t has been shown that obese individuals have an inability to correctly utilise energy from ingested food. This is as a result of the insulin resistance that is a probably cause of weight gain in the obesity disease. In such individuals ingested glucose is not used as a source of energy by skeletal muscle but is instead diverted to adipose tissue where it accumulates and causes abdominal adiposity. The result of this phenomenon is measurable following a meal as the normal thermic effect of food is blunted in such individuals, when compared to lean counterparts (here). As a result thermogenesis is reduced and this can be measured as a smaller temperature rise. Obesity is therefore characterised by a defective metabolism and an inability to correctly utilise energy, with the subsequent result that energy levels, physical activity and oxidation of fuels becomes defective.
Forced energy restriction is the main treatment for obesity. Forced energy restriction involves creating a negative energy balance, such that ingested energy is less than expended energy. This is done primarily though the reduction in the number of calories consumed, but can also involve increased levels of physical activity. If forced energy restriction was an effective cure for obesity, then it would be expected that the lighter individual that results from the treatment would display a reversal of the metabolic abnormalities that are present when body mass is at its greatest. However, forced energy restriction does not reverse these abnormalities. On the contrary, in many cases it causes further deterioration. For example, prior to weight loss the resting metabolic rate of obese individuals is higher than that of lean controls. However, following a forced energy restriction diet the loss of muscle mass causes a reduction in the RMR.
If forced energy restriction diets were a treatment for obesity, we would also expect to see improvements in the utilisation of ingested energy following completion of weight loss. This could be measured as an increase body temperature following a carbohydrate (glucose) containing meal. However, evidence suggests that this does not occur. For example researchers1 investigated the reaction of 8 obese individuals to a glucose load and noted that the thermic effect of this food was lower (1.7 %) compared to lean controls (9.2 %). The researchers also noted that the obese individuals had a reduced adrenaline response from the central nervous system as measured by arterial adrenaline concentrations. Following a 30 kg weight loss, the obese individuals were re-tested but their thermic response from the ingested food was still lower than lean individuals (4.2 % versus 9.2 %, respectively), and arterial adrenaline remained impaired.
These results suggests that weight loss does not reverse the impaired ability of obese individuals to utilise energy. Because these individuals lost 30 kg of weight, it is likely they lost several kg of skeletal muscle. As a result they would almost certainly have developed a lower RMR. The combination of a low RMR with the impaired thermic response to food would have made it highly likely that they would regain any lost body fat. The inability of the obese subjects to utilise energy is reflected in the insulin responses of the subjects. Insulin response to ingested glucose was elevated both before and after weight loss suggesting poor insulin sensitivity. This supports the contention that the poor utilisation of fuel in obesity is caused by insulin resistance, and that the correct treatment for obesity should centre on improving insulin sensitivity through improvements in diet quality.
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