The Brain’s Hunger/Satiety Pathways and Obesity, Animation
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The Brain’s Hunger/Satiety Pathways and Obesity, Animation

March 9, 2020

Food intake and energy expenditure must be
balanced to maintain a healthy body weight. This balance is kept by the central nervous
system, which controls feeding behavior and energy metabolism. Several brain systems are involved, including
the brainstem which receives neuronal inputs from the digestive tract, and the hypothalamus
which picks up hormonal and nutritional signals from the circulation. These two systems collect information about
the body’s nutrient status and respond accordingly. They also interact with the reward and motivation
pathways, which drive food-seeking behavior. The arcuate nucleus, ARC, of the hypothalamus,
emerges as the major control center. There are two groups of neurons, with opposing
functions, in the ARC: the appetite-stimulating neurons expressing NPY and AGRP peptides,
and the appetite-suppressing neurons producing POMC peptide. Appetite-stimulating neurons are activated
by hunger, while appetite-suppressing neurons are stimulated by satiety, or fullness. Neurons of the ARC project to other nuclei
of the hypothalamus, of which the paraventricular nucleus, PVN, is most important. PVN neurons further process the information
and project to other circuits outside the hypothalamus, thus coordinating a response
that controls energy intake and expenditure. Short-term regulation of feeding is based
on how empty or how full the stomach is, and if there are nutrients in the intestine. In the fasting state, an empty stomach sends
stretch information to the brainstem, signaling hunger. It also produces a peptide called ghrelin,
which acts on the arcuate nucleus to stimulate feeding. Ghrelin also acts directly on the PVN to reduce
energy expenditure. Upon food ingestion, distension of the stomach
is perceived by the brainstem as satiety. Ghrelin is no longer produced. Instead, several other gut peptides are released
from the intestine and act on the hypothalamus and other brain areas to suppress appetite
and increase energy expenditure. Long-term regulation, on the other hand, takes
cues from the amount of body fat: low body fat content encourages feeding and energy
preservation, while high body fat suppresses appetite and promotes energy expenditure. Two hormones are involved: leptin and insulin. Insulin is a hormone produced by the pancreas
and is released into the bloodstream upon food ingestion, when blood glucose starts
to rise. Leptin is a hormone secreted by adipose tissues
in a process dependent on insulin. The amount of circulating leptin in the plasma
is directly proportional to the body fat content. Increased leptin levels in the blood signal
to the brain that the body has enough energy storage, and that it has to stop eating and
burn more energy. Leptin and insulin seem to work together on
hypothalamic nuclei, as well as other brain areas, to inhibit food intake and increase
energy expenditure. Obesity results from the dysregulation of
feeding behaviors and energy metabolism. Obesity is most commonly associated with chronic
low leptin activities, which trick the brain into thinking that the body is always starved. This leads to overeating and excessive energy
storage as fats. Both genetic and lifestyle factors contribute
to low leptin signaling, but the contribution of each factor varies widely from person to
person. The major lifestyle factor is a high-fat,
energy-rich diet. In an early stage of high-fat-diet–induced
obesity, increased amounts of saturated fatty acids cross the blood brain barrier and provoke
an inflammatory response in hypothalamic neurons. Inflammation induces stress in these neurons,
blunting their response to leptin. This is known as leptin resistance. Leptin levels are high, but because the cells
cannot react to leptin, the brain interprets it as low and triggers the starvation response. Genetic factors include mutations in the leptin
gene itself, or in one of the numerous downstream genes that are required for leptin action
in various pathways. Leptin deficiency due to gene mutations is
very rare. More common are mutations in the downstream
genes, which render a certain pathway irresponsive to leptin. A major risk factor for childhood obesity
is maternal obesity and mother’s high-fat-diet during pregnancy and lactation. A maternal diet rich in saturated fats can
cause inflammation in the infant’s hypothalamus. It may also prime the reward pathways in infants,
influencing their food choice toward energy-rich foods.

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  2. His hi Alila medical Media! A video about cellular immunity would be amazing. More about infections would be amazing!!

  3. A bigger concern is that insulin blocks leptin at the hypothalamus. Obesity from high saturated fats doesn't happen unless it's on top of a high-carb diet. Don't worry about the fat, worry about the Glucose & Fructose.

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