Acute high blood glucose level attenuates histamine-stimulated acid secretion in male Wistar rats

2014 ◽  
Vol 0 (0) ◽  
Author(s):  
Taofeek O. Usman ◽  
Lawrence A. Olatunji ◽  
Abdul Rasak A. Alada
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Wistar Rats ◽  
Saline Control ◽  
Control Group ◽  
High Blood Glucose ◽  
High Blood Glucose Level ◽  
Perfusion Apparatus ◽  
Male Wistar Rats

AbstractStudies have shown that the hyperglycemic state induced by intravenous glucagon or glucose infusion may lead to inhibition of gastric acid secretion through the inhibition of gastric vagus activity. Histamine is a well-known mammalian acid secretagogue and it stimulates acid secretion through HMale Wistar rats weighing between 200 and 250 g were divided into three groups that received an intravenous infusion of normal saline (control group), glucose (hyperglycemic group), or insulin (hypoglycemic group) followed by injection of histamine to stimulate acid secretion. The oesophageal and duodenal ends of the rats’ stomach were cannulated with polythene tubing and the stomach was perfused at room temperature using a Langendoff perfusion apparatus. The effluent was collected in aliquots over 10 min per sample and its pH was measured.There was a significant (p<0.05) decrease in acid secretion following histamine injection in the hyperglycemic rats, while histamine injection led to an increase (p<0.05) in acid secretion in the hypoglycemic rats.These results show that hyperglycemic state would result in attenuated histamine-stimulated gastric acid secretion, while hypoglycemic state would lead to increased histamine-stimulated gastric acid secretion.

Evaluation of Long Term Alcohol Consumption on Gastric Acid Secretion and the Histomorphometry of the Stomach in Adult Male Wistar Rats

2016 ◽  
Vol 4 (5) ◽  
pp. 7
Author(s):  
Ese C. Adegor ◽  
Anthony E. Ojieh ◽  
Ovocity Eghworo ◽  
Lawrence O. Ewhre ◽  
Tarela M. E. Daubry ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Adult Male ◽  
Wistar Rats ◽  
Male Wistar Rats

scholarly journals RESPON AKTIVITAS TIKUS WISTAR JANTAN AKIBAT KONDISI DIET TINGGI SUKROSA DIUKUR MENGGUNAKAN PEREKAM AKTIVITAS

Jurnal BIOMA ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. 104
Author(s):  
Yanuar Restu Wijaya ◽  
Koekoeh Santoso ◽  
Isdoni Isdoni ◽  
Atin Supiyani
Keyword(s):  
Blood Glucose ◽  
Wistar Rats ◽  
Feeding Activity ◽  
Control Group ◽  
High Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Track System ◽  
Male Wistar Rats ◽  
Auto Track

Excessive energi consumption play a role in increasing blood glucose levels (hyperglycemia), due to the inability of the hormone insulin to compensate the high blood glucose levels. Blood glucose receptor found in the hypothalamus of VMH (Ventro Medial Hypothalamus) and LH (the Lateral Hypothalamus) is able to detect and change the settings for the feeding activity. The aim of this study was to obtain the relationship between high sucrose feeding on male Wistar rats of behavior and activity. This method uses Wistar rats (Rattus norvegicus) as an animal model. Sixteen rats were grouped into 4 treatment groups. The first group was given additional feed 20% sucrose, the second group was given additional feed 40% sucrose, a third group was given additional feed 60% sucrose, and the last as a control group. This feed given continuously for 70 days.Observation of activities conducted using Opto-varimex® auto-track system ver.4.31. The results showed an corellation between activity based doses of sucrose.

scholarly journals Antisecretory Effect of Hydrogen Sulfide on Gastric Acid Secretion and the Involvement of Nitric Oxide

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Seyyed Ali Mard ◽  
Hasan Askari ◽  
Niloofar Neisi ◽  
Ali Veisi
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Control Group ◽  
Antisecretory Effect ◽  
Cox 2 ◽  
Stimulation Of

The present study was designed to investigate the effect of H2S on distention-induced gastric acid secretion. Fifty-two rats were randomly assigned to seven experimental groups. The gastric acid secretion was stimulated by gastric distention. Two groups of rats received L-cysteine or saline for 5 days before stimulation of the gastric acid secretion. Two groups of animals also received NaHS or saline just prior to stimulation of the gastric acid secretion. The effect of L-NAME and propargylglycine was also investigated. The mucosal levels of the gene expression of cyclooxygenase-2 (COX-2), endothelial nitric oxide synthase (eNOS), and H+/K+-ATPaseα-subunit were quantified by qPCR and luminal concentrations of NO were determined. NaHS and L-cysteine decreased the gastric acid output in response to distention. The mRNA expression of H+/K+-ATPaseα-subunit decreased by NaHS and L-cysteine as compared with the control group while gene expression of eNOS and COX-2 was upregulated. The inhibitory effect of NaHS on distention-induced gastric acid secretion was mitigated by pretreatment of L-NAME. These findings suggest the involvement of NO in mediating the antisecretory effect of H2S.

scholarly journals Inhibitory effect of endostatin gene therapy combined with phosphorus-32 colloid on tumour growth in Wistar rats

2016 ◽  
Vol 36 (3) ◽  
Author(s):  
Huiqi Gao ◽  
Jing Zhu ◽  
Yong Li ◽  
Peng Fu ◽  
Baozhong Shen
Keyword(s):  
Wistar Rats ◽  
Tumour Growth ◽  
Combined Therapy ◽  
Inhibitory Effect ◽  
Saline Control ◽  
Control Group ◽  
Healthy Male ◽  
Saline Control Group ◽  
Male Wistar Rats

Eighty healthy male Wistar rats, aged 5 weeks, weighing 100–120 g, were utilized for establishing tumour-bearing models by immediate Walker-256 cancerous ascites injection and randomly divided to four groups (n=20) treated with 0.2 ml solution containing saline, 32P-colloid (0.3 mCi), endostatin gene (20 μg), endostatin gene combined with colloid 32P. The effect of endostatin combined with a small dose of 32P-colloidal on tumour growth in vivo was evaluated and the potential mechanism underlying the combined therapy was explored. We found that 32P-colloid combined with endostatin exhibited higher inhibitory effect upon tumour growth compared with application of 32P-colloid or endostatin alone, although three therapies all significantly inhibited tumour growth compared with saline control group. The higher inhibitory effect of 32P-colloid combined with endostatin upon tumour growth might be attributed to a synergistic effect of inhibiting angiogenesis by endostatin and inducing apoptosis by 32P-colloid, as demonstrated by microvessel density (MVD) and apoptotic index (AI) measurement. Combined therapy of 32P-colloid and endostatin probably serves as a novel and efficacious therapy of tumour growth.

scholarly journals Dihydroquercetin (taxifolin) attenuates dexamethasone activity on prostaglandin E-2 but potentiates thromboxane-A2 action in gastric acid secretion in wistar rats

2020 ◽  
Vol 13 (3) ◽  
pp. 181-188
Author(s):  
Etah Etah Nkanu
Keyword(s):  
Body Weight ◽  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Wistar Rats ◽  
Acid Output ◽  
Thromboxane A2 ◽  
Mucus Secretion ◽  
Gastric Acid Output

The activity of dexamethasone and taxifolin {(2R, 3R)-2-(3, 4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one}supplementation on prostaglandin E2 and thromboxane A2 in gastric acid secretion and anti-ulcer was studied. Twenty male Wistar rats (180g-200g body weight) were used. The rats were randomly selected into four groups containing 5 rats each. Group 1 was the control group fed on normal rat feed. Group 2 received 3mg/kg of Dexamethasone (intraperitoneally) at one day interval. Group 3 received 3mg/kg of Dex. intraperitoneally and 1mg/kg body weight of taxifolin orally while group 4 received 1mg/kg body weight of taxifolin. At the end of 6 weeks, basal and peak gastric acid output was measured by continuous perfusion of rats stomach under anaesthesia with normal saline at the rate of 1ml/min. Gastric acid, mucus secretion, ulcer index, PGE-2 and thromboxane A2 activity were determined according to standard procedures. Results showed a significantly (p<.05) decreased prostaglandin and mucus secretion level and a raised thromboxane concentrations and gastric acid output in dexamethasone administration. Taxifolin significantly (p<.05) lowered thromboxane A2 concentration in Dex treatment while increasing the prostaglandin E2 level. We conclude that Taxifolin decreases dexamethasone- induced gastric acid secretion, increases prostaglandin activity but reduces thromboxane concentration.

Gastric ulceration: the role of thermoxidized palm oil

2016 ◽  
Vol 46 (1) ◽  
pp. 108-119 ◽  
Author(s):  
Agona O Obembe ◽  
Emmanuel O. Ofutet ◽  
Atim B. Antai ◽  
Eme E Osim
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Palm Oil ◽  
Acid Output ◽  
Gastric Ulceration ◽  
Control Group ◽  
Free Access ◽  
Pepsin Secretion ◽  
Content Type

Purpose – The purpose of this paper is to study the effect of chronic consumption of fresh palm oil (FPO) and thermoxidized palm oil (TPO) diet on gastric acid secretion, pepsin secretions, gastric mucus output and gastric cytoprotection. Design/methodology/approach – Adult Wistar rats were randomly assigned into three groups, i.e. control, FPO and TPO groups (n = 10 in each). The control group was fed with normal rat chow only, the FPO group was fed on diet containing 15 per cent v/w FPO and the TPO group was fed with diet containing v/w of thermally oxidized palm oil. All animals had free access to feed and water, and the feeding lasted for 14 weeks. At the end of the feeding period, gastric acid secretion, pepsin secretion, mucus output and gastric ulceration were measured following standard methods. Findings – There was increase in histamine-stimulated gastric acid output in the TPO diet-fed group (p < 0.01) compared with the control and FPO diet-fed groups. No significant change in the mucus output was observed across all the experimental groups; whereas, pepsin secretion was significantly higher (p < 0.05) in the TPO diet-fed group (0.46 ± 0.27) compared with the control (0.14 ± 0.05) and FPO diet-fed groups (0.25 ± 0.01). Ulcer scores in the TPO diet-fed group (15.5 ± 0.33) was significantly higher (p < 0.01) compared with the control (10.0 ± 0.05) and FPO diet-fed (5.0 ± 0.04) groups. Originality/value – Chronic consumption of TPO increased gastric acid and pepsin secretion (gastric-aggressive factors) without a change in the mucus output. This can bring about gastric ulceration; therefore, the liberal use of TPO should be discouraged.

scholarly journals Role of ghrelin in the regulation of gastric acid secretion involving nitrergic mechanisms in rats

2008 ◽  
pp. 563-568
Author(s):  
HM Bilgin ◽  
C Tumer ◽  
H Diken ◽  
M Kelle ◽  
A Sermet
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Control Group ◽  
Albino Rats ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Plasma Nitrite

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R), has been identified in the rat and human gastrointestinal tract. Ghrelin has been proposed to play a role in gastric acid secretion. Nitric oxide (NO) was shown as a mediator in the mechanism of ghrelin action on gastric acid secretory function. However, there is a little knowledge about this topic. We have investigated the role of ghrelin in gastric acid secretion and the role of NO as a mediator. Wistar albino rats were used in this study. The pyloric sphincter was ligated through a small midline incision. By the time, saline (0.5 ml, iv) was injected to the control group, ghrelin (20 μg/kg, iv) was injected to the first experimental group, ghrelin (20 μg/kg, iv) + L-NAME (70 mg/kg, sc) was injected to the second group and L-NAME (70 mg/kg, sc) was administered to the third group. The rats were killed 3 h after pylorus ligation; gastric acid secretion, mucus content and plasma nitrite levels were measured. Exogenous ghrelin administration increased gastric acid output, mucus content and total plasma nitrite levels, while these effects of ghrelin were inhibited by applying L-NAME. We can conclude that ghrelin participates in the regulation of gastric acid secretion through NO as a mediator.

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