AMD-like lesions delayed in mice fed lower glycemic index diet
Nov 14, 2011 - 5:00:00 AM
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We presume the elevated accumulation of AGEs we saw in the retina of the higher GI group is associated with toxicity. The AGEs result from the modification of proteins by excess glucose and this compounds the normal protein damage that happens as we age, says Karen Weikel, first author and a PhD candidate at the Friedman School of Nutrition Science and Policy at Tufts. While previous research has linked higher GI diets to AGE accumulation in the blood, ours appears to be the first to show diet-related AGE presence in tissue, such as the retina, which becomes the site of the eye disease.
By Tufts University, Health Sciences Campus,
[RxPG] BOSTON (November 14, 2011) -- Feeding older mice a lower glycemic index (GI) diet consisting of slowly-digested carbohydrates delays the onset of age-related, sight-threatening retinal lesions, according to a new study from the Laboratory for Nutrition and Vision Research at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University.
The researchers studied middle-aged and older mice that consumed either a higher or lower GI diet. Mice fed the lower GI diet developed fewer and less-severe age-related lesions in the retina than the mice fed the higher GI diet. The lesions included basal laminar deposits, which typically develop after age 60 in the human retina and are the earliest warning sign of Age-Related Macular Degeneration (AMD).
To our knowledge, we have established the first mature, mammalian model indicating a delay in the development of AMD-like lesions as the result of a lower GI diet, says Allen Taylor, PhD, director of the Laboratory for Nutrition and Vision Research at the USDA HNRCA. The only difference between the two groups of mice we studied is the GI of their meals, which suggests that diet alone is enough to accelerate or delay the formation of lesions. These results, coupled with similar observations made by our laboratory in earlier human epidemiologic studies imply that lower GI diets hold potential as an early intervention for preventing onset and progress of AMD.
The dietary glycemic index (DGI) measures the rate at which glucose is delivered to the bloodstream after consuming carbohydrates. Higher GI foods including white bread and white potatoes trigger a rapid delivery of glucose that pushes the body to work overtime to absorb, whereas lower GI foods, like whole grain bread and fruits and vegetables, initiate a slower release of glucose that is more easily processed by cells.
Compared to the mice on the lower GI diet, mice on the higher GI diet demonstrated elevated accumulations of debris known as advanced glycation end products (AGEs) in the whole retina, particularly in the cells of the RPE. The RPE plays a crucial role in maintaining vision and its dysfunction results in the gradual central vision loss that is the hallmark of AMD. AGE accumulation has also been linked to tissue damage in other age-related diseases such as Type 2 diabetes and cardiovascular disease.
We presume the elevated accumulation of AGEs we saw in the retina of the higher GI group is associated with toxicity. The AGEs result from the modification of proteins by excess glucose and this compounds the normal protein damage that happens as we age, says Karen Weikel, first author and a PhD candidate at the Friedman School of Nutrition Science and Policy at Tufts. While previous research has linked higher GI diets to AGE accumulation in the blood, ours appears to be the first to show diet-related AGE presence in tissue, such as the retina, which becomes the site of the eye disease.
The research, published online in October in the journal
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