Does Sugar Really Feed Cancer? Exploring the Facts

Author: University of Utah Health Sciences
Published: 2009/08/17 - Updated: 2025/04/08
Publication Details: Peer-Reviewed, Findings
Category Topic: Cancer and Tumors - Academic Publications

Page Content: Synopsis - Introduction - Main - Insights, Updates

Synopsis: This article examines the controversial topic of whether sugar consumption directly contributes to cancer growth. It provides a nuanced perspective, explaining that while all cells, including cancer cells, require glucose for energy, there is no direct evidence that consuming sugar accelerates cancer growth. Instead, it explores how excess sugar intake may indirectly influence cancer progression through mechanisms like inflammation and metabolic changes. The article is valuable for individuals, including seniors and those with disabilities, as it clarifies misconceptions about dietary sugar and cancer, helping readers make informed decisions about their health and nutrition - Disabled World (DW).

Introduction

During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). Glucose and glutamine are both essential for cell growth, and it was long assumed they operated independently, but Ayer's research shows they are inter-dependent.

Main Content

Researchers at Huntsman Cancer Institute at the University of Utah have uncovered new information on the notion that sugar "feeds" tumors.

The findings may also have implications for other diseases such as diabetes. The research is published in the journal Proceedings of the National Academy of Sciences.

"It's been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth," says Don Ayer, Ph.D., a Huntsman Cancer Institute investigator and professor in the Department of Oncological Sciences at the University of Utah.

During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). Glucose and glutamine are both essential for cell growth, and it was long assumed they operated independently, but Ayer's research shows they are inter-dependent. He discovered that by restricting glutamine availability, glucose utilization is also stopped.

"Essentially, if you don't have glutamine, the cell is short circuited due to a lack of glucose, which halts the growth of the tumor cell" Ayer says.

The research, spearheaded by Mohan Kaadige, Ph.D., a postdoctoral fellow in Ayer's lab, focused on MondoA, a protein that is responsible for turning genes on and off. In the presence of glutamine, MondoA blocks the expression of a gene called TXNIP. TXNIP is thought to be a tumor suppressor, but when it's blocked by MondoA, it allows cells to take up glucose, which in turn drives tumor growth.

Ayer's research could lead to new drugs that would target glutamine utilization, or target MondoA or TXNIP. Ayer says the next step in his research is to develop animal models to test his ideas about how MondoA and TXNIP control cell growth.

"If we can understand that, we can break the cycle of glucose utilization which could be beneficial in the treatment of cancer," Ayer says.

Reference:

Huntsman Cancer Institute at the University of Utah marks its 10th anniversary in 2009. HCI was founded by Jon M. Huntsman to fulfill his dream of finding a cure for cancer through genetic research. In the last 10 years, HCI has grown to become one of America's major cancer research centers. HCI is part of the University of Utah healthcare system and is ranked consistently by U.S. News & World Report as one of the top cancer hospitals in the country.

Insights, Analysis, and Developments

Attribution/Source(s): This peer reviewed publication was selected for publishing by the editors of Disabled World (DW) due to its relevance to the disability community. Originally authored by University of Utah Health Sciences and published on 2009/08/17, this content may have been edited for style, clarity, or brevity.