Role of Calcium Channels in Glucose Uptake Regulation in the In Vitro Model of Polarized Intestinal Epithelium

Abstract

Glucose is the main energy substrate that ensures metabolic processes in the human and animal bodies. Impaired carbohydrate metabolism is often associated with obesity and concomitant diseases, such as cardiovascular diseases, arterial hypertension, insulin resistance, etc. Current data indicate that intestinal glucose absorption is coupled with Ca²⁺ influx, but additional research is needed to confirm this interaction. We used a cellular model of human intestinal epithelium to elucidate the role of Ca²⁺ channels in the regulation of glucose absorption. The results of immunofluorescence and immunoelectron microscopy showed that high cellular glucose loading (50 mM) leads to an increase in the density of TRPV6 calcium channels on the apical membrane of the intestinal epithelium. The level of the calcium sensor STIM1, responsible for store-dependent calcium entry (SOCE), on the contrary, showed a decrease when Caco-2 cells were overloaded with glucose, which was accompanied by a decrease in SOCE. Excessive saturation of Caco-2 cells with glucose also led to a decrease in the expression level of the NF-κB transcription factor p65 subunit responsible for the expression of STIM1. The results showed that Ca²⁺ channels are not only involved in the regulation of glucose uptake, but may themselves be under the control of glucose.