Forget about diet & fat suction

Rats forced to overeat store excess fat, but when offered a normal diet they eat less until the normal weight is regained. Surgical removal of fat mass is followed by increased eating until fat stores are restored. Parabiotic experiments, in which two animals are surgically joined so as to share the same circulatory system, demonstrate the existence of blood-borne factors. Overeating by one joined animal reduces food intake and induces weight loss in the partner. Likewise, when one joined animal becomes obese because of a lesion in the ventromedial hypothalamic nucleus, the other animal reduces its food intake and loses weight, presumably because of enhanced levels of circulating hormones from the obesepartner. However, an ob mutant animal joined to a normal animal eats less and gains less weight, suggesting that the mutation is associated with a lack of a circulating hormone. Leptin binds to a receptor, so that mutations of the leptin receptor should also result in disturbance of long-term regulation of food intake and fat stores. Indeed, the obesity of mutant db/db mice, in which the leptin receptor is defective, is not ameliorated by injection of leptin. In humans, however, the genetic causes of obesity are primarily due to an absence of an appropriate response to leptin, downstream from the leptin receptor, rather than to a deficiency in leptin itself.

How does circulating leptin lead to changes in feeding behavior? There is evidence that leptin produces its action, in part, by regulating the release of neuropeptide Y (NPY). NPY is synthesized by neurons of the arcuate nucleus of the hypothalamus, and these neurons project to other regions of the hypothalamus that control feeding. Release of NPY in the hypothalamus stimulates feeding behavior. Chronic administration of NPY in the brain simulates the phenotype of leptin deficiency and produces hyperphagia, obesity, and inhibition of the production of growth hormone. These findings suggest that leptin acts by inhibiting the actions of NPY. Consistent with this idea, neurons in the arcuate nucleus that express NPY have leptin receptors, and leptin acts on these neurons to inhibit expression of the peptide and its release from the neurons. A critical component of leptin's effect on body weight is its ability to diminish the effects of neurons that secrete NPY and thus decrease the effect of the short-term cues that stimulate feeding. Conversely, low levels of leptin enhance the action of the short-term cues that stimulate feeding.

"Principles Of Neural Science", Eric R. Kandel, 4th_Edition 2000

SO, if you have troubles with your weight, forget about diets or fat suction and just make a your choice to be "Satisfied" by eating less.It is related to satisfaction and as a consequence a set point your body sets it.
I tried this before reading this part of the very interesting very helpful book.


Locus-coeroleus