“…Colesevelam hydrochloride (HCl) is a polyallylamine that has been crosslinked with epichlorohydrin and alkylated with (6-bromohexyl)-trimethylammonium bromide and 1-bromodecane[ 66 ]. In clinical and animal studies on T2DM, obesity, and hyperlipidemia, colesevelam reduced blood glucose[ 67 ], FBG[ 68 ], mediator complex subunit 1, miR-182[ 69 ], HbA1c[ 70 ], hepatic TG, total LDL[ 71 ], very-low-density lipoprotein (VLDL), chylomicron particle[ 72 ], LDL-C[ 73 ], non-HDL-C, ApoB, TGR5/GLP-1-dependent glycogenolysis, FXR-dependent cholesterol, cytochrome P450, Cyp7a1[ 74 ], FGF-19[ 75 ], BA reabsorption[ 76 ], high-sensitivity C-reactive protein[ 77 ], and fructosamine levels[ 78 - 80 ] and increased glycolysis, postmeal glucose tolerance, insulin levels[ 81 ], splanchnic sequestration of meal-derived glucose[ 82 ], GLP-1/GIP levels[ 83 ], total HDL particle levels, miR-96/182/183 expression levels, β-cell function [as revealed by homeostatic model assessment (HOMA)][ 56 ], BA synthesis, ApoA-1 levels[ 54 ], and CCK levels[ 84 ]. As a molecularly engineered, second-generation BA sequestrant, colesevelam has been recommended for reducing LDL-C in patients with primary hypercholesterolemia by inhibiting b-hydroxymethylglutaryl coenzyme A reductase[ 85 ].…”