Consumption of unrefined whole grains are associated with beneficial health effects, whereas refined simple sugars are associated with disease. In particular, high intakes of fructose are suspected of playing a role in the development of obesity, metabolic syndrome, diabetes and cardiovascular disease. This is because when fructose makes up a large percentage of total energy, metabolic changes occur which result in insulin insensitivity. Development of insulin resistance may lead to central adiposity, systemic inflammation and a pro-atherogenic environment. Consumption of fructose for as little as 6 days has been shown to increase rates of de novo lipogenesis, with plasma triglyceride levels rising by up to 200%. Up to 40% of circulating triglycerides can be derived from fructose if it is overfed in healthy humans. In recent decades fructose consumption has increased in most Western nations, mirroring increases in obesity and diabetes.
Researchers1 have investigated the effects of morning fructose consumption on fatty acid synthesis in 6 healthy subjects. The subjects were fed 85 grams of either glucose, a 50:50 fructose glucose mixture or a 75:25 fructose glucose mixture for breakfast, followed 4 hours later by a normal lunch. As expected serum glucose and insulin levels were highest after consumption of the glucose only meal. Lipogenesis was stimulated by both of the fructose meals and resulted in a 2-fold higher level of absolute lipogenesis (17%) when compared to a glucose only meal (8%). Consumption of the fructose meals resulted in plasma triglycerides that were 11 to 29% higher following the subsequent normal lunch, when compared to glucose. In a similar fashion, there was a 76 to 200% greater concentration of very low density lipoprotein (VLDL) after the normal lunch following a fructose meal, when compared to glucose.
These results support previous findings that implicate fructose consumption in metabolic changes that lead to development of metabolic syndrome. In particular, fructose appears to be a potent stimulator of de novo lipogenesis and VLDL synthesis in the liver. Consumption of fructose increases the production of triglycerides following a subsequent non-fructose meal. This may imply that fructose causes an up-regulation of the production of triglycerides from other sources such as plasma fatty acids, dietary fat or adipose tissue. This would also explain the elevated fasting triglyceride levels that are seen with metabolic syndrome, assuming that fructose intake contributes to this condition. Post-lunch increases in de novo lipogenesis following the glucose only meal rose to reach the same level as the fructose only meal, perhaps because this was the maximum possible rate and further intakes of food could not increase lipogenesis further in the fructose groups.