Metabolic syndrome (syndrome X) is characterised by insulin resistance and can lead to obesity. The cause of the insulin resistance in metabolic syndrome is not completely understood, but fructose is thought to play a part in its development. Fructose is a monosaccharide sugar that is metabolised only in the liver where it can be converted to glycogen. If glycogen stores are full, the fate of fructose is conversion to fatty acids in a process called de novo lipogenesis. These fatty acids are then packaged into very low density lipoproteins and exported to skeletal muscle where they are thought to contribute to insulin resistance. Fructose consumption has increased in recent decades due to the introduction of high fructose corn syrup into industrial production of processed foods, and there is speculation that this may have increased the rates of obesity and metabolic syndrome in Western populations.
Research has investigated the metabolic changes and postprandial levels of de novo lipogenesis in response to food. In one study1, overweight and lean male subjects consumed a high carbohydrate (27% lactose and 53% sucrose), low fat meal (80% carbohydrate, 17% protein, 3% fat) following a 17.5 hour fast. The results showed that the high carbohydrate meal caused the overweight men to have higher fatty acid and triglyceride blood concentrations compared to the lean subjects, as well as higher protein oxidation and lower fatty acid oxidation. The overweight subjects also developed hyperinsulinaemia postprandially. The amount of de novo lipogenesis was also significantly higher in overweight subjects before and after the high carbohydrate meal and was correlated positively with body fat levels, fasting serum glucose and insulin concentrations. This suggests that metabolic regulation was different between the lean and overweight subjects.
In the short-term, overweight and lean subjects display different metabolic changes to a high carbohydrate low fat meal. Postprandially, overweight subjects displayed increased de novo lipogenesis and subsequent increased triacylglycerol concentration, but in skeletal muscle fat oxidation decreased. This suggests that despite higher concentrations of circulating fatty acids, overweight subjects were unable to oxidise fatty acids efficiently. The increased protein oxidation might result from the oxidation of amino acids in an attempt to supply adequate energy because of metabolic disturbance to the oxidation of fat. The hyperinsulinaemia and raised fasting blood glucose levels seen in the overweight subjects suggests the development of insulin resistance. The meal was high in sucrose, a disaccharide that contains both glucose and fructose. This high level of sucrose might not be expected in a healthy diet, but could e present in a diet consisting of highly processes sugar rich foods.
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