Ca(2+)-Permeable Channels/Ca(2+) Signaling in the Regulation of Ileal Na(+)/Gln Co-Transport in Mice.
Ca(2+)-Permeable Channels/Ca(2+) Signaling in the Regulation of Ileal Na(+)/Gln Co-Transport in Mice.
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Ca2 通透通道/Ca2 信号传导在小鼠回肠 Na/Gln 协同转运调节中的作用
DOI:
10.3389/fphar.2022.816133
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发表时间:
2022
影响因子:
5.6
通讯作者:
Lü M
中科院分区:
文献类型:
--
作者:
Chu F;Wan H;Xiao W;Dong H;Lü M
Oral glutamine (Gln) has been widely used in gastrointestinal (GI) clinical practice, but it is unclear if Ca2+ regulates intestinal Gln transport, although both of them are essential nutrients for mammals. Chambers were used to determine Gln (25 mM)-induced I sc 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 I sc , especially in the distal ileum. Lowering luminal Na+ almost abolished the Gln-induced ileal I sc , in which the calcium-sensitive receptor (CaSR) activation were not involved. Ca2+ removal from both luminal and serosal sides of the ileum significantly reduced Gln- I sc . Blocking either luminal Ca2+ entry via the voltage-gated calcium channels (VGCC) or endoplasmic reticulum (ER) release via inositol 1,4,5-triphosphate receptor (IP3R) and ryanodine receptor (RyR) attenuated the Gln-induced ileal I sc , Likewise, blocking serosal Ca2+ entry via the store-operated Ca2+ entry (SOCE), TRPV1/2 channels, and Na+/Ca2+ exchangers (NCX) attenuated the Gln-induced ileal I sc . In contrast, activating TRPV1/2 channels enhanced the Gln-induced ileal I sc . We concluded that Ca2+ signaling is critical for intestinal Gln transport, and multiple plasma membrane Ca2+-permeable channels and transporters play roles in this process. The Ca2+ regulation of ileal Na+/Gln transport expands our understanding of intestinal nutrient uptake and may be significant in GI health and disease.
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影响因子:
3.3
作者:
Chen S;Xia Y;Zhu G;Yan J;Tan C;Deng B;Deng J;Yin Y;Ren W
通讯作者:
Ren W
影响因子:
1.2
作者:
Hempstock, Wendy;Ishizuka, Noriko;Hayashi, Hisaysohi
通讯作者:
Hayashi, Hisaysohi
影响因子:
3.5
作者:
Liu, Gang;Ren, Wenkai;Yin, Yulong
通讯作者:
Yin, Yulong
影响因子:
5.6
作者:
Javed K;Cheng Q;Carroll AJ;Truong TT;Bröer S
通讯作者:
Bröer S
DOI:
10.1016/j.cbpa.2017.07.006
发表时间:
2017-10-01
影响因子:
2.3
作者:
Moines, Luciana;Diaz de Barboza, Gabriela;Tolosa de Talamoni, Nori
通讯作者:
Tolosa de Talamoni, Nori