The mechanisms of how glucose restricted diets may offer protection from cancer

This study was published in the Federation of American Societies for Experimental Biology Journal 2010 May;24(5):1442-53

Study title and authors:
Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression.

Li Y, Liu L, Tollefsbol TO.
Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/20019239

WI-38 cells are a type of human cell (used in laboratories) derived from foetal lung tissue. Immortalized WI-38 (WI-38/S) cells, are cells derived from WI-38 cells which have been infected with the simian virus-40 antigen. The simian virus-40 has been found in brain, bone and lung-related cancers. 

hTERT (human telomerase reverse transcriptase), is an enzyme that is found in high numbers in 90% of malignant tumors but in smaller numbers in normal cells. However very low concentrations of hTERT are associated with decreased fertility, impaired wound healing, and reduced production of blood cells and immune system cells. Low hTERT is also associated with shorter lives and increased risk of death from heart disease and infectious diseases.  
 
p16(INK4a) also known as multiple tumor suppressor 1 (MTS-1), is a tumor suppressor protein that regulate the cell cycle and protects against cancer. However high concentrations of p16(INK4a) are associated with faster aging.

This study assessed the effects that glucose restriction has on healthy cells and precancerous cells. WI-38 (normal healthy cells) and WI-38/S (precancerous cells) were cultured in a regular glucose medium or a restricted glucose medium.

The study found:
(a) Normal healthy cells cultured in the glucose restricted medium had an extended lifespan compared to normal healthy cells cultured in the regular glucose medium.
(b) Precancerous cells cultured in the glucose restricted medium had decreased proliferation and increased cell death rates compared to precancerous cells cultured in the regular glucose medium.
(c) Normal healthy cells cultured in the glucose restricted medium had an increase in hTERT compared to normal healthy cells cultured in the regular glucose medium. 
(d) Precancerous cells cultured in the glucose restricted medium had a decrease in hTERT compared to precancerous cells cultured in the regular glucose medium.
(e) Normal healthy cells cultured in the glucose restricted medium had a decrease in p16(INK4a) compared to normal healthy cells cultured in the regular glucose medium.
(f) Precancerous cells cultured in the glucose restricted medium had an increase in p16(INK4a) compared to precancerous cells cultured in the regular glucose medium.

In the glucose restricted medium the normal healthy cells saw their hTERT rise and p16(INK4a) decrease, which would explain the boost in healthy cell growth whereas in the precancerous cells, their hTERT decreased and their anticancer protein p16(INK4a) increased, which explains why these cancer-forming cells died off in large numbers

The results from this study show the mechanisms of how glucose restricted diets may offer protection from cancer.