The review is devoted to the systematization, classification, and generalization of the results of modern scientific research on the role of bile acids as a new class of steroid hormones. The paper presents the evidence for bile acid participation in the regulation of the body energy metabolism, body weight control, as well as the pathogenesis of obesity, diabetes mellitus, insulin resistance, and cardiovascular diseases.
Particular attention is paid to the role of bile acids in the control of nonspecific energy expenditure of the body. The applied aspects of using the novel data about the membrane and intracellular receptors responsible for the development of hormonal regulatory effects of bile acids are analyzed. According to the authors, the modern data on the role of bile acids in the regulation of body functions allow a deeper understanding of the pathogenesis of body weight disorders and associated cardiovascular diseases. The review demonstrates promising directions in the search for specific methods of prevention and correction of these pathological conditions.
This review presents the analysis and systematization of modern data on the molecular mechanisms of autism spectrum disorders (ASD) development. Polyetiology and the multifactorial nature of ASD have been proved. The attempt has been made to jointly review and systematize current hypotheses of ASD pathogenesis at the molecular level from the standpoint of aberrant brain plasticity. The mechanism of glutamate excitotoxicity formation, the effect of imbalance of neuroactive amino acids and their derivatives, neurotransmitters, and hormones on the ASD formation have been considered in detail. The strengths and weaknesses of the proposed hypotheses have been analyzed from the standpoint of evidence-based medicine. The conclusion has been drawn on the leading role of glutamate excitotoxicity as a biochemical mechanism of aberrant neuroplasticity accompanied by oxidative stress and mitochondrial dysfunction. The mechanism of aberrant neuroplasticity has also been traced at the critical moments of the nervous system development taking into account the influence of various factors of the internal and external environment. New approaches to searching for ASD molecular markers have been considered.
The course of preventive oral treatment with a dihydroquercetin-chitosan composition produced a strong antihypoxic effect under conditions of experimental hypobaric hypoxia (arbitrary altitude 12,000 m). The lactate/pyruvate ratio in composition-receiving rats was much lower than in hypoxic animals (by 83%), but higher than in intact specimens (by 29%). The composition of chitosan and dihydroquercetin also possessed a strong antioxidant activity.
We showed that mitochondrial creatine kinase activity can be predicted from the ATP level and that changes in ATP content can be evaluated by activity of mitochondrial creatine kinase under experimental conditions.
MicroRNAs (miRNAs) are short, 22-25 nucleotide long transcripts that may suppress entire signaling pathways by interacting with the 3'-untranslated region (3'-UTR) of coding mRNA targets, interrupting translation and inducing degradation of these targets. The long 3'-UTRs of brain transcripts compared to other tissues predict important roles for brain miRNAs. Supporting this notion, we found that brain miRNAs co-evolved with their target transcripts, that non-coding pseudogenes with miRNA recognition elements compete with brain coding mRNAs on their miRNA interactions, and that Single Nucleotide Polymorphisms (SNPs) on such pseudogenes are enriched in mental diseases including autism and schizophrenia, but not Alzheimer's disease (AD). Focusing on evolutionarily conserved and primate-specifi c miRNA controllers of cholinergic signaling ('CholinomiRs'), we fi nd modifi ed CholinomiR levels in the brain and/or nucleated blood cells of patients with AD and Parkinson's disease, with treatment-related diff erences in their levels and prominent impact on the cognitive and anti-infl ammatory consequences of cholinergic signals. Examples include the acetylcholinesterase (AChE)-targeted evolutionarily conserved miR-132, whose levels decline drastically in the AD brain. Furthermore, we found that interruption of AChE mRNA's interaction with the primatespecifi c CholinomiR-608 in carriers of a SNP in the AChE's miR-608 binding site induces domino-like eff ects that reduce the levels of many other miR-608 targets. Young, healthy carriers of this SNP express 40% higher brain AChE activity than others, potentially aff ecting the responsiveness to AD's anti-AChE therapeutics, and show elevated trait anxiety, infl ammation and hypertension. Non-coding regions aff ecting miRNA-target interactions in neurodegenerative brains thus merit special attention.
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