm to our body, but the fact is that if we want to stay healthy and fit we need to totally boycott the use of these harmful oils. Omega 3 fats and monounsaturated fats like extra-virgin olive oil are involved in improving the growth of good microbes which keep our body healthy and do not cause obesity. The harmful microbes or the bad bacteria cause the production of toxins like the LPS which result in the inflammation of the whole body, also cause diabetes, and thus cause weight gain. Turnbaugh et al. (2009) furnished the first evidence that the transfer of the microbiota of obese mice into mice that is germfree or devoid of any microbes, led to the increase in obesity of the mice. This fact has not only been established in mice but in rodents and even in human beings. The research was performed with the genetically obese mice that were deficient in leptin receptor and came to a conclusion that the microbiota present in the caecum were having about 50% fewer Bacteroidetes that were present in the lean mice also found that a large number of Firmicutes were found in the obese as compared to the unhealthy mice (Ley et al., 2006).
Carriers for Nucleic Acid Delivery to the Brain
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Although large protein ligands such as Tf or antibodies were used successfully for brain delivery, their large size and charge can destabilise nanoparticles and thereby limit their biodistribution in vivo [41]. Smaller peptide ligands are an alternative to protein ligands, especially since display techniques such as messenger RNA (mRNA) or phage display enable the screening of large peptide libraries for binding to target receptors and cells (Table 9.1) [56–58]. Among the most commonly used peptide ligands for BBB transfer is rabies virus glycoprotein (RVG), a 29-amino-acid peptide which binds the nicotinic acetylcholine receptor. RVG bound to a nucleic acid-binding oligo-arginine residue was used for siRNA brain delivery after systemic administration [59]. Since then, nucleic acid formulations for BBB transfer included RVG-decorated PAMAM dendrimers [60], liposomes [61], chitosan nanoparticles [62], poly(mannitol-co-PEI) complexes [63] and exosomes [64], but overall results were not convincing. Other peptide ligands for brain delivery of nucleic acids or nanoparticles include angiopep-2 for LRP-1 binding [65], chlorotoxin, which specifically binds glioma cells and matrix metalloproteinase-2 (MMP-2) [66], EPRNEEK binding the laminin receptor [67], a leptin-derived peptide binding the leptin receptor [68], g7 which promotes brain delivery via AMT [69] or the TfR-binding peptide THR [70]. Small peptide ligands must be presented on the nanoparticle surface to be available for target receptor or cell interaction. In addition, the protease stability of peptides is a major concern when decorated nanoparticles are systemically administered in vivo, as rapid degradation of the ligands results in a loss of targeting capability. The retro-enantio approach inverts the peptide sequence, and L-amino acids are replaced by D-amino acids, resulting in protease-resistant analogues which retain the binding ability of the parent peptide. The TfR binding peptide THR has been converted into the fully protease-resistant THR retro-enantio peptide, which acts as a BBB shuttle for the CNS delivery of a variety of cargoes. [71]. Cyclisation and substitution of natural amino acids by nonnatural residues are further strategies to optimise peptide ligands for systemic brain delivery, as shown for the LDL receptor-binding peptide-22 [72] or the cyclic bee venom-derived peptide MiniAp-4 [73].
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
For female ERαKO mice, both diet and OPFR did not markedly affect Pomc and Cart expression. This is interesting in of itself, as their male counterparts showed marked interactions between these categories for Pomc expression, perhaps indicating that ERα plays a greater role in protection against OPFR-induced alterations to Pomc in males than in females. In females, qPCR analysis revealed an overall significant effect of OPFR to elevate Npy expression (Table 2), as well as Pparg (Table 2). An overall effect of diet was also recorded for Agrp, where expression was lower across exposure groups in HFD-fed females (Table 2). However, post-hoc testing only highlighted a significant reduction in OPFR-exposed females, indicating a potential for OPFR exposure to enhance the impact of HFD on Agrp expression in females lacking ERα. As in males, a significant overall effect of OPFR was reported for both insulin and leptin receptor expression (Table 2). This observation suggests that the potential for OPFRs to increase sensitivity to peripheral leptin and insulin is not impacted by gender.
An ecological study on the spatially varying association between adult obesity rates and altitude in the United States: using geographically weighted regression
Published in International Journal of Environmental Health Research, 2022
Moreover, hypoxia changes the close-period survival tradeoff between the cost for excess body weight and the benefit for increased energy storage (Tschöp et al. 1998; Lippl et al. 2010). Several studies have reported that people living in lowland area, who travel to various altitudes above 2,650 m, experience anorexia and weight loss in the short period of time (Hamad and Travis 2006; Ge et al. 2010; Aeberli et al. 2013). In addition, in a clinical trial, subjects with obesity in hypoxic conditions had lower caloric intake and greater weight loss compare to those in false hypoxic conditions under the same low-intensity activity level (Netzer et al. 2008). Furthermore, previous studies have found that plasma leptin concentrations, which help suppress appetite, in all test subjects increase at higher altitude and in hypoxic conditions, whereas others have found unchanged or decreased levels of plasma leptin concentrations (Vats et al. 2004, 2007; Snyder et al. 2008). Hypoxia promotes leptin signaling by increasing production of leptin receptor. This gives clear explanation on how hypoxic conditions induce anorexia, while other environmental condition stays same (Norese et al. 2002; Voss et al. 2013).
How the quest to improve sheep reproduction provided insight into oocyte control of follicular development
Published in Journal of the Royal Society of New Zealand, 2018
There is strong nutritional regulation of reproduction in sheep with nutritionally induced changes in attainment of puberty, ovulation rate, and embryo, fetal and lamb survival (Scaramuzzi et al. 1993, 2006, 2011; Zieba et al. 2005, 2008). Leptin is known to be involved in appetite control, providing a feedback to the animal regarding the current level of fat deposition (Szczesna & Zieba 2015). Leptin has long been postulated to be a key regulator in the nutritional control of reproduction. Recently we have identified three closely linked mutations in the leptin receptor (LEPR) gene that were negatively associated with reproductive performance. Interestingly, these mutations were associated with suppression of a number of reproductive traits including age at attainment of puberty (Haldar et al. 2014), ovulation rate and embryo survival in ewes with high ovulation rates (Juengel et al. 2016). These findings highlight the potential for mutations in a single gene to affect reproductive outcome through altering multiple reproductive processes in the animal.