Table sugar is chemically called sucrose, and is structurally a glucose molecule bonded to a fructose molecule (with a glycosidic bond). Digestion of sucrose yields one molecule of glucose that is then absorbed to the blood and contributes to blood sugar levels where it can supply energy to skeletal muscles or be used to resynthesise liver glycogen. The fructose moiety of sucrose is absorbed and paases to the liver where it is processed in a number of ways. If liver glycogen levels are low, fructose can contribute to the resynthesis of glycogen. In addition, fructose can be converted to glucose and released into the circulation where it can contribute to the blood glucose concentration. Fructose is found in small concentrations in fruit and generally low intakes of fructose are not problematic if the fruit is in its unrefined whole food form. However, when fructose is processed into a white crystalline powder and intakes increase, it can become a metabolic poison that contributes to the development of insulin resistance.
The metabolic damage caused by crystalline fructose has been demonstrated in both animal and human studies. Initially animal studies were criticised because of the high amounts of fructose used, but more recent estimates of human fructose intakes has shown that these studies are valid. Feeding rodents crystalline fructose for as little as two weeks causes the development of insulin resistance. This is because the fructose overloads the liver with energy and in response the fructose is passed down the de novo lipogenesis pathway to produce fatty acids which can accumulate in liver and skeletal muscle tissue thereby interfering with the insulin signal cascade. Isocaloric substitution of starch for fructose leads to this metabolic dysfunction in both animals and humans, however, this effects can be beneficially modified by the addition of fibre to the diet. In addition, there is good evidence that exercise can also have a beneficial effect on sucrose induced insulin resistance due to the insulin sensitising effects of exercise on skeletal muscle.
For example, in one study1, researchers fed rats either a 64 % cornstarch diet or a 32 % cornstarch diet with 32 % sucrose. Some rats given the mixed starch and sucrose diet were also given either wheat bran fibre or allowed to exercise on wheels in their cages. The results showed that the rats fed the sucrose and starch diet had a significant increase in plasma glucose levels in response to a steady state infusion of glucose, suggesting that insulin sensitivity had declined in comparison to the control diet. The rats fed the sucrose and starch diet with the addition fibre fared better than the rats in the fibre-less sucrose and starch diet but not as well as the control rats on the starch diet. However, those rats able to exercise actually showed improvements in insulin sensitivity compared to the control rats, despite ingesting sucrose. Exercise was therefore able to totally ameliorate the detrimental effects of feeding sucrose, possibly because of the insulin sensitising effects of exercise on skeletal muscle and liver tissue.
Dr Robert Barrington’s Nutritional recommendation: In this study exercise was effective at preventing deteriorations in insulin sensitivity in rats. This is likely due to the glycogen depleting effects of exercise. As glycogen is depleted, ingested fructose is used to replenish these stores and this prevent flux of fructose through the de novo lipogenesis pathway. However, using exercise to prevent declines in insulin sensitivity is not the same as using exercise to reverse insulin resistance once a high fructose diet has cause detrimental metabolic effects. Reversing insulin resistance is much harder especially if a poor diet has been followed for decades. If abdominal obesity has developed from years of fructose abuse, then drastic improvements in diet quality will be needed in addition to exercise in order to reverse the damage. In such circumstances it is doubtful that exercise alone would be successful in improving the metabolic damage.
RdB
