Insulin resistance may the the primary driver of the metabolic changes that cause obesity. Increasingly insulin resistance is thought to develop through adherence to the typical Western diet, a diet that is characterised by high amounts of refined starch and refined crystalline sugar. These two components overload the liver with energy, and this results in the production of fatty acids that accumulate in the liver and skeletal muscle where they interfere with the insulin signal cascade. As insulin resistance develops plasma fasting and postprandial insulin levels rise in response to the insensitive tissue and this leads to a state whereby anabolism is favoured in the metabolic pathways. Insulin allosterically controls many of the enzymes involved in anabolic and catabolic pathways, shunting metabolism towards the synthesis of substrates such as fatty acids and the storage of the products of this synthesis. Reversing insulin resistance is pivotal to fat loss in order to remove this anabolic shunting.
The reversal of insulin resistance has been investigated by researchers. While studies involving human have been performed, many more animal studies have investigated the effects of exercise and dietary changes on insulin resistance. This relates to the ease with which the animal studies can be performed and the greater control of variables available to the researchers. For example, in one study1 experiments were performed on male and female rats. In the experiment male and female rats (in different experiments) were split into three groups. One group was allowed free access to food, another was put through a daily swim test to provide controlled exercise, and a third group had their body weight reduced through adjustment to their food intake. The results of this experiment showed that exercise caused significant reductions in fasting and postprandial insulin levels and also caused significant reductions in the growth of both adipose tissue and lean mass in the rats. These growth inhibiting effects were greater in the male rats.
The reductions in the fasting and postprandial insulin levels in the rats was likely due to the increased insulin sensitivity of peripheral tissue, as seen in human subject in other studies. The authors also pointed out a very strong correlation between the body weights of the animals and the insulin sensitivity they showed. Therefore exercise and dietary restriction of energy have insulin sensitising effects, perhaps because they cause a reduction in body weights. The authors concluded that it was the reduction is body weights that have the main insulin sensitising effects, rather than the physical activity per se. This Is interesting because exercise is known to produce short term insulin sensitising effects in skeletal muscle. Certainly this conclusion is controversial based on other studies in the literature. For example, both exercise and energy restriction cause reductions in blood sugar levels which would have insulin sensitising effects, and it is difficult therefore to claim that the weight reduction was the causative factor in this case.
RdB
