The rise in the number of cases of obesity in the last 3 decades mirrors the 32% rise in dietary fructose between 1977 and 2004. High fructose corn syrup in particular has been implicated as a possible causative factor in obesity, due to its widespread inclusion as a sweetener in soft drinks and processed foods. Animal studies show that fructose over-consumption may promote increases in blood pressure, adiposity, insulin resistance, inflammation and dyslipidaemia, all known risk factors for metabolic syndrome. Studies involving humans have been less consistent, but generally are supportive of the animal studies to date. Adolescent humans consume large amounts of fructose compared to other age groups, mainly because of their consumption of soft drinks and processed and sweetened foods. Nutritional researchers are therefore interested in the effects of fructose consumption on biochemical markers of the metabolic syndrome in this age group.
For example, researchers1 have investigated the effects of total dietary fructose consumption (dietary fructose as well as the fructose component of sucrose) on biomarkers for metabolic syndrome in 559 healthy adolescents aged between 14 and 18 years. Food intakes were assessed by using 24 hour recall diet records, and fat free mass and adiposity was assessed by using dual-energy x-ray absorptiometry and magnetic resonance imaging, respectively. Following adjustment for known confounding variables such as age, sex, race, fat mass, physical activity, energy intake and socioeconomic status, fructose was significantly associated with visceral adipose tissue. There was also a trend across increasing tertiles for an association between fructose intake and systolic blood pressure, fasting glucose, homeostasis model assessment for insulin resistance (HOMA-IR), and C-reactive protein. Downward trends across decreasing tertiles were also reported for adiponectin and high density lipoprotein (HDL) cholesterol.
Fructose consumption may therefore be associated with a number of risk factors for the metabolic syndrome. However, all trends reported were attenuated when the visceral adipose tissue, but not subcutaneous adipose tissue, was used as a covariate. Therefore fructose consumption may increase the risk of developing excess visceral adipose tissue, and this visceral adipose tissue may then causes changes in biomarkers associated with the metabolic syndrome. This supports the hypothesis that fructose over-consumption increases the hepatic fatty acid production which results in lipid droplet accumulation in skeletal muscle tissue. As lipids accumulate, they interfere with normal fatty acid signalling which may lead to insulin resistance and a subsequent increases in visceral, but not subcutaneous, adipose tissue. As visceral adipose tissue accumulates, macrophages migrate in to the tissue and inflammation results from cytokine production. The fact that the risk factors for metabolic syndrome are attenuated by visceral fat loss supports this contention.