Cell Metab: The world is "anti-sugar" to see what cell sub-journals say

Sugar as one of the body's three major energy, proper sugar intake can provide energy for our body, so that we maintain health and happy mood.
Because fructose tastes better than glucose, but has a poor satiety, fructose accounts for about 10 percent of total calorie intake in the United States, but increased fructose intake often leads to obesity and metabolic syndrome.
recent years, several studies have shown that fructose is not only a potential cause of cancer, but also a "complementary fuel" for cancer cell proliferation and metastasis.
GLUT5 is a fructose transport protein.
GLUT5 was significantly increased in non-small cell lung cancer samples to help cancer cells metabolize fructose and multiply under conditions of limited glucose.
, studies have shown that high fructose intake can also lead to accelerated tumor growth.
little is known about fructose metabolism in the liver and small intestine, and an in-depth understanding of fructose metabolism in tumors is of great significance for the diagnosis and treatment of tumors.
recently, Cell Metabolism published online a study by Kayvan R. Keshari and Michael G. Kharas of memorial Sloan-Kettering Cancer Center in the United States called "High Fructose Drives the Serine Synthesis Pathway in Myeloid Acute Leukemic Cells."
the study showed that high fructose in acute myeloid leukemia cells drives the synthesized pathway of serine.
, the researchers studied fructose metabolism in leukemia cells using four leukemia cell line MOLM13 (FLT3-ITD AML), K562 (BCR-ABL CML), THP1 (MLL-AF9 AML) and KASUMI1 (AML1-ETO AML).
results show that high fructose can promote the proliferation of leukemia cells.
and in fructose-rich conditions, leukemia cells significantly rely on the synthesized pathway (SSP) from the head, metabolizeing fructose through ketohexyl kinase (KHK).
high fructose promotes the proliferation of leukemia cells, the researchers tested the expression levels of metabolic enzymes and GLUT5, the main fructose transporter.
the proportion of cells with low levels of GLUT5 in fructose cultures of .2-13C/2-13C lactic acid increased significantly.
Therefore, the level of expression of GLUT5 determines the absorption level of fructose, which is the key factor in determining the difference in fructose metabolism, and the absorption of fructose can regulate the flugy of SSP by the ratio of oxidizing coenzyme (NAD plus)/also prototype coenzyme (NADH).
in addition to low GLUT5 leukemia cells relying on SSP under fructose-rich conditions, the researchers also found that normal hematocytes/progeny cells did not observe changes in SSP fluform under fructose-rich conditions.
speed-limiting enzyme phosphate dehydrogenase (PHGDH), which targets SSP, inhibits the use of fructose by leukemia cells and promotes survival in mice.
high fructose-driven serine synthesis pathway, the researchers found the potential mechanism of fructose metabolism in leukemia cells.
More importantly, SSP plays an important role in the metabolic adaptation of leukemia cells in a high fructose environment, and this dependence is not observed in normal hematocyte CD34 plus cells, so inhibiting SSP can provide a new leukemia treatment strategy.
addition, remind small partners, moderate intake of sugar is also very important Oh!