ASSIGNMENT

Nandana Murali A, NPSY 2022, School of Allied Healthcare and Science, Jain university
Ashwin Shankaran, Department of Psychology, SAHS

Pathways- anorexigenic and orexigenic

To maintain a healthy body weight, one must balance food intake and energy usage. The central
nervous system, which regulates eating habits and energy metabolism, maintains this equilibrium.
Involved brain systems include the hypothalamus, which receives hormonal and nutritional cues
from the circulation, and the brainstem, which receives neuronal inputs from the digestive tract.
Moreover, they affect the reward and motivational pathways that control behaviour related to food
seeking. The arcuate nucleus, or ARC, of the hypothalamus contains two sets of neurons with
conflicting functions: the neurons that stimulate hunger and express the peptides NPY and AGRP and
the neurons that inhibit appetite and produce the peptide POMC. The paraventricular nucleus, or
PVN, is the most significant of the hypothalamic nuclei to which the ARC neurons project. The input
is further processed by PVN neurons, who then send the information to circuits outside the
hypothalamus to coordinate a response that regulates energy intake and expenditure. Based on how
empty or full the stomach is, as well as whether or not the intestines contain nutrients, short-term
feeding management is determined. An empty stomach during a fast transmits stretch signals
to the brainstem representing hunger. It generates ghrelin, a peptide that stimulates hunger by
acting on the arcuate nucleus. Moreover, ghrelin reduces energy use by directly influencing the PVN.
The brainstem interprets the stomach's distension after eating as satiety. The hypothalamus and
other brain regions are affected by a number of additional gastrointestinal peptides, which serve to
decrease appetite and boost energy expenditure. The amount of body fat also serves as a cue for
long-term regulation: low body fat content supports feeding and energy conservation, whereas high
body fat content suppresses appetite and encourages energy expenditure. Leptin and insulin are the
two hormones that are at play.as food is consumed, the pancreas releases the hormone insulin into
the bloodstream, which causes blood glucose levels to rise. Adipose tissues that have been exposed
to insulin release the hormone leptin. Leptin circulation in the plasma is directly correlated with
body fat percentage. Leptin levels in the blood rise, telling the brain to stop eating and start
increasing energy expenditure because the body has ample energy reserves. Together with other
brain regions, the hypothalamic nuclei appear to be where leptin and insulin collaborate to reduce
food intake and boost energy expenditure. The dysregulation of eating habits and energy
metabolism is the cause of obesity. Chronic decreased leptin activity is linked to obesity can deceive
the brain into believing that the body is constantly hungry. Overeating and excessive fat buildup
result from this. A high-fat, high-energy diet is a significant lifestyle determinant. Increased levels of
saturated fatty acids pass the blood brain barrier early in the process of high-fat diet-induced obesity
and cause inflammatory reactions in hypothalamic neurons. Stress brought on by inflammation
reduces these neurons' ability to respond to leptin. Leptin resistance is what is meant by this despite
the fact that cells are unable to respond to lentin, leptin levels are high. The starving reaction is
triggered because the brain interprets it as low. Mutations in the leptin gene or any of the multiple
downstream genes necessary for leptin function in different pathways are examples of genetic
influences. Genetically induced leptin insufficiency is quite uncommon. Most frequently, changes in
the downstream genes make a particular pathway resistant to leptin. Maternal obesity and a high-
fat diet during pregnancy and lactation are significant risk factors for childhood obesity.
Inflammation in the baby's hypothalamus can result from a mother's diet high in saturated fats.
Infants' reward pathways may also be primed, which would affect their preference for calorie-
dense foods.