Abstract
Excess sugar consumption may promote adverse changes in hepatic and total body insulin resistance. Debate continues over the effects of sugars at more typically consumed levels and whether the identity of the sugar consumed is important. In the present study participants (20–60 years old) were randomly assigned to one of five groups, three that consumed low fat milk with added fructose containing sugars in amounts equivalent to the 50th percentile of fructose consumption (US), one which consumed low-fat milk sweetened with glucose, and one unsweetened low-fat milk control group. The intervention lasted ten weeks. In the entire study population there was less than 1 kg increase in weight (73.6 ± 13.0 vs. 74.5 ± 13.3 kg, p < 0.001), but the change in weight was comparable among groups (p > 0.05). There were no changes in fasting glucose (49 ± 0.4 vs. 5.0 ± 0.5 mmol/L), insulin (56.9 ± 38.9 vs. 61.8 ± 50.0 pmol/L), or insulin resistance, as measured by the Homeostasis Model Assessment method (1.8 ± 1.3 vs. 2.0 ± 1.5, all p > 0.05). These data suggest that added sugar consumed at the median American intake level does not produce changes in measures of insulin sensitivity or glucose tolerance and that no sugar has more deleterious effects than others.
Highlights
Diabetes has grown in parallel with the worldwide [1,2,3,4] increase in obesity and is widely linked to it
No study has compared fructose-containing sugars that are normally consumed in the human diet (i.e., high fructose corn syrup (HFCS) and sucrose) vs. fructose by itself with glucose and no added sugar controls
It has been argued that it is the fructose moiety in HFCS and sucrose that may lead to a variety of metabolic abnormalities which suggests that this may be different than glucose
Summary
Diabetes has grown in parallel with the worldwide [1,2,3,4] increase in obesity and is widely linked to it. No study has compared fructose-containing sugars that are normally consumed in the human diet (i.e., HFCS and sucrose) vs fructose by itself with glucose and no added sugar controls. One proposed mechanism for fructose-induced insulin resistance is that fructose consumption may increase de novo lipogenesis (DNL) leading to increased fat in the liver and hepatic insulin resistance [30,31] Data to support these assertions, is limited and, as already indicated, comes from studies that were given very large doses of fructose or glucose, which are typically not consumed in isolation in the human diet. The degree to which the amount of DNL in humans consuming sugars or other carbohydrates typically found in the human diet suggests that it is a very limited pathway comprising no more than 1%–5% of consumed fructose, which may be turned into triglycerides [32,33]
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