Rats are not humans and so care should always be taken when interpreting rodent studies. Rodent physiology differs from human physiology despite the presence of many of the same enzymes and metabolic pathways. However, rodent studies when used in conjunction with evidence from both epidemiology and clinical trials on humans can be useful. For example, rats can be fed restricted diets that can be controlled rigorously by the researchers, something that would be unlikely to occur in a free living human population. In addition the rodents can be sacrificed following feeding and physiological changes analysed in detail. Rats have been used extensively to assess the effects of sugar on metabolism, and from these studies a clear pattern emerges when analysing the data. Sugar is known to cause insulin resistance in rats, just as it does in humans, when ingested at intakes easily obtainable in a human diet.
For example, one group of researchers1 examined the possible deleterious effects of sucrose by feeding rats either a high sucrose or high starch diet for just 4 weeks. The starch or sucrose accounted for 69% of calories (total calories were 74 kcal per day). In addition rats consumed 21 % of calories from protein and 10 % from fat. Infusion of insulin with a radiolabelled glucose solution was used to assess the insulin resistance of the rats in both the sugar and starch groups. Following the sucrose feeding, whole body insulin sensitivity was significantly impaired when compared to starch feeding. Insulin resistance was detected primarily at the liver, with less impairment in peripheral tissues such as the skeletal muscle. However, in the 4 weeks study there was no evidence of an increase in body fat and no changes in energy expenditure were observed.
These result support other evidence by suggesting that sucrose causes insulin resistance in mammals. Although the amount of sucrose fed to the rodents in this study was very high, other studies have used lower intakes of fructose and found similar deleterious effect on insulin resistance (here). Sucrose is a disaccharide that contains both a glucose moiety and a fructose moiety bonded together through a glycosidic bond. Because starch is comprised of chains of glucose molecules and does not cause insulin resistance, it is likely that the cause of insulin resistance is fructose. This has been demonstrated in human and animal feeding studies, whereby administration of even relatively low intakes of crystalline fructose causes the rapid development of hepatic insulin resistance. Fructose is though to induce insulin resistance because it increases de novo lipogenesis rates in the liver and the resultant lipids accumulate in liver tissue where they impair the action of insulin.
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