Researchers at the Rogel Cancer Center at the University of Michigan found that intranuclear receptors activated by synthetic substances in a high-fat diet and a disordered exercise capacity enhancer promote the progression of precancerous pancreatic lesions to pancreatic cancer. Found to promote.
Pancreatic duct adenocarcinoma is a very deadly form cancer Outbreaks are on the rise and there is an urgent need for strategies to prevent and treat the disease.Most of the time Pancreatic cancer Outcomes from preCancerous lesions Called pancreatic intraepithelial neoplasia; it is estimated that approximately 55-80% of adults over the age of 40 have these low-grade precancerous asymptomatic pancreatic lesions.Research published in Nature CommunicationsPrecancerous pancreatic lesions in mice, led by Imad Shureiqi, MD, have been shown to contain high levels of the transcriptional receptor peroxisome proliferator-activated receptor delta (PPARδ), similar to those found in humans.
PPARδ regulates the expression of a wide range of important genes that affect biological processes, including: Lipid metabolism And the formation of cancer. Activation of PPARδ dramatically accelerates the progression of precancerous lesions to pancreatic cancer. Shureiqi previously conducted much of this research at the MD Anderson Cancer Center at the University of Texas. In particular, in collaboration with Xiangsheng Zuo, MD, and Ph.D., he transferred his research to the Rogel Cancer Center at the University of Michigan in 2020.
“Previous observations have shown that PPARδ strongly promotes other gastrointestinal cancers, so I was interested in studying the effects of PPARδ on the development of pancreatic cancer. However, PPARδ in the development of pancreatic cancer. Information about the role of is very limited, “Shureiqi said.
Activation of PPARδ correlates with excessive exposure to specific substances Ligand, Both natural and synthetic. Some ligands occur naturally on a high-fat diet and are associated with an increased risk of pancreatic cancer in human and animal models. High-fat diets are rich in fatty acids, the natural ligand for PPARδ.
Other synthetic forms of PPARδ ligands, such as cardalin (GW501516), are included in exercise supplements aimed at increasing physical fitness and endurance. The GW501516 was originally designed by a pharmaceutical company to encourage the body to use more fat and treat non-cancerous conditions such as obesity and hyperlipidemia. Drug development of GW501516 and other powerful PPARδ agonists for similar medical use has long been discontinued due to their potential precancerous side effects. Studies on how PPARδ affects Colorectal cancer Back in 1999, pharmaceutical companies stopped developing synthetic PPARδ ligands, but unregulated internet retailers still sell substances like cardalin. Advertisements are primarily sold to young people and claim to help increase muscle endurance and burn fat.
Shureiqi explains that researchers initially discovered that these synthetic ligands reduce fatigue in mice. The news came to the major media, nicknamed “exercise with pills.” “Unfortunately, what the media didn’t cover was the dark side of PPARδ. Like muscle cells, synthetic PPARδ ligands help cancer cells get more energy from fat as a fuel source.” He said.
“It’s shocking to me,” continued Shureiqi. “Animal models repeatedly show a strong relationship between PPARδ and cancer promotion in the case of colorectal cancer. stomach cancer.. We are currently getting more information on how it affects pancreatic cancer. “
Key factors that promote the progression of silent precancerous lesions to pancreatic cancer remain poorly defined, especially those that are easy to target. Most of these precancerous lesions do not develop into cancer, but it is still important to understand how they progress in order to find interventions to address the growth rate of pancreatic cancer. The results of this study show that people with asymptomatic precancerous lesions, even at low grades, consume synthetics such as PPARδ natural activators or cardalin, such as high-fat diets. It has been shown to have the potential to increase the risk of developing pancreatic cancer. Future development of effective agents that block the activation of PPARδ may be a new approach to prevent the progression of precancerous lesions to pancreatic cancer. Limiting exposure to a high-fat diet can also be considered for people with a high prevalence of precancerous pancreatic lesions. But so far, the general sale and use of these exercise-promoting synthetic PPARδ activators raises the most pressing concerns.
“This new information should warn individuals about the potential serious health risks of using synthetic PPARδ agonists,” Shureiqi said. “We are trying to spread the message that using these substances is not a good idea. It may increase the endurance of muscles, but it also increases the ability of cancer to grow using energy. increase.”
Rapid acceleration of KRAS mutant pancreatic carcinogenesis through remodeling of tumor immune microenvironment by Yi Liu et al, PPARδ, Nature Communications (2022). DOI: 10.1038 / s41467-022-30392-7
University of Michigan
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High-fat diet and chaotic exercise endurance enhancer associated with pancreatic cancer risk
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