膽囊收縮素
膽囊收縮素(英語:cholecystokinin,簡稱CCK或CCK-PZ)是一种脑肠肽,主要功能是促进脂肪和蛋白质的消化。其名称源自希腊语,包含chole(胆汁)、cysto(囊状)和kinin(移动)三个部分,整体意为“移动胆汁之囊”。它不仅在消化系统中广泛存在,还在中枢及外周神经系统中发挥作用[5]。
膽囊收縮素在此之前名為促胰酶素(pancreozymin),是由小腸的黏膜上皮細胞當中的I細胞所合成,並由十二指腸分泌。当胆囊收缩素被分泌出来后,会刺激胰脏和胆囊分别释放消化酶和胆汁,以帮助消化过程。
除了在消化过程中发挥作用,胆囊收缩素还是一种食欲抑制剂。当胆囊收缩素在体内水平升高时,可以抑制食欲,帮助控制食物的摄入量。最近的證據暗示,膽囊收縮素在促進鴉片類藥物的藥物容許量,如嗎啡和海洛因,扮演著重要角色,並且在經歷鴉片類藥物停藥後的疼痛過敏經歷有著部份的關聯性[6][7]。
膽囊收縮素基因最早在狗(Canis lupus familiaris)的胃肠道中被发现[8],随后在人类(Homo sapiens)、小鼠(Mus musculus)、虹鳟(Oncorhynchus mykiss)、大西洋鲑(Salmo salar)和团头鲂(Megalobrama amblycephala)等多个物种中也有发现[5]。研究表明,不同动物中的膽囊收縮素存在两种甚至三种不同的亚型,并且它们的功能存在差异[5]。例如,在虹鳟中存在CCK-L、CCK-N和CCK-T三种膽囊收縮素亚型,其中CCK-L亚型作为饱腹因子调节摄食,而CCK-N亚型则无显著作用[9]。在红鲷(Pagrus major)中发现CCK基因存在CCK1和CCK2亚型,其中CCK1亚型在消化过程中发挥重要作用,CCK2亚型则通过向脑发送信号调节食物摄入和控制饱腹感[10]。而在白鲷(Diplodus sargus)中,CCK1基因的表达水平不受摄食影响,CCK2基因则参与消化过程的负反馈调节[11]。
膽囊收縮素基因通过与胆囊收缩素受体基因(Cholecystokinin receptor,简称CCKR)相结合,调节动物的摄食、消化等生理过程[12]。在多数动物中,CCKR基因存在CCK1R和CCK2R两种亚型[13]。研究显示,CCK与CCK1R基因结合主要影响消化系统,而CCK与CCK2R基因结合则主要影响中枢神经系统,二者共同参与摄食活动的调节过程[14]。
參考文獻
[编辑]- ^ 1.0 1.1 1.2 GRCh38: Ensembl release 89: ENSG00000187094 - Ensembl, May 2017
- ^ 2.0 2.1 2.2 GRCm38: Ensembl release 89: ENSMUSG00000032532 - Ensembl, May 2017
- ^ Human PubMed Reference:. National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ Mouse PubMed Reference:. National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ 5.0 5.1 5.2 禁食和复投喂对大口黑鲈胆囊收缩素及其受体基因表达的影响. 水生生物学报. 2023-08-15, 47 (8): 1220–1227. doi:10.7541/2023.2022.0175.
- ^ Kissin I, Bright CA, Bradley EL. Acute tolerance to continuously infused alfentanil: the role of cholecystokinin and N-methyl-D-aspartate-nitric oxide systems. Anesth. Analg. 2000, 91 (1): 110–6 [2013-12-02]. PMID 10866896. doi:10.1097/00000539-200007000-00021. (原始内容存档于2007-12-06).
- ^ Fukazawa Y, Maeda T, Kiguchi N, Tohya K, Kimura M, Kishioka S. Activation of spinal cholecystokinin and neurokinin-1 receptors is associated with the attenuation of intrathecal morphine analgesia following electroacupuncture stimulation in rats. J. Pharmacol. Sci. 2007, 104 (2): 159–66. PMID 17558184. doi:10.1254/jphs.FP0070475.
- ^ Ivy, A. C.; Oldberg, E. Contraction and Evacuation of Gall-Bladder Caused by Highly Purified "Secretin" Preparation.. Experimental Biology and Medicine. 1927-11-01, 25 (2): 113–115. doi:10.3181/00379727-25-3724.
- ^ Jensen, H; Rourke, IJ; Møller, M; Jønson, L; Johnsen, AH. Identification and distribution of CCK-related peptides and mRNAs in the rainbow trout, Oncorhynchus mykiss.. Biochimica et biophysica acta. 2001-01-26, 1517 (2): 190–201. PMID 11342099. doi:10.1016/s0167-4781(00)00263-3.
- ^ Huong, Tran Thi Mai; Murashita, Koji; Senzui, Ayaka; Matsumoto, Toshiro; Fukada, Haruhisa. Cholecystokinin 1 and 2 in red seabream Pagrus major: molecular cloning, response to feeding, and a potential indicator of dietary protein source quality. Fisheries Science. 2020-09, 86 (5): 835–849. doi:10.1007/s12562-020-01443-z.
- ^ Micale, V; Campo, S; D'Ascola, A; Guerrera, MC; Levanti, MB; Germanà, A; Muglia, U. Cholecystokinin in white sea bream: molecular cloning, regional expression, and immunohistochemical localization in the gut after feeding and fasting.. PloS one. 2012, 7 (12): e52428. PMID 23285038. doi:10.1371/journal.pone.0052428.
- ^ Yu, N; Smagghe, G. CCK(-like) and receptors: structure and phylogeny in a comparative perspective.. General and comparative endocrinology. 2014-12-01, 209: 74–81. PMID 24842717. doi:10.1016/j.ygcen.2014.05.003.
- ^ Dufresne, M; Seva, C; Fourmy, D. Cholecystokinin and gastrin receptors.. Physiological reviews. 2006-07, 86 (3): 805–47. PMID 16816139. doi:10.1152/physrev.00014.2005.
- ^ Balaskó, M.; Rostás, I.; Füredi, N.; Mikó, A.; Tenk, J.; Cséplő, P.; Koncsecskó-Gáspár, M.; Soós, S.; Székely, M.; Pétervári, E. Age and nutritional state influence the effects of cholecystokinin on energy balance. Experimental Gerontology. 2013-11, 48 (11): 1180–1188. doi:10.1016/j.exger.2013.07.006.