Gastric ulceration: the role of thermoxidized palm oil

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.

Effect of low molecular weight organic compound sodium 2-(2-hydroxyphenoxy)acetyl)-L-prolinate on rat gastric secretion stimulated by carbachol

Тto investigate the effects of low molecular organic compound (LMOC) on gastric acid secretion (GAS), pepsin output and the activity of Н+,К+-ATPase in the conditions of carbachol stimulation. GAS stimulated by carbachol was measured by method of isolated perfused stomach, pepsin output was analyzed by colorimetric method for 120 minutes and the activity of Н+,К+-ATPase was assessed spectrophotometrically by the level of anorganic phosphate on 20 white laboratory rats. GAS, pepsin output and the Н+,К+-ATPase activity were decreased under the carbachol stimulation after injection of LMOC. LMOC decreases the gastric acid and pepsin secretion in terms of carbachol stimulation. The inhibition of Н+,К+-ATPase activity is considered as mechanism of antisecretory property of LMOC.