Key Signals Produced by Gut Microbiota Associated with Metabolic Syndrome, Cancer, Cardiovascular Diseases, and Brain Functions

肠道菌群产生的关键信号与代谢综合征、癌症、心血管疾病和脑功能相关

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Abstract

Gut microbiota have a significant impact neurotransmitters, short-chain fatty acids (SCFAs), immune signaling molecules, and gut hormones. These signaling molecules interact with receptors on the gut wall, immune cells, or the enteric nervous system (ENS), and reach the central nervous system (CNS) via the Vagus nerve (VN). SCFAs interact with G protein-coupled receptors (GPCRs), Toll-like receptors (TLRs), and proliferator-activated receptors (PPARs), influencing inflammatory reactions, gut motility, nutrient absorption, hormone secretion, neurochemical signaling, and brain functions. Olfactory receptor OR51E1 influences blood pressure, vascular reactivity, and arterial stiffness. Activation of the brainstem nucleus tractus solitarius (NTS) by glucagon-like peptide 1 (GLP-1) influences mood, cognition, and gastrointestinal motility. Prolactin-releasing peptide (PrRP) binds to its receptor (PrRPR), suppressing food intake, and regulating stress, cardiovascular reactions, and circadian rhythms. In-depth studies on how gut microbiota control cognitive behavior, mood, and neuropsychiatric disorders are lacking. G protein receptor 119 (GPR119) suppresses appetite and may find an application in the treatment of type 2 diabetes and obesity. The binding of butyrate to nuclear factor kappa B (NF-κB) and proliferator-activated receptor γ (PPARγ) regulates the production of pro-and anti-inflammatory cytokines. This suppresses protein CD36, preventing the uptake of oxidized low-density lipoprotein (ox-LDL) and cardiovascular diseases (CVDs). This review focuses on a few prominent health conditions related to CVDs, i.e., metabolic syndrome (MetS), cancer, and brain functions. Information in this review is based on animal and preclinical studies published in repositories such as PubMed, the National Institutes of Health (NIH), NIH PubChem, ScienceDirect, MDPI, Frontiers, Cell Press, and the CAS Content Collection.

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