膽囊收縮素
膽囊收縮素(英語:cholecystokinin,簡稱CCK或CCK-PZ)是一種腦腸肽,主要功能是促進脂肪和蛋白質的消化。其名稱源自希臘語,包含chole(膽汁)、cysto(囊狀)和kinin(移動)三個部分,整體意為「移動膽汁之囊」。它不僅在消化系統中廣泛存在,還在中樞及外周神經系統中發揮作用[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。當膽囊收縮素被分泌出來後,會刺激胰臟和膽囊分別釋放消化酶和膽汁,以幫助消化過程。
除了在消化過程中發揮作用,膽囊收縮素還是一種食慾抑制劑。當膽囊收縮素在體內水平升高時,可以抑制食慾,幫助控制食物的攝入量。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,如嗎啡和海洛英,扮演着重要角色,並且在經歷鴉片類藥物停藥後的疼痛過敏經歷有着部份的關聯性[6][7]。
膽囊收縮素基因最早在狗(Canis lupus familiaris)的胃腸道中被發現[8],隨後在人類(Homo sapiens)、小鼠(Mus musculus)、虹鱒(Oncorhynchus mykiss)、大西洋鮭(Salmo salar)和團頭魴(Megalobrama amblycephala)等多個物種中也有發現[5]。研究表明,不同動物中的膽囊收縮素存在兩種甚至三種不同的亞型,並且它們的功能存在差異[5]。例如,在虹鱒中存在CCK-L、CCK-N和CCK-T三種膽囊收縮素亞型,其中CCK-L亞型作為飽腹因子調節攝食,而CCK-N亞型則無顯著作用[9]。在紅鯛(Pagrus major)中發現CCK基因存在CCK1和CCK2亞型,其中CCK1亞型在消化過程中發揮重要作用,CCK2亞型則通過向腦發送信號調節食物攝入和控制飽腹感[10]。而在白鯛(Diplodus sargus)中,CCK1基因的表達水平不受攝食影響,CCK2基因則參與消化過程的負反饋調節[11]。
膽囊收縮素基因通過與膽囊收縮素受體基因(Cholecystokinin receptor,簡稱CCKR)相結合,調節動物的攝食、消化等生理過程[12]。在多數動物中,CCKR基因存在CCK1R和CCK2R兩種亞型[13]。研究顯示,CCK與CCK1R基因結合主要影響消化系統,而CCK與CCK2R基因結合則主要影響中樞神經系統,二者共同參與攝食活動的調節過程[14]。
參考文獻
- ^ 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. 水生生物學報. 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. (原始內容存檔於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.