Fructose consumption has increased considerably over the past five decades, largely due to the widespread use of high-fructose corn syrup as a sweetener1. It has been proposed that fructose promotes the growth of some tumours directly by serving as a fuel2,3. Here we show that fructose supplementation enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer without causing weight gain or insulin resistance. The cancer cells themselves were unable to use fructose readily as a nutrient because they did not express ketohexokinase-C (KHK-C). Primary hepatocytes did express KHK-C, resulting in fructolysis and the excretion of a variety of lipid species, including lysophosphatidylcholines (LPCs). In co-culture experiments, hepatocyte-derived LPCs were consumed by cancer cells and used to generate phosphatidylcholines, the major phospholipid of cell membranes. In vivo, supplementation with high-fructose corn syrup increased several LPC species by more than sevenfold in the serum. Administration of LPCs to mice was sufficient to increase tumour growth. Pharmacological inhibition of ketohexokinase had no direct effect on cancer cells, but it decreased circulating LPC levels and prevented fructose-mediated tumour growth in vivo. These findings reveal that fructose supplementation increases circulating nutrients such as LPCs, which can enhance tumour growth through a cell non-autonomous mechanism.

TLDR - “In all cases, diets supplemented with HFCS resulted in faster tumour growth compared with control diets”

I’m having trouble finding the full text of the paper, normal avenues 🦜 are a little behind

https://pubmed.ncbi.nlm.nih.gov/39633044/

  • jetOPMA
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    8 days ago

    The puzzle is

    “Dietary fructose supports tumour growth in vivo but fructose is not efficiently metabolized by cancer cells in vitro”

    "As expected, we saw extensive metabolism of glucose in all of the experiments as represented by 13 C enrichment in lactate. To the contrary, we observed minimal metabolism of the fructose label in all of the cell lines analysed. "

    Cancer cells thrive on glucose, but not fructose, yet fructose intake directly yields cancer cell growth. Puzzle deepens.

    I’m probably getting the details wrong: Ketohexokinase levels are low in most cancer cells, but the liver (when exposed to fructose) will express LPCs which then the cancer cells convert into phosphatidylcholines… basically this is a pathway for fructose to feed cancer cells (indirectly with the help of the liver)

    I’m not sure what LPC means - liver progenitor cell perhaps?