Obesity and insulin-resistance in childhood

Insulin-resistance is the most common metabolic complication of obesity. Fatness per sé is associated with insulin-resistance but it is mainly visceral, hepatic and skeletal muscle fat mass distribution that promotes and maintains insulin-resistance. Fat infiltration in the liver, pancreas and skeletal muscle is associated with a lower glucose uptake in the muscle, a lower insulin-mediated suppression on hepatic glucose production, a lower insulin-sensitivity, a greater susceptibility to diabetes and metabolic syndrome. Proliferative and differentiative capacity of fat cells contribute to the development of the metabolic complications of obesity. In fact, in the case of high proliferative and differentiative capacity, the mesenchimal precursor of the adipocite will give origin to mature adipocites high in number and low in volume, with a lower infiltration of the skeletal muscle, liver and pancreas. On the contrary in the case of low proliferative and differentiative capacity of the precursor, a hypertrophic obesity will develop, with low number of adipocites with high volume and a high infiltration of the organs. Skeletal muscle metabolism plays an important role in the fat balance regulation and, therefore, fat mass. Training and prolonged muscular work increases intramuscular fat oxidation, favouring insulin action and reducing insulin-resistance associated with intramuscular fat concentration. A high insulin sensitivity and a high insulin response are obesity risk factors in children. On the contrary, during puberty, insulin resistance associated with the increase of fat mass and with the changes of fat mass distribution seems to oppose, at least in females, further fat gain in adulthood. A high sensitivity to the insulin and a high insulinic answer seem to be obesity risk factors in the adult subjects. Several studies performed on children about the relationship between obesity and insulin-resistance are few and contradictory amongst them. These studies evidence that high insulin-sensitivity favours the increase of adiposity in non-obese children. Afterwards children's insulin-resistance associated to increase of fat mass opposes to a new increase of adiposity, at least in the girls.