Evidence suggests that animals fed high fructose diet have increases in adiposity, body weight and energy intake. There are now many such studies in the nutritional literature involving a wide range of animals, but centred mainly on rodents, particularly rats. In fact much of the work on fructose has been performed on animals because their diets can be rigorously controlled in environments that would not be ethical for human subjects. Animal studies are also advantageous because their shorter life spans means that growth rates are much higher and so study length can be shorter. Therefore less details are available regarding the effects of fructose on humans. However, research that has been performed suggests that that the effects of fructose on animals are applicable to humans, and although initial criticism of animal studies was based on the high levels of fructose consumed by the animals, subsequent studies have shown that such high levels are ingested by some human subjects.
For example, human subjects who drank 1150 grams of soft drink containing high fructose corn syrup for 3 weeks had increased ad libitum energy intake and body weight compared to control subjects. Subjects with type 2 diabetes fed 50 to 60 grams of fructose per day also experienced significant increases in body weight over 24 weeks compared to controls. Consumption of 28 % of energy as sucrose, a molecule containing 50 % fructose, experienced increased energy intake, increased body weight and increased adiposity in just 10 weeks. Therefore human studies are in broad agreement with animal studies, in that fructose increases fat mass, body weight and energy intake. Unlike glucose, fructose does not stimulate the release of insulin. This is a pertinent point here because insulin is thought to act as a feedback signal to the hypothalamus to limit further energy intake. The implication is them that fructose bypasses the normal insulin induced appetite regulatory mechanism and so does not curtail appetite postprandially.
Insulin signalling in the central nervous system may therefore curtain energy intake. Fructose therefore does not have this effects and this may explain the increase in energy consumption, adiposity and body weight seen with fructose ingestion. However, leptin is another hormone that is known to be involved in appetite regulation, body weight and adiposity. Could fructose affect leptin secretion? Leptin may be stimulated by insulin, in so far as glucose uptake to cells may trigger the release of leptin. Further flux through glycolysis, which would occur after insulin release may also stimulate leptin release. Increasing the carbohydrate content of meals may also increase circulating leptin, all of which suggests that insulin stimulates leptin release. As fructose does not stimulate the release of insulin, it stands to reason that it therefore does not stimulate the release of leptin. In animals studies glucose can stimulate insulin release and subsequently leptin secretion rises. However, fructose does not have this effect.
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