A groundbreaking study conducted by researchers at The University of Texas MD Anderson Cancer Center has unveiled a compelling link between the consumption of sugar-sweetened beverages and the progression of metastatic colorectal cancer. This preclinical research, recently published in the high-impact journal Nature Metabolism, provides the first direct evidence that the glucose and fructose blend commonly found in sodas and fruit juices actively fuels cancer metastasis through a metabolic enzyme called sorbitol dehydrogenase (SORD). These findings could usher in new dietary and therapeutic strategies to combat one of the deadliest aspects of colorectal cancer.
Metastasis — the spread of cancer cells from the original tumor site to distant organs — remains the principal cause of mortality in colorectal cancer patients. Until now, the molecular mechanisms by which diet, especially sugary beverage intake, might influence the metastatic progression of colorectal cancer have been elusive. The MD Anderson team, led by Dr. Jihye Yun, assistant professor of Genetics, deployed sophisticated laboratory models to dissect how the combined sugars glucose and fructose uniquely stimulate colorectal cancer cells to become more mobile and invade the liver, which is the most frequent metastasis site in patients.
Dr. Yun’s group discovered that exposure to mixtures of glucose and fructose, mimicking the sugar composition in typical sweetened drinks, activates SORD — an enzyme pivotal in catalyzing the oxidation of sorbitol to fructose, thus modulating carbohydrate metabolism. This activation amplifies glucose flux and initiates a cholesterol biosynthesis pathway, fueling cellular mechanisms critical for cancer cells’ motility and metastatic capacity. Intriguingly, the cholesterol pathway stimulated by SORD activity is the same target inhibited by statins, a widely used class of drugs for cardiovascular disease prevention. This biochemical intersection suggests unexplored possibilities for repurposing statins as adjuvant therapies to slow or prevent colorectal cancer metastasis.
By selectively blocking the SORD enzyme in experimental models, the researchers observed a significant deceleration of metastatic dissemination, even in the presence of high sugar mixtures. These results not only solidify SORD’s role as a metabolic driver of cancer progression but also highlight it as a promising therapeutic target. The metabolic rewiring caused by the glucose-fructose combo contrasts sharply with the effects of glucose or fructose alone, neither of which triggered the aggressive metastatic phenotype, underscoring the unique pathological synergy of these sugars.
The study follows earlier work from the same laboratory that challenged the conventional assumption that sugary drink consumption influences colorectal cancer risk merely through obesity-related mechanisms. Instead, even moderate intake of these beverages directly enhanced tumor growth in early-stage colorectal cancer, independently of obesity. The current research extends these insights by focusing on late-stage cancer dynamics, illustrating that diet not only affects cancer risk but also profoundly modulates disease progression at advanced stages.
From a molecular biology standpoint, SORD’s role in the sorbitol pathway acts as a metabolic switch that tips cancer cells toward increased energy production and membrane remodeling, necessary prerequisites for invasion and colonization of distant tissues. The cholesterol biosynthesis pathway activated downstream further provides essential lipids for membrane fluidity, signaling complexes, and other structural components that support metastatic competency. This intricate metabolic crosstalk elucidates how simple dietary sugars can be harnessed by cancer cells to augment malignancy.
Clinically, these findings come at a critical time when nutritional recommendations for colorectal cancer patients often include high-calorie liquid supplements laden with glucose and fructose to maintain weight and stamina. While these supplements serve immediate nutritional needs, the study raises red flags about potential unintended consequences on metastatic progression. This paradox highlights the pressing need for nuanced dietary guidelines that balance caloric requirements without exacerbating cancer dissemination.
The implications of this research extend beyond patient care to public health policies targeting sugar consumption. As colorectal cancer remains a leading cause of cancer deaths worldwide, the evidence linking sugary drink intake to metastasis advocates for stronger advisories and interventions aimed at reducing these beverages in vulnerable populations. Furthermore, uncovering metabolic enzymes like SORD as mediators of cancer aggressiveness opens new frontiers for drug development and precision oncology approaches.
Experts emphasize that although these findings are based on preclinical models, they warrant urgent clinical investigation to validate the translational potential of targeting SORD or repurposing statins in colorectal cancer patients. The convergence of metabolic research and cancer biology exemplified in this study epitomizes a paradigm shift toward understanding how systemic metabolic environments influence tumor behavior.
Dr. Yun and her colleagues envisage future clinical trials exploring whether pharmacological inhibition of SORD combined with dietary modifications can attenuate metastatic progression and improve patient survival. They also advocate for integrating metabolic enzyme profiling into personalized cancer treatment plans to identify individuals with heightened metabolic vulnerabilities.
This extensive inquiry was supported by the National Cancer Institute (NCI), the Pew-Stewart Scholars for Cancer Research program, the Cancer Prevention and Research Institute of Texas (CPRIT), alongside other notable fellowships, underscoring important institutional commitment to uncovering diet-cancer interactions. The comprehensive mechanistic insights unveiled reflect years of rigorous experimental work grounded in cutting-edge genetic, biochemical, and metabolic methodologies.
In conclusion, this research fundamentally reshapes our understanding of how the glucose-fructose combination in everyday sugary drinks does more than provide empty calories — it acts as a biochemical catalyst of colorectal cancer metastasis. Targeting the metabolic axis mediated by SORD holds unprecedented promise for disrupting this lethal process while reinforcing the critical message that diet and metabolism are inseparable from cancer pathophysiology. As the field advances, these discoveries beckon a future where cancer treatment incorporates metabolic and dietary strategies as central pillars.
Subject of Research: Colorectal cancer metastasis and metabolic effects of glucose-fructose consumption
Article Title: Fructose and glucose from sugary drinks enhance colorectal cancer metastasis via SORD
News Publication Date: 19-Sep-2025
Web References:
MD Anderson Cancer Center
Colorectal Cancer Info at MD Anderson
Original paper in Nature Metabolism
References: 10.1038/s42255-025-01368-w
Image Credits: Not specified
Keywords: Colorectal cancer, cancer metastasis, sugary drinks, glucose-fructose blend, sorbitol dehydrogenase (SORD), cholesterol pathway, statins, cancer metabolism
Tags: colorectal cancer metastasis mechanismsdietary strategies for cancer preventionglucose fructose blend and cancer cellsimpact of diet on cancer progressionliver metastasis in colorectal cancermetabolic enzymes and cancer metastasisnew findings in cancer researchpreclinical studies on cancer treatmentsoft drinks and health riskssorbitol dehydrogenase in cancer metabolismsugary drinks and colorectal cancerUniversity of Texas MD Anderson research
