The mechanism the ensure complete absorption of glucose from the intestinal lumen
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Answer:
glucolosis and kreb cycle
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Explanation:
Mechanisms of Glucose Absorption in the Intestine
Complex carbohydrates reaching the small intestine must be hydrolyzed to monosaccharides such as glucose or galactose in order to be transported across the intestinal mucosa. The classical pathway of glucose absorption is across the intestinal brush-border membrane (BBM), which was predominantly mediated by SGLT1, a membrane protein that couples two molecules of Na+ together with one molecule of glucose. The passive move out of the basolateral surface of enterocytes contains a facilitated-diffusion glucose transporter (GLUT2) which allows glucose to move from the IEC into the extracellular medium near the blood capillaries [15] (Figure 1). The absorption of glucose may be adjusted by other transporters, such as GLUT2 [16,17,18]. Translocation of GLUT2 from cytoplasmic vesicles into the apical membrane markedly increases the capacity of glucose uptake by the enterocyte [19,20,21]. Thus, any factor that influences the activities of SGLT1 and GLUT2 will also alter the absorption and metabolism of glucose.
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Figure 1
Absorption of digested food (glucose) from the intestinal lumen into the blood, and transportation of the absorbed nutrients via mesenteric circulation to target cells.
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3. Detection Methods of Glucose Absorption in Vitro
At present, glucose absorption can be studied by two methods in vitro and in vivo. In vitro methods include tissue and cell experiments: (1) The Ussing chamber experiment uses intestinal tissues. Schultz and Zalusky were the first to use the short-circuit current to examine the electrical properties of rabbit ileum [22,23]. Specifically, they demonstrated via electrophysiological and radioisotopic experiments that the addition of glucose to the mucosal solutions resulted in a rapid increase in the transmural potential difference [24]. So this glucose-induced change in short-circuit currents was regarded as rates of glucose and Na+ transports across the epithelium; (2) Then there is the application of the isotope tracer method in intestinal tissue and IEC. d-(6-3H) Glucose or 14C glucose is used as the tracer to detect glucose absorption into intestinal tissue or IEC [25]; (3) To examine glucose absorption into a cell, glucose is absorbed into a cultural cell after glucose is added to the cell culture medium for a period of time, and the medium is then taken out for determining the concentrations of glucose by the hexokinase method or the glucose oxidizes/peroxides (GOD-POD) method [26].
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4. Regulation of Glucose Absorption by Potassium Channels
4.1. Potassium Channels in Small Intestinal Epithelial Cells
The concentration of K+ inside the cell is roughly 20-fold larger than the outside. K+ channels function to conduct potassium ions down their electrochemical gradient to maintain ion equilibrium, and provide electrochemical driving force to maintain cell function [27,28,29]. K+ channels represent the largest and most heterogeneous family of ion channels and membrane proteins. They are widely expressed in both excitable and non-excitable cells [27,30,31]. In epithelial cells, K+ channels are expressed in a polarized fashion and serve two principal functions for transepithelial transports: the generation of membrane potential and the recycling of K+ [32]. As in duodenal epithelial cells, an intermediate-conductance Ca2+-activated K+ channel (IKCa) can provide a driving force for duodenal bicarbonate secretion [33]. On the intestinal mucosa surface, intermediate conductance K+ channels (KCNN4) can provide a driving force for Cl− secretion via both cystic fibrosis transmembrane conductance regulator(CFTR ) and Ca2+-activated Cl− channels (CaCC) that are mediated by cAMP and Ca2+ [34]. K+ channels also regulate cell volume in isosmotic conditions in small intestinal epithelial cells [35]. Therefore, K+ channels may be involved in various physiological processes of small intestinal epithelial cells. Especially, we deal with the regulatory mechanism of glucose absorption by K+ channels.
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