Tumor growth can be directly fed with high fructose corn syrup

The consumption of sugary drinks has been badociated with a worldwide epidemic of obesity and an increase in colorectal cancer incidence rates among young and middle-aged adults, suggesting a potential link between these types of beverages, obesity and the development of colorectal cancer.

Studies indicate that excessive consumption of sugary sugar beverages results in obesity and that obese men are at increased risk of colorectal cancer; but it is not clear if BSNs contribute directly to the formation of tumors. Obesity and metabolic syndrome are important confounding factors that can indirectly affect tumor development by altering the physiological and endocrine systems of several organs.

Genetically modified mouse models containing deleted adenomatous polyposis coli genes were used to study the direct links between cancer and HFCS. APC is a caretaker of colorectal cancer; by removing the protein, the animals are predisposed to the development of cancers of the intestine; without it, normal intestinal cells do not stop growing and do not die to form an early-stage polyp, and 90% of patients with CRC have this type of CPA mutation.

Mouse models deficient in APC and control mice had free access to sugar water with 25% HFCS composed of a 45:55 glucose / fructose ratio; both groups became obese in 2 months and the controls developed a metabolic syndrome. Another group of modified animals was syringe-fed with a daily amount of HFC water equivalent to a can of soft drink consumed by a human; these animals did not become obese or did not develop a metabolic syndrome; however, after 2 months, they developed larger and higher grade tumors than those developed in control mice with unsweetened water. Similar results were obtained in different models developing tumors in the colon rather than in the small intestine.

The researchers suggest "Chronic consumption of small amounts of high fructose corn syrup facilitates tumor growth in cases of PCA deficiency, regardless of obesity and metabolic syndrome. Tumors at an early stage can occur by chance and without notice. Even modest consumption of HFCS can stimulate tumor growth and progression regardless of obesity. This may explain why the increase in HFCS consumption over the last three decades is correlated with the increase in CRC rates in the 25 to 50 age group in the United States .

While studying the mechanism by which HFCS can promote tumor growth, the APC – / – models that were administered by syringe with a moderate amount of HFCS were found to have high glucose and fructose levels in the column; tumors effectively using both types different routes. Fructose appears to be retained by tumors; the amounts reaching the liver and serum were reduced in modified animals with tumors, which meant that fructose was trapped by the tumor rather than transported to the liver and blood.

Although metabolized differently, fructose and glucose have a calorific value and similar structures. Techniques such as radiolabeling were used to trace the fate of each in modified animals in order to discover that fructose was being converted to fructose-1 phosphate in tumors; the altered metabolism of the tumor cells and the fatty acids generated favored tumor growth. "The results suggest that the role of fructose in tumors is to enhance the role of glucose in the synthesis of fatty acid synthesis.Cancer cells can use the resulting abundance to form cell membranes and for the molecules to signaling are developing and have a significant inflammatory effect "

Then, the APC-deficient mice were modified so as not to possess genes encoding the KHK enzyme involved in the metabolism of fructose, or FASN, which is a key enzyme in fatty acid synthesis. The modified animals deficient in one or the other did not develop larger tumors than those observed in the APC deficient mice of origin, even when they were fed the same way. "The results reveal that CRC uses HFCS as a fuel to increase tumor growth rates; and shows a direct molecular mechanism for the correlation between sugar consumption and colorectal cancer. "

It was concluded that "High fructose corn syrup contributes to intestinal tumorigenesis in mice by accelerating de novo glycolysis and lipogenesis, with effects independent of obesity and metabolic syndrome. HFCS rapidly increases glucose and fructose levels in the intestinal lumen and serum, allowing intestinal tumors to resume their growth. "

"Fructose is not essential for the survival and growth of normal cells, suggesting that therapies targeting fructose metabolism deserve to be explored. Avoiding sugary drinks such as these as much as possible instead of depending on drugs would reduce the availability of sugar in the colon. " according to the researchers. "Further research is needed to determine if the results can be extrapolated to humans. Taken together, the results suggest that the therapeutic targeting of fructose metabolism may be a strategy for slowing the progression of colorectal cancer. "