After ingestion, fructose is absorbed from the mid to distal small bowel and almost completely metabolised by the liver, independent of the hormone insulin. Unlike glucose, fructose does not stimulate insulin release. Metabolism of fructose depletes intracellular energy stores (ATP), and induces uric acid production.14
The principal products of hepatic fructose metabolism are triglycerides, which are then released into the circulation.
While fructose is processed, conversion of glucose to glycogen (glycogenesis) in the liver is blocked. The reduction in glucose metabolism, in turn, causes insulin levels to rise so that glucose is taken up in alternative sites, such as muscle tissue. Such high insulin levels leads to compensatory insulin resistance in muscle tissue.14 This mechanism may explain how fructose has little acute effect on serum glucose levels, but importantly, impairs glycaemic control after long-term exposure to high doses. Further details of fructose physiology are presented elsewhere.14
Using animal studies, researchers have documented adverse metabolic effects of refined fructose consumption. Rodents fed on high fructose and sucrose diets, but not high glucose diets develop features of the metabolic syndrome, such as hyperinsulinaemia, hyperuricaemia and hypertriglyceridaemia.14
In contrast to animal data, links between fructose and adverse health outcomes have not been so convincingly demonstrated in humans, although longer exposure studies and higher doses of fructose (>200g/day or the equivalent of two cups of sugar) tend to produce clearer adverse health outcomes. For example, small intervention studies have shown that high doses of fructose provoke insulin resistance within one week,15 whereas smaller doses (14 Whilst 200g is greater than the average New Zealand daily intake (70g/day), variation in consumption means that a substantial proportion of New Zealanders are likely to ingest more than 100g/day. A rise in systolic blood pressure of 7mmHg was observed after intake of 200g of fructose per day for 14 days in a randomised trial (n=74).16 This study also found adverse effects on triglycerides, fasting insulin and metabolic syndrome outcomes. Other effects include modest weight gain in some short term studies.17 The health effects of long term, high dose exposure of fructose, which occurs in some subsets of the population have not been studied in experimental trials.
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Johnson RJ, Perez-Pozo SE, Sautin YY, et al. Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes? Endocr Rev. 2009;30(1):96-116. - Havel P. Dietary Fructose: Implications for Dysregulation of Energy Homeostasis and Lipid/Carbohydrate Metabolism. Nutrition Reviews. 2005;63(5):133-57.
- Perez-Pozo SE, Schold J, Nakagawa T, et al. Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response. Int J Obes. 2009.
- Raben A, Vasilaras TH, Moller AC, et al. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin Nutr. 2002;76(4):721-9.
source refined sucrose is half fructose. corn syrup is roughly half fructose. fruits have fructose and sucrose, but are less concentrated and at least have fiber and polyphenols to slow digestion.
More work needs to be done to show that small amounts of fructose (like those obtained by a diet including fruits but not much refined sugar or corn syrup) are harmful and should be reduced. Perhaps the harm is very small, or nonexistent. But for sure, large amounts are harmful and cause obesity, diabetes, high blood pressure, and heart disease. It’s definitely above average to consume over 400g of sugar and thus over 200g of fructose, daily, but probably 1/3 of American teens+adults do (complete guess).