Oh boy! It’s something to do with our diet again! New developments in Metabolic Syndrome

Over the last few decades, Americans have increased their caloric intake substantially.  Aside from eating more, we are making less healthy eating decisions.  Research has indicated several implications from our choices including increased risk for cardiovascular disease and stroke.  Metabolic syndrome predisposes one to future development of cardiovascular disease (Evangelou 2014). 

Metabolic syndrome is characterized by a series of homeostatic imbalances.  Symptoms include elevated blood pressure, hyperglycemia, and hypercholesterolemia (Evangelou 2014).  Metabolic syndrome is also characterized by obesity (Evangelou 2014).  There are several ways to disrupt normal metabolism but researchers have zeroed in on a normal metabolic byproduct within the body that is also the byproduct from substances in our diet.  Fructose and purines from our diet have been shown to be broken down or lead to uric acid production through liver glycolysis and metabolism respectively (DeBosch et al. 2014).  Normally, uric acid is excreted from the body through urine after it is absorbed from the blood by the kidneys (Evangelou 2014).  Elevated levels of uric acid seen in metabolic syndrome suggest that there is a change in the local physiology that helps to remove this byproduct. 

Researchers at Washington University School of Medicine located in St. Louis developed a murine model lacking GLUT9, uric acid transporter within the gut, and protein product of the SLC2A9 gene (DeBosch et al. 2014).  Aside from having decreased uric acid transport from the gut, these mice developed hallmarks of metabolic syndrome between 6 and 8 weeks (DeBosch et al. 2014).  Interestingly enough, the kidney functioned as normal (DeBosch et al. 2014) though it is not clear that this study saw short term adaptations in response to elevated blood uric acid levels.  Possible adaptations include a decreased flow rate within the glomerulus to increase the filtration rate.  

So what does this mean?  Usually when research comes out and says that something related to the diet is linked to a disorder, there is a motion to start avoiding foods that contain that compound.  However, in this situation, we can’t avoid uric acid all together because it is a normal byproduct of metabolism within our bodies (Evangelou 2014).  Decreasing our fructose intake and foods that contain purines may help in the future because these foods lead to uric acid production which can increase uric acid blood levels.  Future research hopes to develop the implications of high fructose intake on metabolic syndrome by studying mice on a high fructose diet (DeBosch et al. 2014).  Our diet can predispose use to a lot of complications including metabolic syndrome, so as a nation, it would be worthwhile to continue making better decisions and educating others in regards to diet.          

References

DeBosch BJ, Kluth O, Fujiwara H, Schürmann A, Moley K. 2014. Early-onset metabolic syndrome in mice lacking the intestinal uric acid transporter SLC2A9.Nature Communications [Internet]. 5 DOI: 10.1038/ncomms5642. Available from: http://www.nature.com/ncomms/2014/140807/ncomms5642/full/ncomms5642.html

Evangelou, J. 2014. New culprit identified in metabolic syndrome. Science Daily [Internet]. [cited 2014 Nov 27]; Aug 8. Available from: http://www.sciencedaily.com/releases/2014/08/140808123941.htm