Consumption of sugar in Western nations has increased in recent decades partly due to increased intakes of sugar sweetened soft drinks. Epidemiological studies show that high consumption of such drinks can increase the risk of developing detrimental blood lipid profiles, insulin resistance, non-alcoholic fatty liver, cardiovascular disease, metabolic syndrome and type 2 diabetes. Traditionally it was thought that the detrimental effects of increased intakes of sugar sweetened drinks was because of the increased insulin secretion and increased circulating glucose levels as a result of consuming simple sugars with no fibre. However, sweetened drinks often contain low glycaemic index sugars such as fructose that do not cause large increases in insulin and glucose levels. Instead, fructose is absorbed by the liver and stimulates uncontrolled de novo lipogenesis which results in the secretion of very low density lipoproteins (VLDL) that can lead to insulin resistance.
Researchers1 have compared the adverse effects of consuming of fructose and glucose sweetened drinks to determine if the detrimental effects are due to changes in insulin and blood glucose concentrations. Thirty nine subjects (age 40 to 72 years, body mass index of 25 to 35kg/m2) were admitted to a metabolic unit and administered an energy balanced diet containing 55% of calories as complex carbohydrates. Subjects were then allowed to return home where they consumed their normal ad libitum diets but the researchers provided a fructose or glucose sweetened drink that provided 25% of their energy requirements. The subjects followed this diet for 8 weeks and then for a further 2 weeks in the metabolic unit. Measurements of glucose and insulin profiles, as well as fasting plasma glycated albumin were taken at baseline and during week 2, 8 and 10.
The results showed that consumption of the fructose sweetened drink lowered the postprandial blood glucose and insulin concentrations and the 23 hour area under the curves for both circulating glucose and insulin, compared to the baseline diet and the glucose-sweetened drink. In addition, fructose consumption resulted in a lower concentration of plasma glycated albumin at 10 weeks compared to glucose consumption. Taken as a whole, these results suggest that the detrimental effects of fructose on lipid profiles and insulin resistance are independent of changes to insulin and blood sugar concentrations and therefore must relate to specific effects of fructose. This supports other data that shows the lipid profile changes from sugar sweetened drink consumption are as a result of the hepatic metabolism of fructose to fatty acids, which then subsequently enter circulation and interfere with insulin sensitivity.
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