Gastrin,somatostatin,G and D cells of gastric ulcer in rats

AIM: To investigate the relationship among gastrin,somatostatin, G and D calls in gastric ulcer and in its healing process in rats.METHODS: Fourty-nine Wistar rats were divided into 7groups. The gastric ulcer model was induced by acetic acid successfully. The gastrin and the somatostatin in rat plasma, gastric fluid and antral tissue were measured by radioimmunoassay(RIA). G and D cells in antral mucosa were analyzed with polyclonal antibody of gastrin and somatostatin by immunohistochemical method and Quantimet 500 image analysis systemRESULTS: In gastric ulcer, the level of gastrin in plasma,gastric fluid, and antral tissue increased, that ofsomatostatin declined, and the disorder gradually recoveredto the normal level in the healing process.Immunohistochemical technique of G and D cells in antralmucosa demonstrated that the number of G cells increasedand that of D cells decreased, both areas of G and D cellsdeclined, the ratio of number and area of G/D increased ingastric ulcer, and the disorder gradually recovered in thehealing process.CONCLUSION: In gastric ulcer, the increased gastrinsecreted by G cells, the declined somatostatin secreted by Dcells, and the disordered G/D cell ratio can lead togastrointestinal dysfunction.

Gastrin and antral G cells in course of Helicobacter pylori eradication: Six months follow up study

AIM: To assess long-term effects of Helicobacter pylori (H pylori) eradication on antral G cell morphology and function in patients with and without duodenal ulcer (DU).METHODS: Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 H pylori positive patients, 8 had DU (H pylori+DU) and 31 gastritis (H pylori +G). Control groups consisted of 11 uninfected dyspeptic patients (CG1) and 7 healthy volunteers (CG2). Basal plasma gastrin (PGL), antral tissue gastrin concentrations (ATGC), immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.RESULTS: We demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy.Elevated PGL were registered in all H pylori+patients (H pylori +DU: 106.78±22.72 pg/mL, H pylori+G: 74.95±15.63,CG1: 68.59±17.97, CG2:39.24±5.59 pg/mL, P＜0.01).Successful eradication (e) therapy in H pylori+patients lead to significant decrease in PGL (H pylori+DU: 59.93±9.40and H pylori+Ge: 42.36±10.28 pg/mL, P＜0.001). ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in H pylori+gastritis, but not in DU patients. In the H pylori+DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups (P＜0.01), but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased (P＜0.01) in H pylori+Ge group after successful eradication therapy (294±32 and 0.31±0.02,respectively), in comparison to values before eradication (416±40 and 0.48±0.09). No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.CONCLUSION: H pylori infection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the H pylori infection influence antral G cell morphology and function.

Effect of gastrin on protein kinase C and its subtype in human colon cancer cell line SW480

INTRODUCTIONGastrin is atrophic gastrointestinal hormone whichis secreted by G cell.Gastrin has long beenconsidered a growth stimulatory hormone formucosa of the gastrointestinal tract.The growthresponses of certain colorectal cancer cells,andxenografts,can be stimulated by endogenousgastrin.Protein kinase C (PKC) is a family ofisozymes that plays a crucial role in transducingsignals of many hormones,growth peptides,

CacyBP/SIP nuclear translocation induced by gastrin promotes gastric cancer cell proliferation

AIM:To investigate the role of nuclear translocation of calcyclin binding protein,also called Siah-1 interacting protein(CacyBP/SIP),in gastric carcinogenesis.METHODS:The expression of CacyBP/SIP protein in gastric cancer cell lines was detected by Western blot.Immunofluorescence experiments were performed on gastric cancer cell lines that had been either unstimulated or stimulated with gastrin.To confirm the immunofluorescence findings,the relative abundance of CacyBP/SIP in nuclear and cytoplasmic compartments was assessed by Western blot.The effect of nuclear translocation of CacyBP/SIP on cell proliferation was examined using MTT assay.The colony formation assay was used to measure clonogenic cell survival.The effect of CacyBP/SIP nuclear translocation on cell cycle progression was investigated.Two CacyBP/SIPspecific siRNA vectors were designed and constructed to inhibit CacyBP/SIP expression in order to reduce the nuclear translocation of CacyBP/SIP,and the expression of CacyBP/SIP in stably transfected cells was determined by Western blot.The effect of inhibiting CacyBP/SIP nuclear translocation on cell proliferation was then assessed.RESULTS:CacyBP/SIP protein was present in most of gastric cancer cell lines.In unstimulated cells,CacyBP/SIP was distributed throughout the cytoplasm;while in stimulated cells,CacyBP/SIP was found mainly in the perinuclear region.CacyBP/SIP nuclear translocation generated a growth-stimulatory effect on cells.The number of colonies in the CacyBP/SIP nuclear translocation group was significantly higher than that in the control group.The percentage of stimulated cells in G1phase was significantly lower than that of control cells(69.70%±0.46%and 65.80%±0.60%,control cells and gastrin-treated SGC7901 cells,P=0.008;72.99%±0.46%and 69.36%±0.51%,control cells and gastrin-treated MKN45 cells,P=0.022).CacyBP/SIPsi1effectively down-regulated the expression of CacyBP/SIP,and cells stably transfected by CacyBP/SIPsi1 were then chosen for further cellular assays.In CacyBP/SIPsi1 stably transfected cells,CacyBP/SIP was shown to be distributed throughout the cytoplasm,irregardless of whether they were stimulated or not.After CacyBP/SIP nuclear translocation was reduced,there had no major effect on cell proliferation,as shown by MTT assay.There had no enhanced anchoragedependent growth upon stimulation,as indicated by colony formation in flat plates.No changes appeared in the percentage of cells in G0-G1 phase in either cell line(71.09%±0.16%and 70.86%±0.25%,control cells and gastrin-treated SGC7901-CacyBP/SIPsi1 cells,P=0.101;74.17%±1.04%and 73.07%±1.00%,control cells and gastrin-treated MKN45-CacyBP/SIPsi1cells,P=0.225).CONCLUSION:CacyBP/SIP nuclear translocation promotes the proliferation and cell cycle progression of gastric cancer cells.

αV integrin:A new gastrin target in human pancreatic cancer cells

AIM:To analyse αV integrin expression induced by gas-trin in pancreatic cancer models. METHODS:αV integrin mRNA expression in human pan-creatic cancer cells was analysed using a "cancer genes" array and confirmed by real-time reverse transcription-polymerase chain reaction (PCR). Western blotting and semi-quantitative immunohistochemistry were used to examine protein levels in human pancreatic cancer cell lines and pancreatic tissues, respectively. The role of αV integrin on gastrin-induced cell adhesion was examined using blocking anti-αV integrin monoclonal antibodies. Adherent cells were quantified by staining with crystal violet.RESULTS: Using a "cancer genes" array we identified αV integrin as a new gastrin target gene in human pancreatic cancer cells. A quantitative real-time PCR approach was used to confirm αV integrin gene expression. We also demonstrate that Src family kinases and the PI 3-kinase, two signalling pathways specifically activated by the CCK-2 receptor (CCK2R), are involved in gastrin-mediated αV integrin expression. In contrast, inhibition of the ERK pathway was without any effect on αV integrin expression induced by gastrin. Our results also show that gastrin modulates cell adhesion via α V integrins. Indeed, in vitro adhesion assays performed on fibronectin show that gastrin significantly increases adhesion of pancreatic cancer cells. The use of blocking anti-αV integrin monoclonal antibodies completely reversed the increase in cell-substrate adhesion induced by gastrin. In addition, we showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, leads to the overexpression of αV integrin. This process may contribute to pancreatic tumour development observed in these transgenic animals. CONCLUSION:αV integrin is a new gastrin target in pancreatic cancer models and contributes to gastrin effects on cell adhesion.

EFFECTS OF MEDICINAL MOXIBUSTION ON SERUM GASTRIN,URINARY D-XYLOSE EXCRETORY RATE AND T CELL SUBGROUPS IN SPLEEN DEFICIENCY PATIENTS

The medicinal moxa stick made by moxa wool combining with Chinese medicines of supporting the body resistance and strengthening the spleen was used to treat 74 cases of spleen deficiency, the other 41 patients as control were treated by pure moxa stick. After treatment, the serum gastrin, urinary D - xylose excretory rate and T cell subgroups in patients with spleen deficiency have been greatly improved as compared with those before treatment in two groups (P< 0.01 or 0.05). Comparing the changes of the indexes between treatment group and control group, there were significant(P<0.05), or markedly significant(P<0.01) differences. It indicated that the medicinal moxibustion could improve the secreting and absorbing functions of digestive tract and the cellular immune function in patients with spleen deficiency.

胃泌素释放肽前体、鳞状细胞癌抗原在非小细胞肺癌中的表达及临床意义

目的探讨胃泌素释放肽前体(ProGRP)、鳞状细胞癌抗原(SCCA)在非小细胞肺癌(NSCLC)中的表达及临床意义。方法选取122例NSCLC患者和93例健康体检者,分别作为观察组和对照组。采用化学发光法检测两组受试者血清ProGRP、SCCA水平,比较不同组织学类型NSCLC患者ProGRP、SCCA的水平和阳性表达率,比较两组受试者和不同临床特征NSCLC患者的ProGRP、SCCA阳性表达率。绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),分析ProGRP、SCCA单独及联合检测对NSCLC的诊断价值。结果鳞状细胞癌患者的血清SCCA水平高于腺癌及大细胞癌患者,差异均有统计学意义(P﹤0.05)。鳞状细胞癌患者SCCA的阳性表达率高于腺癌患者,差异有统计学意义(P﹤0.05)。观察组患者ProGRP、SCCA的阳性表达率分别为90.98%、78.69%,分别明显高于对照组的8.60%、6.45%,差异均有统计学意义(P﹤0.01)。有淋巴结转移NSCLC患者ProGRP、SCCA的阳性表达率均明显高于无淋巴结转移患者(P﹤0.01)。ROC曲线显示,ProGRP联合SCCA检测诊断NSCLC的AUC为0.797(95%CI:0.714~0.880),灵敏度为90.59%,特异度为89.25%,均高于二者单独检测。结论ProGRP、SCCA在NSCLC患者中阳性表达率均较高,且其表达与淋巴结转移有关,二者联合检测对NSCLC具有较高的诊断价值。

多次小剂量STZ处理建立糖尿病大鼠模型及EGF与Gastrin联合应用对胰岛素分泌的影响

目的通过多次小剂量STZ处理建立糖尿病大鼠模型,观察EGF/Gastrin联合应用对模型大鼠胰岛功能的影响。方法采用35mg·Kg-1腹腔注射STZ-枸橼酸钠缓冲液,每周1次,连续4周,建立大鼠糖尿病模型。采用生化分析和组织染色的方法观察血糖和胰岛细胞的改变。成模大鼠随机分为三组:Insulin治疗组,EGF/Gastrin联合治疗组及DM对照组。EGF/Gastrin组给予EGF(1μg·Kg-1)/Gastrin(3μg·Kg-1),每日1次皮下注射,连续14日;Insulin组给予长效胰岛素2U/d,连续14日;DM对照组及正常对照组给予枸橼酸钠缓冲液。观察血浆中胰岛素和C肽的改变,评估胰岛细胞功能。结果 35只实验组大鼠中有33只血糖值≥11.1mmol·L-1,占总数的94%。Insulin组大鼠和EGF/Gastrin组大鼠血糖值同DM组相比显著降低。DM组中血清胰岛素及C肽含量显著低于正常对照组(P<0.05),而Insulin组及EGF/Gastrin组均显著高于DM组(P<0.05)。组织学结果观察发现,成模大鼠的胰岛数量明显减少,分布不均匀并出现不同程度的萎缩,出现空泡变性。Insulin免疫组织化学染色结果显示,成模大鼠胰岛内Insulin染色阳性的细胞明显减少;且残存胰岛β细胞Insulin染色强度低于正常对照组,Insulin组及EGF/Gastrin组大鼠胰岛中Insulin表达细胞明显增多,有部分细胞呈强阳性表达。结论 EGF和Gastrin联合应用能够促进糖尿病大鼠胰岛功能的恢复。

胃癌患者血清胃泌素释放肽前体、鳞癌相关抗原和糖类抗原72-4的变化及意义

目的探讨胃癌患者血清胃泌素释放肽前体(ProGRP)、鳞癌相关抗原(SCC)及糖类抗原72-4(CA72-4)水平变化及临床意义。方法选取68例胃癌患者(胃癌组)、37例胃部良性病变患者(胃部良性病变组)、30例健康受试者(非胃部疾病组)作为研究对象。比较3组研究对象入院时血清ProGRP、SCC、CA72-4水平;分析胃癌组患者血清ProGRP、SCC、CA72-4水平与病理参数的关系;对出院后胃癌组患者随访24个月,采用多因素Logistic回归分析明确胃癌患者随访预后的影响因素,绘制受试者工作特征(ROC)曲线并计算曲线下面积(AUC),分析血清ProGRP、SCC、CA72-4对胃癌患者随访期间死亡的预测效能。结果胃癌组血清ProGRP、SCC、CA72-4水平高于胃部良性病变组和非胃部疾病组,胃部良性病变组血清ProGRP、CA72-4水平高于非胃部疾病组,差异有统计学意义(P<0.05);胃癌组中,TNM分期为Ⅲ~Ⅳ期、组织学分级为中低分化、有淋巴结转移患者血清ProGRP、CA72-4水平分别高于Ⅰ~Ⅱ期、高分化、无淋巴结转移患者,组织学分级为中低分化患者血清SCC水平高于高分化患者,差异有统计学意义(P<0.05)。随访24个月,胃癌组存活49例(存活组)、死亡19例(死亡组),死亡组患者入院时血清ProGRP、SCC、CA72-4水平均高于存活组,差异有统计学意义(P<0.05)。多因素Logistic回归分析结果显示,血清ProGRP、SCC、CA72-4均为胃癌患者随访预后的独立影响因素(P<0.05);血清ProGRP、SCC、CA72-4对胃癌患者随访期间死亡均有良好的预测效能(AUC=0.766、0.705、0.828),且三者联合的预测效能更佳(AUC=0.899)。结论胃癌患者血清ProGRP、SCC、CA72-4水平异常升高(与TNM分期、组织学分级、淋巴结转移状态有关),三者联合检测对患者随访期间死亡具有很好的预测效能。

EGF/Gastrin联用对实验性1型糖尿病大鼠胰岛β细胞再生的影响

目的观察EGF/Gastrin联用对实验性1型糖尿病大鼠胰岛β细胞再生的影响,为糖尿病的治疗开辟新途径。方法选用Wister大鼠,一次性腹腔注射STZ(55 mg.kg-1)诱导1型糖尿病模型。实验分3组:正常对照组、糖尿病组及EGF/Gastrin组。EGF(1μg.kg-1)/Gastrin(3μg.kg-1)每日一次,连续14日。实验结束检测各组大鼠的空腹血糖、血清Insulin及C肽等生化指标;进行HE染色,观察胰岛形态学变化。结果 EGF/Gastrin组大鼠空腹血糖明显低于糖尿病组(P<0.05);血清Insulin、C肽含量及胰岛β细胞数量均明显高于糖尿病组(P<0.05)。结论 EGF/Gastrin联用能够降低糖尿病大鼠的血糖,并使血清Insulin和C肽含量增加,胰岛β细胞数量增多,功能得到改善。

鳞状细胞癌抗原、胃泌素释放肽前体、神经元特异性烯醇化酶对肺癌的诊断价值

目的探讨鳞状细胞癌抗原(SCCA)、胃泌素释放肽前体(ProGRP)、神经元特异性烯醇化酶(NSE)对肺癌的诊断价值。方法选取43例肺癌患者和35例肺部良性疾病患者分别作为肺癌组和良性组。采用化学发光分析仪、自动生化仪检测两组患者的血清ProGRP、NSE和SCCA水平。比较两组患者的SCCA、ProGRP和NSE水平,分析肺癌发生的影响因素和SCCA、ProGRP、NSE单独及联合检测对肺癌的诊断价值。结果肺癌组患者SCCA、ProGRP和NSE水平均明显高于良性组,差异均有统计学意义(P﹤0.01)。SCCA、ProGRP及NSE均是肺癌发生的独立危险因素(P﹤0.05)。SCCA、ProGRP及NSE联合检测诊断肺癌的AUC、灵敏度、特异度均高于三者单独检测。结论SCCA、NSE和ProGRP均在肺癌患者中高表达,可作为肺癌良好的血清肿瘤标志物,且联合检测对肺癌有较好的诊断价值。

壳多糖酶3样蛋白1在肺癌诊断中的临床价值

目的探讨壳多糖酶3样蛋白1(CHI3L1)在肺癌诊断中的临床价值。方法选取2022年1-12月安徽医科大学第一附属医院北区收治的106例肺癌患者为肺癌组,同期收治的76例肺良性疾病患者作为肺良性疾病组及20例健康体检者作为对照组,采用酶联免疫吸附试验法检测CHI3L1水平,化学发光法检测癌胚抗原(CEA)、神经元特异性烯醇化酶(NSE)、细胞角蛋白19片段(CYFRA21-1)、鳞状细胞癌抗原(SCC-Ag)、胃泌素释放肽前体(ProGRP)水平。结果肺癌组血清CEA、ProGRP、NSE、CYFRA21-1、CHI3L1水平较对照组明显升高,差异有统计学意义(P<0.05)。肺癌组血清CEA较肺良性疾病组明显升高,而血清CHI3L1较肺良性疾病组明显下降,差异有统计学意义(P<0.05)。与肺腺癌、肺鳞癌患者比较,小细胞肺癌患者血清NSE、ProGRP水平较高,差异有统计学意义(P<0.05);与肺腺癌、小细胞肺癌患者比较,肺鳞癌患者血清CYFRA21-1水平较高,差异有统计学意义(P<0.05)。与对照组比较,肺癌组Ⅰ~Ⅱ期患者血清NSE、CYFRA21-1、CHI3L1水平明显升高,差异有统计学意义(P<0.05)。对CEA、ProGRP、NSE、CYFRA21-1、CHI3L1进行多因素Logistic逐步回归分析,发现NSE、CHI3L1对肺癌的发生产生影响。CHI3L1、NSE联合检测诊断肺癌的灵敏度为96.2%,特异度为90.0%,曲线下面积为0.965。结论血清CHI3L1可辅助肺癌的诊断与鉴别诊断,CHI3L1、NSE联合检测有助于临床对肺癌的早期发现,具有良好的临床应用价值。

血清Pro-GRP、NSE在非小细胞肺癌化疗前后的水平变化及临床意义

目的分析血清胃泌素释放肽前体(Pro-GRP)、神经元特异性烯醇化酶(NSE)在非小细胞肺癌(NSCLC)化疗前后的水平变化及临床意义。方法收集2020年2月—2022年2月本院收治的NSCLC患者126例为观察组,另选取同期于本院进行体检的健康体检者108例为对照组。对比观察组与对照组患者Pro-GRP、NSE水平,分析观察组患者化疗前后Pro-GRP、NSE水平变化情况;分析影响NSCLC患者化疗效果的危险因素;分析Pro-GRP、NSE单独及联合检测对NSCLC患者化疗效果的预测价值。结果观察组患者化疗前Pro-GRP、NSE水平均高于对照组,差异有统计学意义(t=11.584,P<0.001;t=4.951,P<0.001),且观察组化疗前Pro-GRP、NSE水平均高于化疗后,差异有统计学意义(t=5.901,P<0.001;t=2.633,P=0.008)。化疗后,有效组共有患者98例,无效组共有患者28例。2组患者吸烟史、慢性病史、远处转移情况、Pro-GRP水平及NSE水平比较,差异均有统计学意义(P<0.05)。Logistic回归分析结果显示:有吸烟史、有慢性病史、有远处转移、Pro-GRP升高及NSE升高是影响NSCLC患者化疗效果的危险因素(P<0.05)。受试者工作特征(ROC)曲线结果显示,Pro-GRP+NSE预测NSCLC患者化疗效果的曲线下面积(AUC)为0.911,95%CI:0.861~0.962,敏感度为0.871,特异度为0.862。结论NSCLC患者化疗后血清Pro-GRP、NSE水平降低,而通过检测Pro-GRP、NSE水平可对患者化疗效果进行预测,且2个指标联合预测的价值更高。

非小细胞肺癌患者SCC、ProGRP及CEA水平变化及临床意义

目的探讨非小细胞肺癌(NSCLC)患者鳞状细胞癌相关抗原(SCC)、胃泌素释放肽前体(ProGRP)及癌胚抗原(CEA)水平变化及临床意义。方法回顾性分析2020年5月至2023年2月于首都医科大学附属北京友谊医院展开治疗的132例NSCLC患者的临床资料,设为A组;另抽取同期于本院治疗的71例肺良性病变患者,设为B组。比较两组患者SCC、ProGRP及CEA水平,分析不同临床特征NSCLC患者SCC、ProGRP及CEA水平,运用受试者工作特征(ROC)曲线分析SCC、ProGRP及CEA对NSCLC的诊断价值。结果A组患者血清SCC、ProGRP及CEA水平均高于B组患者,差异有统计学意义(P<0.05)。血清SCC、ProGRP、CEA及三者联合诊断NSC的AUC分别为0.691、0.815、0.822、0.832。不同病理类型、分化程度、临床分期及淋巴结转移的NSCLC患者血清SCC、ProGRP及CEA水平比较差异有统计学意义(P<0.05)。结论不同病理类型、分化程度、临床分期及淋巴结转移的NSCLC患者血清SCC、ProGRP及CEA存在差异,血清SCC、ProGRP及CEA均可有效辅助诊断NSCLC,且三者联合诊断能提高诊断效能。

Gastrin,somatostatin,and experimental disturbance of the gastrointestinal tract in rats

INTRODUCTIONThe field of gastrointestinal hormones has expanded at a dizzying rate[1-4].Gastrointestinal hormones as regulatory peptides that appear to be major components of bodily integration and have important regulatory actions on physioligical function of the gastrointestinal tract .The successful isolation of some gastrointestinal hormones and the development of sensitive methods for their detection have led to the unexpected finding that they also exist in the brain .

Effect of gastrectomy on G-cell density and functional activity in dogs

INTRODUCTION Billroth gastrectomy has some advantages ofinhibiting acid secretion,low ulcer recurrence andlow mortality. However, postoperativecomplications,such as dumping syndrome andreflux gastritis,often occurred as a result ofpylorectomy.To minimize these complications,pylorus-preserving gastrectomy(PPG)had beenperformed for gastric ulcer with satisfied clinicalresults.Positive correlation was not found betweenulcer recurrence and serum gastrin level.In

Influence of IFNα-2b and BCG on the release of TNF and IL-1 by Kupffer cells in rats with hepatoma

INTRODUCTIONKupffer cells are residential macrophages in the liver ,which play a critical role in the maintenance of normal liver function and in immunal surveilance of hepatocellular carcinoma (HCC) and other cancers[1].The biological immune modulants have cancers[2].In our previous studies ,the combined use of biological immune modulants showed better dffects .

Differentiations of 5-HT and GAS cells in the digestive canals of Rana chensinensis tadpoles

In the current study, 5-nydroxytryptamine （5-HT） and gastrin （GAS） cells in the digestive canals of Rana chensinensis tadpoles at different developmental stages were investigated by immunohistochemistry. Results showed that the 5-HT cells were only detected in the duodenum before metamorphosis began, and were extensively distributed in the stomach, duodenum, small intestine, and rectum thereafter, with the highest counts found in the duodenum and rectum when metamorphosis was completed. The GAS cells were only distributed in the stomach and duodenum, and only rarely detected in the duodenum before metamorphosis began, but increased in the stomach during metamorphosis and showed zonal distribution in the gastric mucosa when metamorphosis was completed. Metamorphosis is a critical period for amphibians, during which structural and functional physiological adaptations are required to transition from aquatic to terrestrial environments. During metamorphosis, the differentiations of 5-HT cells in the gastrointestinal canals of tadpoles could facilitate mucus secretion regulation, improve digestive canal lubrication, and help water- shortage food digestion in terrestrial environments. Conversely, GAS cell differentiations during metamorphosis might contribute to the digestive and absorptive function transition from herbivore to omnivore.

Physiological and clinical significance of enterochromaffin-like cell activation in the regulation of gastric acid secretion

Gastric acid plays an important role in digesting food (especially protein), iron absorption, and destroying swallowed micro-organisms. H+ is secreted by the oxyntic parietal cells and its secretion is regulated by endocrine, neurocrine and paracrine mechanisms. Gastrin released from the antral G cell is the principal physiological stimulus of gastric acid secretion. Activation of the enterochromaffin-like (ECL) cell is accepted as the main source of histamine participating in the regulation of acid secretion and is functionally and trophically controlled by gastrin, which is mediated by gastrin/CCK-2 receptors expressed on the ECL cell. However, long- term hypergastrinemia will induce ECL cell hyperplasia and probably carcinoids. Clinically, potent inhibitors of acid secretion have been prescribed widely to patients with acid-related disorders. Long-term potent acid inhibi- tion evokes a marked increase in plasma gastrin levels, leading to enlargement of oxyntic mucosa with ECL cell hyperplasia. Accordingly, the induction of ECL cell hy- perplasia and carcinoids remains a topic of considerable concern, especially in long-term use. In addition, the activation of ECL cells also induces another clinical con- cern, i.e., rebound acid hypersecretion after acid inhibi- tion. Recent experimental and clinical findings indicate that the activation of ECL cells plays a critical role both physiologically and clinically in the regulation of gastric acid secretion.

Changes of G cells and D cells in the antral mucosa in rat experimental gastric ulcer

Objective: To investigate the association of changes in G and D cells in the antral mucosa with the production of gastrin and somatostatin during gastric ulcer and the healing process. Methods: Experimental gastric ulcer was induced with acetic acid in 42 Wistar rats and another 7 normal rats served as control. Changes in the production of gastrin and somatostatin in the plasma, gastric fluid and the antral tissues of the rats were measured by radio immunoassay, and the number and distribution of G and D cells were respectively determined by immunochemistry and Quantimet500 image analysis system. Results: In rats with gastric ulcer, the gastrin levels in the plasma, gastric fluid and the antral tissues increased while somatostatin levels were reduced, which were corrected in the healing process. Immunochemistry demonstrated the increase in the number of G cells in the antral tissues with decrease in D cell number, and the area covered by both cells shrank. The G cell to D cell number and area ratios