Schwarts and Baskin highlighted how the central nervous system controls food consumption through two effector pathways. Some neuropeptides and monoamines synthesized and released through nerve pathways are able to modify, once they reach the brain, the consumption of food and the choice of the type of food.
These two effector pathways can be recognized as "anabolic effector system" and "catabolic effector system".
. The anabolic effector system inhibits:- the activity of the SNS (sympathetic nervous system)
- l "SNS activity in BAT (brown adipose tissue)
- hence the optional thermogenesis which leads to a certain energy loss only in the form of heat.
This inhibition of the SNS implies:
- stimulation of the LPL (lipoprotein lipase) activity responsible for the storage of fats in adipose cells
- hence, lipogenesis
- increased production and release of insulin
- increased production and release of glucocorticoids (cortisol and its prohormones).
So this effector system only and elusively stimulates the conservation of excess energy, almost completely inhibiting heat dissipation - inhibiting thermogenesis, as mentioned before, blocks the loss of caloric surplus through the production of body heat.
For the moment we will not discuss the hormones responsible for the activation of this neuronal pathway, but know that: prolonged fasting, weight loss and type 1 diabetes (therefore also the prolonged glucose deficiency) lead to the activation of this nervous pathway and prepare the "body to store the caloric surplus and increase the" need for food ".
