胆囊收缩素在畜禽生产中的应用

胆囊收缩素(CCK)是一种具有广泛生物学活性的脑肠肽,它存在于体内许多部位并通过受体介导多种重要的生理功能.作为一种饱感因子,CCK具有抑制动物摄食的功能.在畜禽生产上,CCK受体颉颃剂、CCK免疫及CCK抗体已有应用并取得了较好的效果.     

含CCK抗体卵黄粉和丙谷胺对生长猪生产性能、养分消化率和内分泌激素的影响

采用单因子试验设计,将30头体重(34.93±2.46)kg的DLY生长猪随机分为5个处理,研究饲粮添加不同水平丙谷胺和含CCK抗体卵黄粉对生长猪生产性能、养分消化率和内分泌激素的影响。5个处理分别为对照组(C)、C+含CCK抗体卵黄粉400mg/kg、C+含CCK抗体卵黄粉800mg/kg、C+丙谷胺500mg/kg和C+丙谷胺1000mg/kg。结果表明:添加CCK抗体卵黄粉400mg/kg组试猪全期日增重(ADG)提高11.10%(P>0.05),饲料增重比(F/G)降低8.33%(P>0.05)。丙谷胺500mg/kg组全期ADG提高6.02%(P>0.05),F/G降低7.54%(P>0.05),同时饲粮干物质、有机物和粗蛋白质的消化率显著改善(P<0.05)。添加含CCK抗体卵黄粉或丙谷胺均有降低试猪第1周末采食前后及试验结束时血清尿素氮含量的趋势。同时,添加含CCK抗体卵黄粉有降低试猪第1周末采食前后血清CCK浓度的趋势。含CCK抗体卵黄粉或丙谷胺对血清瘦素和胰岛素含量均无显著影响。     

含胆囊收缩素抗体卯黄粉对断奶仔猪生产性能及养分消化率的影响

本试验旨在研究含胆囊收缩素(CCK)抗体卵黄粉对断奶仔猪生产性能、日粮养分消化率及血清CCK浓度的影响.90头(30±2)日龄断奶约克仔猪[平均体重(7.05±0.20)kg]随机分为5个处理,分别饲喂基础日粮和基础日粮中添加100、200、300 mg/kg和400 mg/kg含CCK抗体卵黄粉的试验日粮,每个处理6个重复,每个重复3头仔猪.试验期28 d.结果表明,与基础日粮组相比,添加含CCK抗体卵黄粉可提高仔猪全期平均日增重(ADG)和平均日采食量(ADFI),降低料内比(F/G),其中200 mg/kg组ADG提高12.14%(P＞0.05),ADFI提高6.92%(P＞0.05),F/G降低4.62%(P＞0.05).同时,日粮粗蛋白质消化率随含CCK抗体卵黄粉添加量的增加呈二次曲线变化(P=0.044).添加含CCK抗体卵黄粉后,仔猪血清CCK浓度下降,200 mg/kg组降低35.6%(P＞0.05).综合来看,添加200 mg/kg 含CCK抗体卵黄粉组效果最好.     

CCK、CCKAR对动物采食量影响的研究进展

胆囊收缩素(Cholecystokinin,CCK)又称作促胰酶素,是一种能引起胆囊收缩和促进胰液中各种酶分泌的胃肠道多肽激素.CCK广泛存在于消化系统、中枢及外周神经系统对动物采食具有抑制作用.猪缩胆囊素受体(Cholecystokinin A receptor,CCKAR)在动物采食量、饱度以及肥胖方面起调节控制作用.本文综述了近些年来CCK CCKAR对动物采食量影响的研究状况.     

胆囊收缩素主动免疫产蛋鸡的营养生理效应研究

用胆囊收缩素(CCK)主动免疫产蛋鸡，研究产蛋鸡血清和卵黄中CCK特异性抗体的产生规律及不同CCK免疫剂量对产蛋鸡生产性能和胰腺、胆囊发育及内分泌激素的影响。结果显示：用CCK-8主动免疫产蛋鸡，可以提高血清和卵黄CCK抗体水平，降低血液中CCK水平；CCK抗体的产生量在第1次加强免疫后即可接近高峰，第2、第3次加强免疫可维持较高的抗体水平。CCK主动免疫产蛋鸡后，对蛋鸡胰腺、胆囊发育、胰蛋白含量以及蛋鸡体内的生长激素、胰岛素和瘦素水平均没有显著影响，同时对蛋鸡采食量和料蛋比等生产性能也没有显著影响。用CCK主动免疫产蛋鸡，在不影响蛋鸡正常生理功能的同时，可以获得含特异性CCK抗体的卵黄。     

饲粮蛋白质水平对家兔食欲肽基因表达的影响

本试验旨在探讨饲粮蛋白质水平对家兔食欲肽基因表达的影响。选择体重相近的30日龄断奶伊拉肉兔30只,随机分为3组,分别饲喂蛋白质水平为12.8%、16.0%和19.2%的试验饲粮,每组10个重复,每个重复1只兔。预试期7d,正试期35d。试验结束后,采集弓形核、十二指肠、空肠和回肠,测定弓形核中阿片促黑色素原(POMC)、可卡因-苯丙胺调节转录物(CART)、神经肽Y(NPY)、刺鼠基因相关蛋白(AgRP)、胆囊收缩素(CCK)和肠道中CCK基因的相对表达量。结果显示:十二指肠CCK基因的相对表达量显著高于空肠、回肠和弓形核(P0.05);与16.0%和12.8%蛋白质饲粮组相比,19.2%蛋白质饲粮组十二指肠中CCK基因的相对表达量显著增加(P0.05),而其回肠中CCK基因的相对表达量无显著变化(P0.05);与16.0%和12.8%蛋白质饲粮组相比,19.2%蛋白质饲粮组弓形核中POMC和CART基因的相对表达量显著增加(P0.05),而其弓形核中NPY和AgRP基因的相对表达量无显著变化(P0.05)。由此得出,饲喂低蛋白质水平(12.8%~16.0%)饲粮家兔的食欲增加与肠道和中枢中脑肠肽有关。与低蛋白质水平饲粮相比,高蛋白质水平(19.2%)饲粮显著提高十二指肠中CCK和弓形核中CART和POMC基因的相对表达量,表明这些基因形成食欲网络共同参与饲粮蛋白质调控家兔食欲的过程。此外,回肠和弓形核中CCK、弓形核中NPY和AgRP基因对饲粮中蛋白质水平变化不敏感。     

四君子汤对脾虚大鼠胃肠运动功能和胃肠激素影响

为研究四君子汤对脾虚大鼠胃肠运动和胃肠激素含量影响,用营养性半固体糊灌胃法测定大鼠胃排空率和肠推进率,采集胃窦基础电位信号,ELISA法测定胃肠组织中CCK、MTL蛋白水平。结果显示,与对照组比,脾虚组胃排空率下降,肠推进率上升,胃电振幅和频率均降低;胃窦内CCK明显升高(P0.05),十二指肠和空肠内CCK显著降低(P0.05);MTL在脾虚大鼠消化道内呈整体降低趋势,仅在空肠内极显著降低(P0.01)。与脾虚组比,治疗组胃排空率升高,肠推进率下降,胃电振幅和频率均回升;胃窦内CCK明显降低(P0.05),十二指肠和空肠内CCK显著升高(P0.05);消化道内MTL含量整体回升。由此可见,四君子汤可以平衡紊乱的胃肌电活动,调节脾虚大鼠的胃肠运动,调节消化道内局部CCK和MTL含量。     

胆囊收缩素对动物采食量的影响

胆囊收缩素(cholecystokinin,CCK)的基本生理功能是收缩胆囊和促进胰酶分泌。目前的研究表明,CCK对于动物饱感的产生和采食量的调节具有重要作用,这对于提高畜牧业的养殖效率具有重要意义。本文综述了胆囊收缩素参与动物采食量调节的效果,作用机制,影响CCK分泌的因素以及抗CCK免疫在动物养殖中的应用。     

使猪长得快的疫苗

美国一公司制出了一种能使猪吃得更多,长得快的化合物。这种化合物是一种由胆囊收缩素(CCK)片段组成的疫苗,CCK是由猪和     

胆囊收缩素主动免疫对猪生产性能及胴体品质、肉质的影响

此试验研究胆囊收缩素(CCK)主动免疫对猪生产性能及胴体品质、肉质的影响。试验结果表明,CCK主动免疫诱发高强度的免疫应答,试验组抗体滴度在第71天比对照组高67.73%,差异极显著(P<0.01);试验组猪的日增重比对照组提高21.23%,日采食量提高16.23%,料重比降低4.86%,但均差异不显著;试验猪屠宰体重比对照组增加12.68%,背膘厚、胴体长、眼肌面积与对照组差异不显著,CCK主动免疫对猪的肉色评分、大理石纹评分、pH、滴水损失以及肌肉的脂肪/蛋白质比例没有影响。结果显示,CCK主动免疫诱发试猪高强度的免疫应答,提高猪的生产性能,但不影响猪的胴体品质和肉质。     

党参和白术对脾虚北京鸭肠道CCK、VIP、SSmRNA表达的影响

采用利血平建立北京鸭脾虚模型,观察健脾益气中药党参和白术对脾虚北京鸭十二指肠和空肠CCK、VIP、SSmRNA表达的影响。结果表明:脾虚组鸭十二指肠和空肠CCK、SSmRNA表达都显著(P<0.05、P<0.01)低于正常组;党参预防组、治疗Ⅱ组以及白术治疗Ⅱ组治疗效果均显著,可使十二指肠和空肠CCK、SSmRNA表达回复到正常水平。说明党参具有预防脾虚的作用,且单独高剂量(中药浓度2g/mL)使用党参和白术能达到治疗脾虚的目的,其作用机理是通过调节胃肠激素在体内的平衡达到治疗脾虚泄泻的目的。     

四君子汤对北京鸭十二指肠、空肠CCK、VIP mRNA表达的影响

本试验探讨了四君子汤对实验性脾虚鸭十二指肠、空肠胆囊收缩素（cholecystokinin，CCK）和血管活性肠肽（vasoactive intestinal peptide，VIP）mRNA表达的调控作用。采用利血平法建立北京鸭实验性脾虚模型，用半定量RT—PCR法检测了十二指肠、空肠CCK和VIP mRNA表达的变化。结果：（1）四君子汤预防组十二指肠CCK、VIP mRNA表达极显著高于脾虚组（P〈0．01），空肠CCK、VIP mRNA显著高于脾虚组（P〈0．05），四君子汤预防组和正常对照组之间无显著差异；（2）四君子汤治疗组十二指肠CCK、VIP mRNA表达极显著高于自然恢复组（P〈0．01），空肠CCK、VIP mRNA表达显著高于自然恢复组（P〈0．05）。四君子汤对北京鸭实验性脾虚症引起的十二指肠、空肠CCK和VIP表达降低有明显的上调作用，提示四君子汤上调CCK和VIP的表达可能是其健脾助消化机理之一。     

Elevation of plasma cholecystokinin concentration following a meal is increased by gonadectomy in male cats

An overweight or obese body condition commonly develops after gonadectomy (GX) in domestic cats. The cause appears to be a rapid, quantal (approximately 12%), increase in food intake that is sustained and probably mediated by withdrawal of gonadal hormone. Recently, an interaction of gonadal hormone and cholecystokinin (CCK) effectiveness has been suggested. A reduction in the satiating potency of intestinal CCK was presently hypothesized to contribute to the disturbance of food intake control caused by GX in domestic cats. Pre- and post-prandial intestinal CCK secretion as indicated by plasma CCK concentrations were determined in 16 adult male cats (5.1 +/- 0.1 kg) 8 weeks before and 57 weeks after eight of the cats were gonadectomized. During ad libitum intake of a commercial dry, expanded diet, body weight increased from 22% to 28% in gonadectomized cats and was unchanged in intact cats. Baseline CCK concentrations were not different between gonadectomized and intact cats. Amounts of diet ingested during CCK determinations were 15-19% of daily metabolizable energy requirement and were not different between gonadectomized and intact cats. The post-prandial area under the curve (AUC; 0-400 min) CCK concentration increased linearly with meal size (p < 0.01) and was not correlated with body weight. Area under the curve CCK concentration, when normalized for meal size, was 34% greater (p < 0.01) in gonadectomized cats than that in intact cats. The findings indicate GX increases meal-induced intestinal CCK secretion and therefore, do not support the study hypothesis. The findings indicate GX may slow digestion and absorption and attenuate inhibition of food intake by CCK.     

The trophic effect of cholecystokinin on the pancreas declines in rats on total parenteral nutrition

Total parenteral nutrition (TPN) results in atrophy of the pancreas, while cholecystokinin (CCK) can significantly stimulate the exocrine pancreas in rodents. This study was designed to examine whether CCK may improve the atrophy of the pancreas in rats on TPN treatment. Forty-eight Sprague-Dawley rats were divided into orally fed and TPN groups and were infused with CCK at a dose of 5 μg/kg/h or the CCK-receptor antagonist devazepide at a dose of 200 μg/kg/h for 10 days. Infusion of CCK caused hypercholecystokininemia (hyperCCKemia) and decreased the atrophy of the pancreas resulting from TPN. The hyperplastic response to CCK in orally fed rats was decreased in the rats given TPN. Devazepide did not influence the pancreatic variables. This study further confirmed that CCK stimulates the exocrine pancreas and decreases the atrophy of the exocrine pancreas resulting from TPN. Our present findings suggest that the trophic effect of CCK on the exocrine pancreas declines in TPN.     

Sulfated cholecystokinin‐8 increases ghrelin secretion but does not affect oxyntomodulin in Holstein steers

The effect of appetite regulatory hormone cholecystokinin (CCK) on the secretions of oxyntomodulin (OXM) and ghrelin, and the effect of ghrelin on the secretions of CCK and OXM were studied in ruminants. Eight Holstein steers, 7 months old, 243 ± 7 kg body weight (BW), were arranged in an incomplete Latin square design (8 animals × 4 treatments × 4 days of sampling). Steers were intravenously injected with 10 µg of sulfated CCK‐8/kg BW, 20 µg of acyl ghrelin/kg BW, 100 µg of des‐acyl ghrelin/kg BW or vehicle. Blood samples were collected from ?60 min to 120 min relative to time of injection. Plasma concentrations of ghrelin, sulfated CCK and OXM were measured by double‐antibody radioimmunoassay. Plasma acyl ghrelin was increased to peak level (428.3 ± 6 pg/mL) at 60 min after injection of CCK compared with pre‐injected levels (203.3 ± 1 pg/mL). These results showed for the first time, that intravenous bolus injection of CCK increased ghrelin secretion in ruminants. In contrast, injection of ghrelin did not change CCK secretion. Administration of ghrelin or CCK has no effect on plasma OXM concentrations. In conclusion, our results show that administration of CCK increased ghrelin secretion but did not affect OXM release in ruminants. Ghrelin did not affect the secretions of CCK and OXM.     

Neuroendocrine regulation of growth hormone secretion in sheep. IV. Central and peripheral cholecystokinin

The result of alterations in the levels of CCK, in the blood and in the cerebrospinal fluid, on the functioning of the growth hormone axis has been examined in sheep. Male Coopworth sheep of about 40 kg liveweight were given various doses of CCK either intracerebroventricularly (icv) or intravenously (iv). Other similar sheep were given various doses of a CCK antagonist (loxiglumide) by the same routes. Bolus iv administration of either 35 μg or 200 μg of CCK had no effect on plasma GH levels. When given icv, however, CCK resulted in a marked (P<0.01) prolonged depression in plasma GH levels. The decrease in GH secretion could be partially attenuated by concurrent administration of loxiglumide, but was completely unaffected by concurrent administration of anti-somatostatin serum icv. Loxiglumide alone had no effect on plasma GH levels when given at up to 200 μg icv, but intravenous administration of 8 mg of the CCK antagonist resulted in an increase in plasma GH concentrations (P<0.05). Plasma levels of somatostatin, glucose and cortisol were unaffected by both icv and iv administration of CCK. These results show that CCK can have a strong GH-inhibiting effect in the brain. Furthermore, this effect seems to be independent of hypothalamic somatostatin, suggesting another GH-inhibiting system exists.     

Effects of cholecystokinin-receptor antagonists on Fos-like immunoreactivity stimulated by sulfated cholecystokinin-8 in neurons of the myenteric plexus and hindbrain of rats

OBJECTIVE: To evaluate the role of cholecystokinin (CCK)-receptor antagonists in the activation of enteric and hindbrain neurons by sulfated CCK-8. ANIMALS: 81 male Sprague-Dawley rats. PROCEDURE: Rats were allocated to 10 groups (5 to 22 rats/group). Each rat received 2 IP injections (15 minutes between injections). The first injection consisted of a specific CCK2-receptor (CCK2R) antagonist (L365,260; 150, 500, or 1,000 microg/kg), a specific CCK1-receptor (CCK1R) antagonist (devazepide; 150 microg/kg), or 1% dimethyl sulfoxide (DMSO [ie, vehicle]), and the second injection consisted of sulfated CCK-8 (10 microg/kg) or saline (0.9% NaCl) solution. Rats were anesthetized and perfused with 500 mL of Krebs saline solution, and the myenteric plexuses of the duodenum and jejunum were collected. Rats were then perfused with 500 mL of phosphate-buffered 4% formaldehyde solution; rats were then euthanatized, and the hindbrain of each was harvested. Tissues were stained by use of a diaminobenzidine reaction enhanced with nickel to reveal Fos-like immunoreactivity (Fos-LI), a marker of neuronal activation, in the aforementioned neurons. RESULTS: Sulfated CCK-8 significantly increased Fos-LI in the myenteric and hindbrain neurons, compared with values for the DMSO injections. All dosages of L365,260 failed to attenuate this increase; however, injection of devazepide attenuated the increase in Fos-LI. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of the results of this study reveals that sulfated CCK-8 activates myenteric and hindbrain neurons of rats primarily through CCK1 R. It provides evidence that CCK2R are lacking or not functional in the gastrointestinal tract of rats.     

Effect of feeding fat or intrajugular infusion of glucagon-like peptide-1 and cholecystokinin on dry matter intake, digestibility, and digesta rate of passage in growing wethers

A cause and effect relationship between glucagon-like peptide 1 (7, 36) amide (GLP-1) and cholecystokinin (CCK) and DMI regulation has not been established in ruminants. Three randomized complete block experiments were conducted to determine the effect of feeding fat or infusing GLP-1 or CCK intravenously on DMI, nutrient digestibility, and Cr rate of passage (using Cr(2)O(3) as a marker) in wethers. A total of 18 Targhee × Hampshire wethers (36.5 ± 2.5 kg of BW) were used, and each experiment consisted of four 21-d periods (14 d for adaptation and 7 d for infusion and sampling). Wethers allotted to the control treatments served as the controls for all 3 experiments; experiments were performed simultaneously. The basal diet was 60% concentrate and 40% forage. In Exp. 1, treatments were the control (0% added fat) and addition of 4 or 6% Ca salts of palm oil fatty acids (DM basis). Treatments in Exp. 2 and 3 were the control and 3 jugular vein infusion dosages of GLP-1 (0.052, 0.103, or 0.155 μg?kg of BW(-1)?d(-1)) or CCK (0.069, 0.138, or 0.207 μg?kg of BW(-1)?d(-1)), respectively. Increases in plasma GLP-1 and CCK concentrations during hormone infusions were comparable with increases observed when increasing amounts of fat were fed. Feeding fat and infusion of GLP-1 tended (linear, P = 0.12; quadratic, P = 0.13) to decrease DMI. Infusion of CCK did not affect (P > 0.21) DMI. Retention time of Cr in the total gastrointestinal tract decreased (linear, P < 0.01) when fat was fed, but was not affected by GLP-1 or CCK infusion. In conclusion, jugular vein infusion produced similar plasma CCK and GLP-1 concentrations as observed when fat was fed. The effects of feeding fat on DMI may be partially regulated by plasma concentration of GLP-1, but are not likely due solely to changes in a single hormone concentration.     

Stimulation of the exocrine pancreas via a third CCK-receptor subtype?

The physiological role of the cholecystokinin1 receptor (CCK1R) and the cholecystokinin/gastrin receptor (CCK2R) in the enzyme release from the exocrine pancreas in various mammal species has been debated. Experiments in pigs have indicated that physiological levels of cholecystokinin-33 (CCK-33) elicit pancreatic enzyme release via CCK2Rs located in the gastro-duodenal region. Since gastrin and CCK have similar affinity for the CCK2R, the aim was to examine if gastrin can elicit a similar enzyme response as CCK, after infusion via the gastric artery. Weaned pigs were anaesthetised and surgically prepared with appropriate catheters. Pentagastrin (n = 6) or CCK-33 (n = 6), 13 pmol/kg, was infused via the gastric artery into the gastro-duodenal region and 20 min. later 130 pmol/kg of the same hormone was infused via the jugular vein to the general circulation. Pancreatic juice was collected in intervals after each infusion and analysed for its protein and enzyme (trypsin) content. CCK-33 gave rise to significantly higher protein and trypsin output compared to pentagastrin for both doses and infusion routes. The results indicate that low doses of CCK-33 infused to the duodenal region do not stimulate the exocrine pancreas via the CCK2R since the result can't be reproduced with pentagastrin. Since previous studies have indicated that CCK1R is not involved the present results indicate that a third CCK-receptor subtype might be involved in the stimulation of the exocrine pancreas.     

Ontogeny expression of ghrelin,neuropeptide Y and cholecystokinin in blunt snout bream,Megalobrama amblycephala

Ghrelin, neuropeptide Y (NPY) and cholecystokinin (CCK) all have important roles in the regulation of feeding in fish and mammals. To better understand the role of the three peptides in appetite regulation in the early developmental stages of blunt snout bream (Megalobrama amblycephala), partial cDNA sequences of ghrelin, NPY and CCK genes were cloned. And then, real‐time quantitative PCR and RT‐PCR were used to detect and quantify the mRNA expressions of these genes from zygotes to larvae of 50 days after hatching (DAH). Ghrelin, NPY and CCK were all expressed throughout the embryonic and larval development stages, and the expression levels were higher in larval stages than in embryonic stages. Ghrelin and NPY mRNA expressions were upregulated at 1, 3, 5 DAH, while CCK mRNA expression was reduced significantly at 3 DAH. The mRNA expression levels of three genes in larvae varied significantly until 30 DAH. In adult fish, all three peptides were detected to be expressed in brain and several peripheral tissues. Ghrelin mRNA was mainly expressed in the intestine, whereas NPY and CCK mRNAs were mainly expressed in the brain. Taken together, these results indicate that ghrelin, NPY and CCK may have roles in early development and participate in the regulation of feeding of larvae in blunt snout bream and will be helpful for further investigation into feed intake regulation in adults of this species.