lundi 16 septembre 2013

More on fructose and Met syndrome


"We are now suffering a huge epidemic of metabolic syndrome... and we can correlate the onset of the epidemic with the increased consumption of sugars,"
"The changes in the wild type mice were brought on by fructose converted from glucose via the polyol pathway, wrote Miguel A. Lanaspa, DVM, PhD, asssistant research professor of medicine at the University of Colorado, and his co-authors.
The polyol pathway is triggered by high serum glucose. When that happens, aldose reductase (AR) metabolizes glucose to sorbitol, which is converted to fructose by sorbitol dehydrogenase."










So is it endogenous fructose, exogenous fructose or both? In humans we don't know but fructose is in the box...

Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome




Abstract


Carbohydrates with high glycaemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations are known to induce the polyol pathway and increase fructosegeneration in the liver. Here we show that this hepatic, endogenously produced fructose causes systemic metabolic changes. We demonstrate that mice unable to metabolize fructose are protected from an increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels and hyperleptinaemia after exposure to 10% glucose for 14 weeks. In normal mice, glucose consumption is accompanied by aldose reductase and polyol pathway activation in steatotic areas. In this regard, we show that aldose reductase-deficient mice are protected against glucose-induced fatty liver. We conclude that endogenous fructose generation and metabolism in the liver represents an important mechanism by which glucose promotes the development of metabolic syndrome.


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