Chu Fenglan, Wan Hanxing, Xiao Weidong, Dong Hui, Lü Muhan
Department of Gastroenterology, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Department of Gastroenterology, Xinqiao Hospital, Army Medical University, Chongqing, China.
Front Pharmacol. 2022 Feb 23;13:816133. doi: 10.3389/fphar.2022.816133. eCollection 2022.
Oral glutamine (Gln) has been widely used in gastrointestinal (GI) clinical practice, but it is unclear if Ca regulates intestinal Gln transport, although both of them are essential nutrients for mammals. Chambers were used to determine Gln (25 mM)-induced through Na/Gln co-transporters in the small intestine in the absence or the presence of selective activators or blockers of ion channels and transporters. Luminal but not serosal application of Gln induced marked intestinal , especially in the distal ileum. Lowering luminal Na almost abolished the Gln-induced ileal , in which the calcium-sensitive receptor (CaSR) activation were not involved. Ca removal from both luminal and serosal sides of the ileum significantly reduced Gln- . Blocking either luminal Ca entry the voltage-gated calcium channels (VGCC) or endoplasmic reticulum (ER) release inositol 1,4,5-triphosphate receptor (IPR) and ryanodine receptor (RyR) attenuated the Gln-induced ileal , Likewise, blocking serosal Ca entry the store-operated Ca entry (SOCE), TRPV1/2 channels, and Na/Ca exchangers (NCX) attenuated the Gln-induced ileal . In contrast, activating TRPV1/2 channels enhanced the Gln-induced ileal . We concluded that Ca signaling is critical for intestinal Gln transport, and multiple plasma membrane Ca-permeable channels and transporters play roles in this process. The Ca regulation of ileal Na/Gln transport expands our understanding of intestinal nutrient uptake and may be significant in GI health and disease.
口服谷氨酰胺（Gln）已在胃肠道临床实践中广泛应用，但尽管二者都是哺乳动物的必需营养素，钙是否调节肠道谷氨酰胺转运尚不清楚。采用小室来测定在不存在或存在离子通道和转运体的选择性激活剂或阻滞剂的情况下，谷氨酰胺（25 mM）通过小肠中的钠/谷氨酰胺共转运体诱导的[具体指标未给出]。向肠腔而非浆膜施加谷氨酰胺可诱导显著的肠道[具体指标未给出]，尤其是在回肠末端。降低肠腔钠几乎消除了谷氨酰胺诱导的回肠[具体指标未给出]，其中不涉及钙敏感受体（CaSR）激活。从回肠的肠腔和浆膜两侧去除钙显著降低了谷氨酰胺诱导的[具体指标未给出]。阻断通过电压门控钙通道（VGCC）的肠腔钙内流或通过肌醇1,4,5 - 三磷酸受体（IPR）和兰尼碱受体（RyR）的内质网（ER）钙释放减弱了谷氨酰胺诱导的回肠[具体指标未给出]。同样，阻断通过储存 - 操作性钙内流（SOCE）、瞬时受体电位香草酸亚型1/2（TRPV1/2）通道和钠/钙交换体（NCX）的浆膜钙内流也减弱了谷氨酰胺诱导的回肠[具体指标未给出]。相反，激活TRPV1/2通道增强了谷氨酰胺诱导的回肠[具体指标未给出]。我们得出结论，钙信号传导对肠道谷氨酰胺转运至关重要，多个质膜钙通透通道和转运体在此过程中发挥作用。回肠钠/谷氨酰胺转运的钙调节扩展了我们对肠道营养物质摄取的理解，可能对胃肠道健康和疾病具有重要意义。
