A diet containing large amounts of fructose is even more unhealthy than you probably realised. Fructose not only leads to gradual weight increase, it also boosts the activity of the stress hormone cortisol. Serbian biochemists have demonstrated this effect in rats that were given fructose water to drink.
Nearly all the processed foods we eat contain increasing amounts of fructose in the form of sugar, glucose-fructose syrup or fruit juice. This fructose-based diet that the food industry is serving us is making us fat. Not only because it contains large amounts of hidden energy, but also because a high-fructose diet messes up our appetite and our metabolism. [Hepatology. 2007 Mar;45(3):778-88.] Go ask Robert Lustig.
Biochemists at the University of Belgrade published in the Journal of Nutritional Biochemistry the results of a study in which they examined another potentially fattening aspect of fructose: the effect of cortisol in fat cells.
Throughout the world there are a couple of dozen laboratories that are working on developing slimming aids that deactivate this hormone in fat deposits by blocking the enzyme 11-beta-HSD-1. This is the enzyme that converts the inactive hormone cortisone into the active hormone cortisol. Cortisol is a stress hormone that inhibits muscle growth but stimulates the growth of fat cells.
The Serbian researchers studied two groups of male lab rats. One group was given ordinary drinking water [Control]; the other was given drinking water that contained 10 percent fructose [Fructose].
After nine weeks the rats in the fructose group ate more than the animals in the control group. The fructose rats had slightly more abdominal fat than the control rats, but the difference was not statistically significant.
The amount of free fatty acids [NEFA] in the blood of the fructose rats was significantly higher than the amount in the control rats. If you burn the free fatty acids there’s no problem. If you don’t, a high concentration of free fatty acids in your blood spells disaster in the long term. The fatty acids build up in your muscles and organs and end up sabotaging their functioning.
The fructose diet didn’t increase the number of cortisol receptors [GR] in the fat cells, but the researchers did find considerably higher numbers of cortisol receptors in the cell nuclei. These were probably receptors activated by cortisol, which then pass on instructions to the DNA in the fat cells.
In the fat cells the researchers found more 11-beta-HSD-1 and more H6PDH. H6PDH is an enzyme that provides energy to 11-beta-HSD-1, so it can carry out its work.
The researchers were not able to confirm the theory that 11-beta-HSD-1 and H6PDH blockers are slimming aids. They didn’t observe a significant increase in the abdominal fat of their lab animals, but their study does suggest that a low-fructose diet is interesting for anyone wanting to reduce their cortisol levels.
Fructose consumption enhances glucocorticoid action in rat visceral adipose tissue
Biljana N. Bursa?, Ana D. Djordjevic, Ana D. Vasiljevi?, Danijela D. Vojnovi? Milutinovi?, Nataša A. Veli?kovi?, Nataša M. Nestorovi?, Gordana M. Mati?
Received 5 July 2012; received in revised form 3 September 2012; accepted 13 September 2012. published online 18 December 2012.
The rise in consumption of refined sugars high in fructose appears to be an important factor for the development of obesity and metabolic syndrome. Fructose has been shown to be involved in genesis and progression of the syndrome through deregulation of metabolic pathways in adipose tissue. There is evidence that enhanced glucocorticoid regeneration within adipose tissue, mediated by the enzyme 11beta-hydroxysteroid dehydrogenase Type 1 (11?HSD1), may contribute to adiposity and metabolic disease. 11?HSD1 reductase activity is dependent on NADPH, a cofactor generated by hexose-6-phosphate dehydrogenase (H6PDH). We hypothesized that harmful effects of long-term high fructose consumption could be mediated by alterations in prereceptor glucocorticoid metabolism and glucocorticoid signaling in the adipose tissue of male Wistar rats. We analyzed the effects of 9-week drinking of 10% fructose solution on dyslipidemia, adipose tissue histology and both plasma and tissue corticosterone level. Prereceptor metabolism of glucocorticoids was characterized by determining 11?HSD1 and H6PDH mRNA and protein levels. Glucocorticoid signaling was examined at the level of glucocorticoid receptor (GR) expression and compartmental redistribution, as well as at the level of expression of its target genes (GR, phosphoenolpyruvate carboxyl kinase and hormone-sensitive lipase). Fructose diet led to increased 11?HSD1 and H6PDH expression and elevated corticosterone level within the adipose tissue, which was paralleled with enhanced GR nuclear accumulation. Although the animals did not develop obesity, nonesterified fatty acid and plasma triglyceride levels were elevated, indicating that fructose, through enhanced prereceptor metabolism of glucocorticoids, could set the environment for possible later onset of obesity.