Introduced in the 1970s as an abundant and cheap sweetening agent, high-fructose corn syrup has become so popular that every American now consumes about sixty pounds a year.
Whenever Diabetes Health publishes an article about high fructose corn syrup (HFCS), we receive mountains of printed material from corn industry advocates. They argue that the effects of HFCS cannot be extrapolated from research because the "studies look at the effects of fructose independently." They claim, in the words of Christopher Mohr, MS, RD, LDN, of the Corn Refiners Association, that "the absence of glucose makes pure fructose fundamentally different from HFCS."
Diabetes Health doesn't have the wherewithal at the moment to examine all sides of the argument. We suggest that if the topic interests you, you do your own due diligence and come to your own conclusion. In the meantime, Yale University researchers say that a study in mice shows that diets heavy in high-fructose corn syrup can lead to insulin resistance. At the same time they found that if they blocked the activity of a gene called PGC-1B, mice on a high-fructose diet were protected from insulin resistance.
Introduced in the 1970s as an abundant and cheap sweetening agent, high-fructose corn syrup has become so popular that every American now consumes about sixty pounds a year. For that reason, the sweetener has become a source of concern to doctors and scientists who treat metabolic disorders. Because the liver more readily metabolizes fructose into fat than it does glucose, high fructose consumption can lead to non-alcoholic fatty liver disorder, often a precursor to insulin resistance and type 2 diabetes.
While earlier studies had pointed to a gene called SREBP-1, which regulates the manufacture of lipids in the liver, as the primary cause for increased fatty acids and triglycerides in that organ, researchers weren't sure just how it worked.
When the Yale researchers found that PGC-1B might be responsible for boosting expression levels of SREBP-1, they tested their suspicion by blocking its activity in mice that were being fed a four-week diet high in fructose. Blocking PGC-1B lowered the expression levels of SREBP-1 and other fat building genes in their livers, reversed their insulin resistance, and led to a tripling of glucose uptake in their fatty tissue.
Practical benefits from this line of research could lead to a gene-specific therapy designed to help lower insulin resistance.