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L- cells is the name for intermediate large vesicles.
The identifying hormone (historically) is
Examples of colocalization of hormones and/or their gene transcripts (most of recent data is from mouse):
Limited analyses of human intestinal samples have also suggested the expression of G-Protein Coupled Receptor 43 (GPR43) and G-Protein Coupled Receptor 41 (GPR41) in the L cell population. L cells are mainly localized in the distal ileum and colon, where the microbiota is exposed to fiber. Overall, these studies have demonstrated G-Protein Coupled Receptor 43 (GPR43)- and G-Protein Coupled Receptor 41 (GPR41)-dependent effects of acetate and propionate to stimulate Glucagon Like Peptide 1 (GLP-1) release, suggesting, but not proving, a direct link to improved glucose metabolism through the incretin effects of this hormone.
Therefore, most studies have focused on the direct effects of SCFAs on the secretion of GLP-1, a physiological enhancer of insulin secretion following nutrient intake.
Indole, a metabolite produced from the dissimilation of tryptophan, is able to modulate the secretion of glucagon-like peptide-1 (GLP-1) from immortalized and primary mouse colonic L cells. Indole increased GLP-1 release during short exposures, but it reduced secretion over longer periods. These effects were attributed to the ability of indole to affect two key molecular mechanisms in L cells. On the one hand, indole inhibited Voltage-gated potassium channel, increased the temporal width of action potentials fired by L cells, and led to enhanced Ca 2+ entry, thereby acutely stimulating GLP-1 secretion. On the other hand, indole slowed ATP production by blocking NADH dehydrogenase, thus leading to a prolonged reduction of GLP-1 secretion.
Activation of FFAR 2 or GPR 41 leads to L-cells' PYY and GLP 1 secretion, which affect several tissues, including the cardiovascular system, the pancreas, and the brain
A previous study has shown that GLP-2 secretion from the L cell is increased by feeding a prebiotic to obese (ob/ob) mice, leading to the well-known effects of GLP-2, which is the function to improve the intestinal barrier and thereby reduce the parameters of metabolic inflammation.
They stimulate the carbohydrate uptake, slow down the intestinal transit, regulate appetite and insulin release