Saturday, 18 August 2007

sugar consumption = premature aging

There are several factors which contribute to aging in modern society: mainly genetics, diet, stress and lifestyle factors. I have often wondered whether sugar does really cause aging most especially when i develop sugar cravings usually satiated by chocolate and my newly found craze of Nando's chocolate mousse. However I have never actually looked at these studies which support the findings that sugar induces premature aging but mainly just believed the hype in the media. So, I decided to briefly review a recent manuscript which asks this question and conducts experiments at the molecular level, and confirms previous findings. So as i speak, i believe i am spiralling into premature death by chocolate.
A manuscript by Berge et al. (2007) demonstrated that normal human epidermal keratinocytes (primary cells) treated with 100 mM glucose or 0.1 mM gyoxal* for three days induced premature aging. Their experimental methods included examining the phenotype of cells, cell proliferation and cell viability assays, an assay to examine glycoxidatively damaged proteins, and examination of differentiation markers of the cell.
Findings: Using cell proliferation and cell viability assays, the cell number, proliferation rate and viability was measured and found to have decreased in a dose-dependent manner at a glucose concentration of 100 mM and above relative to controls. In contrast, 0.1 mM of glyoxal and above induced a reduction in the previously mentioned parameters in a dose-dependent manner relative to controls. The LD50 for glucose and glyoxal was 200 mM and 50 uM, respectively. The authors state that the possible reason for the difference in LD50 values could be due to glyoxal having a higher reactivity and easier penetration of the cell membrane. Examination of cell morphology demonstrated that cells treated with the same levels of sugar induced vacuolation (formation of vacuoles) and increase in cell size, both of which are characteristic of senescent** cells. Results from assays targeted to measuring aging cells, including the senescence-associated beta-galactosidase and protein glycoxidation***, were significantly higher in cells treated with the sugars compared to control cells after three days of treatment. Glucose caused a 52% and 58% increase and glyoxal a 44% and 68% increase in the senescence-associated beta-galactosidase and protein glycoxidation assays, respectively. Glycoxidation of proteins targets these proteins to be degraded by the proteasome because they are of no use or unwanted by the cell. Proteasomal degradation is one of a few ways in which unwanted proteins are targeted and removed by our cells. As a measure of unwanted protein removal, the group measured proteasomal activity and found that glucose-treated cells had an 11% increase in proteasomal activity. Glyoxal treated cells had a 3% decrease which the authors state as "unchanged". Differentiation was examined using involucrin level measurement against a differentiation agent, calcium. Using a positive control of 1.2 mM calcium, glucose treatment of cells resulted in involucrin levels lower than the positive control whereas glyoxal treatment resulted in involucrin levels similar to and higher than the positive control.
Conclusions: Glucose concentrations of 100 mM and glyoxal concentrations of 0.1 mM and the above indicators of cell senescence in human epidermal keratinocytes have re-confirmed that sugar is able to induce premature aging.

That Mars bar doesn't look so appetising now, does it?


Source: Berge, U, Behrens, J and Rattan, SI. Sugar-Induced Premature Aging and Altered Differentiation in Human Epidermal Keratinocytes. Annals of New York Academy of Science. Volume 1100: 524-529 (2007).


* The paper refers to the term glyoxal, which i assume is methylglyoxal. Methylglyoxal is a by-product of glycolysis (sugar breakdown).

** Cellular senescence, which is when cells arrest in a non-dividing state, is synonomous with aging in the biological context.

***Glycoxidation is the oxidative alteration of a protein by a sugar and forms advanced glycation end products which are known contributors of aging.

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