During many years, the milk fat has been unfairly undervalued due to its association with higher levels of cardiovascular diseases, dyslipidaemia or obesity, among others. However, currently, this relationship is being re-evaluated because some of the dairy lipid components have been attributed potential health benefits. Due to this, and based on the increasing incidence of cancer in our society, this review work aims to discuss the state of the art concerning scientific evidence of milk lipid components and reported anticancer properties. Results from the in vitro and in vivo experiments suggest that specific fatty acids (FA) (as butyric acid and conjugated linoleic acid (CLA), among others), phospholipids and sphingolipids from milk globule membrane are potential anticarcinogenic agents. However, their mechanism of action remains still unclear due to limited and inconsistent findings in human studies.
Lipid metabolism, genetics and cancerCancer is the term to define a group of diseases characterized by uncontrolled growth and spread of cells affecting any part of the body. These 'out-of-control' cells also have the ability to invade surrounding lymph nodes, tissues or organs (metastatic cancer) as well as spread to distant sites in the body. This uncontrolled, oncogene-driven proliferation of cancer cells, lacking an efficient vascular system, quickly depletes the nutrient and oxygen supply from the normal vasculature and becomes hypoxic [1]. Due to this, one of the main hallmarks of cancer is a metabolic reprogramming consistent with the Warburg effect: increased glucose uptake and fermentation to lactate to promote growth, survival, proliferation and long-term maintenance [2]. Thus, normal cells use glycolysis to produce pyruvate that is transferred to the mitochondria to produce acetyl-CoA for further utilization in the tricarboxylic acid cycle (Figure 1), but cancer cells produce citrate that is converted in the cytoplasm into acetyl-CoA by the ATP citrate-lyase (ACL) [3].Moreover, cancer cells can also rely on acetate uptake from three different sources: foods (e.g. meat, cheese, pickles), intestinal microbiota (fibre fermentation, besides resulting in short-chain fatty acid (SCFA), propionate and butyrate) and liver (while fasting, acyl-CoA thioesterase 12 (ACOT12) is activated and hydrolyses acetyl--CoA) [4]. Thus, although membranes are passively permeable to acetic acid (pK a : 4.75), intestinal pH (5.5-7) favours anionic forms and therefore exists three active transport mechanisms involving: (i) monocarboxylate transporters (MCTs; coupling acetate plus SCFA uptake and excretion of bicarbonate), (ii) sodium--coupled MCTs (SMCTs; that primarily uptake butyrate) and finally (iii) proton-coupled MCTs (co-transport of SCFA and H + ) [4]. The latter form seems to be the main mechanism in colon and many other cancer types [5].