Potential Mechanisms of Gut-Derived Extracellular Vesicle Participation in Glucose and Lipid Homeostasis

Abstract

The intestine participates in the regulation of glucose and lipid metabolism in multiple facets. It is the major site of nutrient digestion and absorption, provides the interface as well as docking locus for gut microbiota, and harbors hormone-producing cells scattered throughout the gut epithelium. Intestinal extracellular vesicles are known to influence the local immune response, whereas their roles in glucose and lipid homeostasis have barely been explored. Hence, this current review summarizes the latest knowledge of cargo substances detected in intestinal extracellular vesicles, and connects these molecules with the fine-tuning regulation of glucose and lipid metabolism in liver, muscle, pancreas, and adipose tissue.

Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons

“…EVs originating from specific bacterial strains, or those engineered to carry beneficial microbiota-derived molecules, might be capable of modifying the gut microbiota. Such alterations could potentially improve nutrient absorption and overall metabolism in CC patients [ 246 ].…”

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

“…Mechanistically, the high concentration of glucose in the intestinal lumen of the small intestine first upregulates SGLT1 expression to maintain the overall physiological needs of the organism. Furthermore, a high rate of SGLT1 transport depolarizes the BBM and further activates Ca 2+ uptake [ 37 , 38 ]. Consequently, elevated intracellular Ca 2+ concentration activates the PKC pathway to mediate myosin II phosphorylation [ 39 , 40 ].…”

A case for the study of native extracellular vesicles

“…A key mode of communication between cells involves extracellular vesicles (EVs), which incorporate donor cell-derived signals (both membrane-bound and intracellular) that are delivered to acceptor/recipient cells ( 1 ). This process profoundly affects key biological activities, including transfer of processed antigen from activated B cells to follicular dendritic cells in the lymph nodes ( 2 ), glucose and lipid metabolism via gut-liver communication ( 3 ), synaptic activity and plasticity between neurons and glia ( 4 , 5 ) and at the feto-maternal interface ( 6 ). Consequently, alteration or amplification of EV-mediated intercellular communications foster pathophysiological processes ( 7 ).…”