The Effect of Diet Supplementation with Pomegranate and Bitter Melon on Lipidomic Profile of Serum and Cancerous Tissues of Rats with Mammary Tumours.

Agnieszka Białek,Małgorzata Jelińska,Tomasz Lepionka,Małgorzata Białek,Małgorzata Czerwonka,Marian Czauderna

doi:10.3390/antiox9030243

Abstract

The aim of this study was to present overall lipid profile of organisms with ongoing neoplastic process and applied diet supplementation with pomegranate seed oil (PSO) and bitter melon extract (BME). The following were quantified in serum and cancerous tissues of rats suffering from mammary tumours: fatty acids, conjugated fatty acids and sterols, their oxidised metabolites (malondialdehyde and oxysterols) and lipoxygenase (LOX) metabolites of polyunsaturated fatty acids. The obtained results indicate that abnormalities in lipid metabolism accompany neoplastic process. These differences concern all classes of lipids and most pathways of their transformation, with the special emphasis on lipid peroxidation and LOX-mediated metabolism. Cancer process appears to be so detrimental that it may conceal positive influence of dietary modifications. The lack of anticarcinogenic properties of PSO and BME in this model may be due to their antioxidant properties or elevated levels of conjugated linoleic acids (CLA), which change CLA isomer activity from anti- to pro-tumorigenic. As CLA are the product of conjugated linolenic acids (CLnA) endogenous metabolism, high CLA levels may be explained by applied diet enrichment.

Highlights

Since 1920, when Warburg observed that cancer cells show avid glucose uptake and tend to convert it to lactate through the glycolytic pathway regardless of whether oxygen is present (Warburg Effect) [1], many differences in metabolic pathways distinguishing cancer cells from normal cells have been described
We demonstrated that dietary supplements such as pomegranate seed oil (PSO) - source of conjugated linolenic acids (CLnA) and bitter melon fruits aqueous extract (BME) interfere in fatty acids (FA) metabolism and LOX metabolites formed in physiological state [18]
An overall FA profile of serum samples of animals suffering from mammary tumours was rather stable as total share of saturated FA (SFA), monounsaturated FA (MUFA) and polyunsaturated FA (PUFA) did not differ among experimental groups (Table 1)

Summary

Introduction

Since 1920, when Warburg observed that cancer cells show avid glucose uptake and tend to convert it to lactate through the glycolytic pathway regardless of whether oxygen is present (Warburg Effect) [1], many differences in metabolic pathways distinguishing cancer cells from normal cells have been described. Increased glutaminolysis [2], increased nucleotides synthesis [3] and abnormalities in lipid metabolism [4,5,6] are recognised as characteristic features—hallmarks of cancer cells. Oncoproteins directly reprogram the metabolism of cancer cells and make them follow certain metabolic pathways [5]. Proliferating cancer cells either activate their endogenous de novo synthesis or increase the uptake of lipids and lipoproteins from bloodstream [4,9]. Many studies reported an upregulated lipolysis and lipid oxidation in cancer cells, making FA oxidation a dominant bioenergetic pathway, e.g., in prostate cancer cells [5]

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