2 research outputs found
Gut microbiota is an endocrine organ
The gut microbiota affects the processes of food digestion, intestinal peristalsis, controls the work of the intestinal epithelium, has protective properties against pathogenic microorganisms, activating local immunity and stimulating the secretion of mucus by intestinal cells. Besides the gut microbiota participates in the metabolism of proteins, fats and carbohydrates, mediates the processes of gluconeogenesis, glycogenolysis, lipogenesis and lipolysis, and affects on feelings of hunger and satiety. All these processes occur because the gut microbiota produces active metabolites throughout their life activity. Gut microbiota and active metabolites of the gut microbiota activate the synthesis of hormones. The gut microbiota affects the synthesis of hormones such as glucagon-like peptide-1, glucagon-like peptide-2, YY-peptide, glucose-dependent insu-linotropic peptide, ghrelin, leptin, cholecystokinin, serotonin, and insulin. Disturbance of the secretion of these hormones is one of the links in the pathogenesis of endocrine diseases such as diabetes and obesity. Thus, the gut microbiota is an endocrine organ. Changes in the composition and functions of the gut microbiota lead to metabolic disorders.This article describes the effect of gut germs and active metabolites of the gut microbiota on the synthesis hormones by means of receptor mechanisms, genes, and enzymes
A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand
The mutational spectrum of the mitochondrial DNA (mtDNA) does not resemble any of the known mutational signatures of the nuclear genome and variation in mtDNA mutational spectra between different organisms is still incomprehensible. Since mitochondria are responsible for aerobic respiration, it is expected that mtDNA mutational spectrum is affected by oxidative damage. Assuming that oxidative damage increases with age, we analyse mtDNA mutagenesis of different species in regards to their generation length. Analysing, (i) dozens of thousands of somatic mtDNA mutations in samples of different ages (ii) 70053 polymorphic synonymous mtDNA substitutions reconstructed in 424 mammalian species with different generation lengths and (iii) synonymous nucleotide content of 650 complete mitochondrial genomes of mammalian species we observed that the frequency of A(H) > G(H) substitutions (H: heavy strand notation) is twice bigger in species with high versus low generation length making their mtDNA more A(H) poor and G(H) rich. Considering that A(H) > G(H) substitutions are also sensitive to the time spent single-stranded (TSSS) during asynchronous mtDNA replication we demonstrated that A(H) > G(H) substitution rate is a function of both species-specific generation length and position-specific TSSS. We propose that A(H) > G(H) is a mitochondria-specific signature of oxidative damage associated with both aging and TSSS