Abstract
BackgroundBoth in vitro and epidemiological studies indicate that dietary polyunsaturated fatty acids may play a protective role against peptic ulcer in humans. Adipose tissue fatty acid composition is thought to reflect dietary fatty acid intake. The aim of the present study is to investigate adipose and gastric mucosa fatty acid levels in relation to gastric ulceration status.MethodsFifty two adult outpatients undergoing upper gastrointestinal tract endoscopy participated in the study. Adipose tissue samples were taken from the abdomen and buttock during the endoscopy procedure and samples from gastric tissue were taken from a subsample of 30 subjects. The presence of Helicobacter pylori was determined using the CLO test. Capillary gas chromatography was used for the extraction of 36 and 42 adipose tissue and gastric mucosa lipids respectively.ResultsThe monounsaturated fatty acids (MUFAs) C18:1n-12c, C16:1n-5, C16:4n-1 and the polyunsaturated fatty acids (PUFAs) C16:3n-4, C20:3n-3, C20:4n-6, C21:5n-3 and C18:2n-9c,12t of the gastric mucosa were present in higher proportions in ulcer negative patients. These unsaturated fatty acids, however, each contributed less than 1% on average to total fatty acid content. In addition, higher average levels of eicosapentaenoic acid (EPA) C20:5n-3 and docosahexaenoic acid (DHA) C22:6n-3 were detected in abdominal and buttock samples in CLO negative controls, compared to CLO positive controls. Adipose tissue and gastric mucosa n-6 and trans fatty acid levels were positively linearly correlated (r = 0.37 and 0.41 for n-6 and trans fatty acids respectively).ConclusionCertain minor MUFAs and PUFAs of the gastric mucosa appear to be present in higher proportions in ulcer negative patients. Overall, the findings provide only weak evidence of an association between the gastric mucosal fatty acids and the presence of gastric ulceration. The higher average levels of EPA and DHA in abdominal and buttock adipose tissue in CLO negative controls could be an indicator that dietary FAs inhibit Helicobacter pylori growth. Larger studies are necessary to provide evidence of a biologically relevant effect.
Highlights
Both in vitro and epidemiological studies indicate that dietary polyunsaturated fatty acids may play a protective role against peptic ulcer in humans
A positive linear correlation was found between the fatty acid clusters at each of the two adipose tissue sites: saturated fatty acids (SFA) (r = 0.73, p < 0.0001), monounsaturated fatty acids (MUFA) (r = 0.81, p < 0.0001), polyunsaturated fatty acids (PUFA) (r = 0.84, p < 0.0001), n-3 cluster (r = 0.54, p < 0.0001), n-6 cluster (r = 0.83, p < 0.0001), trans (r = 0.612, p < 0.0001), MUFA:PUFA ratio (r = 0.86, p < 0.0001), MUFA:SFA ratio (r = 0.74, p < 0.0001), n-3:n-6 ratio (r = 0.63, p < 0.0001) and the sum of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (r = 0.88, p < 0.0001) using measurements from the 42 subjects who had samples from both sites
It is possible that the consumption of PUFAs inhibits the growth of H. pylori and the colonization of the gastric mucosa, a hypothesis that is in agreement with previous studies showing that ingested dietary PUFAs inhibit the growth of H. pylori in vitro [5,28]
Summary
Both in vitro and epidemiological studies indicate that dietary polyunsaturated fatty acids may play a protective role against peptic ulcer in humans. The aim of the present study is to investigate adipose and gastric mucosa fatty acid levels in relation to gastric ulceration status. The pathophysiology of peptic ulcer disease has centered on an imbalance between aggressive and protective factors in the stomach [1]. Twenty five years have elapsed since Marshall and Warren's discovery of the link between Helicobacter pylori (H. pylori) infection and peptic ulcer disease [2]. Epidemiological evidence suggests that the declining prevalence of peptic ulcer disease may be partially attributable to increased consumption of polyunsaturated fatty acids (PUFAs), a hypothesis supported by in vitro evidence of toxicity of such substances to H. pylori [5]
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