[Physiopathology and treatment of obesity].
Obesity results from an energy imbalance affecting both energy intake and output to various degrees. In some individuals hyperphagia may be the obvious cause of the imbalance, whereas in other obese patients a defective thermogenic capacity unable to adapt energy expenditure to a variable intake plays an important role. The mechanisms of this thermogenic defect are not well understood: decreased sensitivity to the thermogenic effects of the sympathetic nervous system and insulin resistance may be implicated. The thermogenic defect favours weight gain; it is likely that body weight reaches a plateau (th obese state) when the body weight gain is accompanied by a rise in basal metabolic rate which compensates the thermogenic defect. The excess in body weight becomes a compensated state which allows the whole energy intake to be expended. The principles of the protein sparing modified fast (low carbohydrate and lipid, but high protein intake) are outlined. After the end of the hypocaloric diet  period the recommendations for maintaining the new body weight should stress the need to maintain a low lipid intake but allow carbohydrate intake (mainly starch). It is important to realize that the energy needs of the patient are lowered after weight loss.
D000273:Adipose Tissue; D001833:Body Temperature Regulation; D001835:Body Weight; D004038:Diet, Reducing; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D004041:Dietary Fats / Q000008:administration & dosage; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D008297:Male; D009765:Obesity / Q000178:diet therapy / Q000503:physiopathology* / Q000628:therapy*; D005082:Physical Exertion
D004040:Dietary Carbohydrates; D004041:Dietary Fats
Physiopathologie et traitement de l'obésité.