Effects of gut microbiota–derived extracellular vesicles on obesity and diabetes and their potential modulation through diet

Abstract

Obesity and diabetes incidence rates are increasing dramatically, reaching pandemic proportions. Therefore, there is an urgent need to unravel the mechanisms underlying their pathophysiology. Of particular interest is the close interconnection between gut microbiota dysbiosis and obesity and diabetes progression. Hence, microbiota manipulation through diet has been postulated as a promising therapeutic target. In this regard, secretion of gut microbiota–derived extracellular vesicles is gaining special attention, standing out as key factors that could mediate gut microbiota-host communication. Extracellular vesicles (EVs) derived from gut microbiota and probiotic bacteria allow to encapsulate a wide range of bioactive molecules (such as/or including proteins and nucleic acids) that could travel short and long distances to modulate important biological functions with the overall impact on the host health. EV-derived from specific bacteria induce differential physiological responses. For example, a high-fat diet–induced increase of the proteobacterium Pseudomonas panacis–derived EV is closely associated with the progression of metabolic dysfunction in mice. In contrast, Akkermansia muciniphila EV are linked with the alleviation of high-fat diet–induced obesity and diabetes in mice. Here, we review the newest pieces of evidence concerning the potential role of gut microbiota and probiotic-derived EV on obesity and diabetes onset, progression, and management, through the modulation of inflammation, metabolism, and gut permeability. In addition, we discuss the role of certain dietary patterns on gut microbiota–derived EV profile and the clinical implication that dietary habits could have on metabolic diseases progression through the shaping of gut microbiota–derived EV.

A thousand metagenome-assembled genomes of Akkermansia reveal phylogroups and geographical and functional variations in the human gut

“…Lv et al 10.3389/fcimb.2022.957439 In recent years, the geographic deviation among different subspecies has been described in several gut bacteria such as Prevotella copri (Tett et al, 2019) and Eubacterium rectale (Karcher et al, 2020). These findings suggested that not only the geographical factor but also other unknown factors (e.g., diet difference between populations (Cheng et al, 2021;Dıéz-Sainz et al, 2022), or movement of individuals) are probably the forces for speciation of the gut bacteria. Similarly, except for Amuc III, Amuc I, II, and IV were observed in the gut microbiota of American children in the study of Kirmiz et al (2020).…”

A Predictive Model Based on the Gut Microbiota Improves the Diagnostic Effect in Patients With Cholangiocarcinoma

“…Previous studies suggested that gut microbiota was associated with body weight ( Cuevas-Sierra et al., 2019 ), and obesity might be a risk factor for CCA progression and postoperative recurrence ( Merath et al., 2019 ; Zhou et al., 2020 ; Yugawa et al., 2021 ). There was evidence concerning the potential role of gut microbiota and probiotic-derived extracellular vesicles (EVs) on obesity via the modulation of inflammation, metabolism, and gut permeability ( Díez-Sainz et al., 2021 ). Although the clinical variables for CCA development were not included in our model, it was striking that genera Burkholderia-Caballeronia-Paraburkholderia were positively correlated with BMI, and biomarker genera had a higher abundance in individuals with BMI ≥23.01.…”

Exploring New Drug Targets for Type 2 Diabetes: Success, Challenges and Opportunities

“…In addition, it was found that gut microbiota participates in drug metabolism by producing specific enzymes, such as reductase and hydrolytic enzymes, thus affecting the efficacy, toxicity, and bioavailability of drugs. Various antibiotics also alter the diversity and composition of gut microbiota which leads to dysbiosis, and it was found to be linked with progression of various neurodegenerative as well as metabolic disorders [ 73 , 74 , 75 ].…”