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A high-fat diet will increase the possibility of cancer
A high-fat diet will increase the possibility of cancer. A high-fat diet will make the normal liver behave like cancerous tissue, increasing the possibility of cancer.
When exposed to a high-fat diet, metabolic changes occur in normal untransformed liver cells, and this fat-induced change is similar to the metabolic state of aggressive liver cancer cells.
Hepatocellular carcinoma (HCC) is a high-mortality malignant tumor originating from normal liver cells, accounting for 90% of primary liver cancer, and ranking third on the global cancer-related death list. Obesity, smoking and diabetes are known to be the main risk factors for liver cancer.
Today, the incidence of obesity and liver cancer is increasing year by year worldwide. Therefore, understanding how excess fat leads to liver cancer is essential for identifying the pathogenesis and finding effective treatments.
Recently, researchers from VIB-KU Leuven Cancer Biology Center in Belgium published a research paper titled “Fat induces glucose metabolism in non-transformed liver cells and promotes liver tumorigenesis” in Cancer Research.
The study found that when exposed to a high-fat diet, normal untransformed liver cells undergo metabolic changes, and this fat-induced change is similar to the metabolic state of aggressive liver cancer cells. In short, when the liver is exposed to excess fat, normal liver tissue is more likely to become cancerous. This discovery will
Diet, obesity and liver cancer are directly linked.
The effective utilization of tissue environment and nutrients are important regulators of cellular processes. Many cancer-related studies have shown that, compared with primary tumors, the effective utilization of nutrients can directly regulate cell metabolism by defining metabolic dependence, metabolic heterogeneity within the tumor, and metastatic components. These studies emphasize the importance of studying cell metabolism in the context of increasing nutrient supply.
In this study, the research team studied normal tissue metabolism under disease conditions and compared the metabolism between different tissues. By comparison, they observed a signal-independent metabolic link of nutrient availability.
First, the researchers tested the metabolic changes in the liver tissue of mice fed a high-fat diet at the early stage when no tumors appeared and at the late stage of tumor formation. They found that before there was any clue that cancer was developing, liver cells used glucose in the same way as tumors. This way of consuming a lot of glucose is one of the well-known characteristics of cancer, the famous “Warburg effect”.
Subsequently, the researchers studied what happens when the tumor is fully formed and measured the sensitivity of the mice to glucose.
The corresponding author of the study, Professor Sarah-Maria Fendt of the Cell Metabolism and Metabolic Regulation Laboratory of the VIB-KU Leuven Cancer Biology Center said: “It’s surprising that despite diabetes, people who are fed a high-fat diet get cancer. Mice can consume glucose in the blood as easily as healthy mice.”
As we all know, too much fat is the main cause of insulin resistance. It suppresses insulin signals in the liver and skeletal muscles. Insulin resistance can also reduce glucose uptake in the liver and skeletal muscle and increase liver gluconeogenesis. The important thing is that fat can directly change the metabolism of non-transformed cells in the liver.
Using the most advanced glucose-13C6 tracking technology, researchers observed how glucose molecules are used in cells and tissues. They found that regardless of whether the mice were fed a high-fat diet or a normal diet, the tumor tissue would break down glucose in a consistent manner.
These findings indicate that when normal liver cells transform into cancer cells, their metabolism will continue to increase glucose consumption. Since a high-fat diet can cause these changes before cancer, this means that under a high-fat diet, non-cancer liver tissue is more likely to become cancerous.
Mice fed a high-fat diet showed increased production of lactic acid when stimulated by glucose. Subsequently, the team tested whether this similar change would occur in the human body. They tested the metabolic response of 20 healthy volunteers after taking glucose pills and observed a correlation between waist circumference and lactic acid production.
The research team also studied the underlying mechanism of this effect, and they found that before any cancer occurs, liver tissue exposed to high fat seems to use another type of fat metabolism in a cell compartment called peroxisomes. way. Using liver cancer cells, the researchers confirmed that peroxisome metabolism increases cellular stress and glucose uptake.
This study confirmed that a high-fat diet can promote the formation of liver cancer in mice, and regardless of the diet background, the glucose metabolism changes of all mouse tumors are similar to those of non-transformed mouse liver exposed to fat. This means that fat can induce glucose-mediated metabolic changes in non-transformed liver cells, and this change is exactly similar to the metabolic changes found in hepatocellular carcinoma.
(source:internet, reference only)