To review recent evidence linking excessive fructose consumption to health risk markers and development of components of the Metabolic Syndrome.
Consumption of fructose, the sweetest of all naturally occurring carbohydrates, has increased dramatically in the last 40 years and is commonly used commercially in soft drinks, juice, and baked goods.
A large body of evidence associates consumption of fructose and other sugar-sweetened beverages with insulin resistance, intrahepatic lipid accumulation, and hypertriglyceridemia. In the long term, these risk factors may contribute to the development of type 2 diabetes and cardiovascular diseases.
Further, fructose consumption is considered to be a culprit in metabolic syndrome as a lipogenic compound that associates with excess ectopic fat accumulation, particularly in the liver.
This review focuses on the links between fructose consumption and metabolic syndrome, highlighting specifically the effects of fructose on hepatic lipid homeostasis and metabolism.
The methodology utilized in this review was not described.
Accumulating evidence supports the fact that fructose is an important mediator for the development of NAFLD and a main driver for de novo lipogenesis. This concept is supported by a recent meta-analysis including 6326 participants and 1361 cases with NAFLD. However, it is still debated whether fructose, when consumed in isocaloric amounts, causes more liver fat accumulation than other energy-dense nutrients.
Despite weaknesses in study design such as small cohorts, variable or short duration and varying dosage, many studies seem to indicate that hypercaloric fructose feeding increases liver fat content and that this response is aggravated in obese subjects.
Fructose seems to influence multiple metabolic pathways in the liver that results in enhanced lipogenesis, generation of uric acid, ER stress, and inflammation. The association between uric acid and insulin resistance raised the interest of uric acid as a potential biomarker in metabolic syndrome and several studies have established that serum uric acid is a risk factor.
Recent French recommendations for sugar intake concluded that long-term consequences of potential small increases of uric acid by fructose/sugar intake remain insufficient. Likewise, critical analysis of the available data left open the casual link between fructose intake and hyperuricemia.
Several studies have consistently reported increased responses of fasting and postprandial triglyceride levels and 24-hour profiles to short term feeding of fructose as compared to glucose in both lean and obese subjects. These perturbations directly lead to other lipid abnormalities including elevation of apoB levels, accumulation of small dense LDL, and increased remnant lipoproteins, combined with reduced HDL cholesterol which all are components of the atherogenic lipid triad, a strong risk factor for CVD.
Multiple studies have also reported fructose as a critical factor contributing to NAFLD progression by modulating intestinal microbiota. Microbial composition have been shown to differ between healthy individuals and NAFLD patients, and a diet enriched in fructose not only induced NAFLD but also negatively affected the gut barrier and the microbiota composition, leading to impaired microbiota.
Consistent data evidence that excess fructose intake as a central component of unhealthy lifestyle has detrimental effects on multiple cardiovascular risk factors.
It is clear that added sugars have become a threat to cardiometabolic health. These facts call for the restriction of dietary sugars, especially SSB consumption to limit fructose intake to achieve better cardiometabolic health.
Do you have questions about low-calorie sweeteners? Want to learn more about maintaining a healthy lifestyle? You asked and we listened. Our resident Registered Dietitians answered the most popular questions about low-calorie sweeteners.