Hunger and satiety

Definitions & Key takeaways

Hunger and satiety are regulated by a complex network of hormones and neurotransmitters that interact with the central nervous system. This network is responsible for signaling to the brain when you're hungry, what foods you should eat, and when you're full.

Some of the most important hormones involved in hunger and satiety include ghrelin, leptin, peptide YY (PYY), and cholecystokinin (CCK). Ghrelin is produced in the stomach and stimulates the release of stomach acids to digest food. Leptin is produced by fat cells and signals to the brain when you've had enough food. PYY is released by the small intestine after eating and inhibits hunger signals. CCK is also released after eating and reduces hunger by slowing gastric emptying.

The hormones involved in hunger and satiety are regulated by a complex network of hormones and neurotransmitters that interact with the central nervous system. This network is responsible for signaling to the brain when you're hungry, what foods you should eat, and when you're full.

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Introduction0:00–0:57

The hypothalamus is a small part of your brain that lies just above the pituitary gland. It controls various body functions like hunger, thirst, body temperature and hormones released by the pituitary gland.
The three parts of the hypothalamus that regulate food intake are called the ventromedial nuclei. The lateral hypothalamic area and the arcuate nucleus, the ventral medial nuclei is the satiety center.
And when stimulated, it causes the sensation of fullness. On the other hand, the lateral hypothalamic area is the feeding center.
And when stimulated, it causes the sensation of hunger. Finally, there's the arcuate nucleus, which is like a switchboard that receives various signals from the gastrointestinal tract.
This nucleus sends neuron fibers that regulate the feeding center and the satiety center. All right, let's say you forgot to buy lunch and it's the late afternoon.

Hunger Pathway0:57–2:08

Two things happen to trigger your hunger. First, mckanna receptors in your stomach, detect that your stomach is empty.
So they fire slowly through the vagus nerve to a cluster of neurons in the medulla called the solitary nucleus. The solitary nucleus then sends nerve fibers to the arcuate nucleus in the hypothalamus.
The arcuate nucleus then activates the phoenix center through orexigenic neurons and inhibits the satiety center through anorexigenic neurons.
Orexigenic refers to something that stimulates the appetite and anorexigenic refers to something that inhibits the appetite.
In addition to this, the decreased firing of the McKinna receptors and low blood glucose levels triggers PD. One also known as ghrelin cells or GR cells for short in the lining of the stomach to secrete the hormone ghrelin into the body.
Ghrelin is the hunger hormone and it travels directly to the arcuate nucleus further causing it to stimulate the feeding center and inhibiting the satiety center.
All right. Now, let's say you decide to eat a tasty enchilada that enchilada stretches out your stomach and it increases the firing of the mckanna receptors.

Satiety Pathway2:08–4:45

This information goes through the vagus nerve and causes the arcuate nucleus to decrease stimulation of the feeding center and increase stimulation of the satiety center.
When food reaches the small intestine, it's broken down into glucose amino acids and fats. And these nutrients are detected by chemo receptors in the stomach and intestines.
These chemo receptors send signals through the enteric nervous system of the gastrointestinal tract. And that stimulates enteroendocrine cells which secrete various hormones, first fats and proteins cause eye cells in the duodenum and jejunum to release the hormone cholecystokinin or CCK proteins also cause L cells in the ileum and colon to secrete the hormone peptide yy and glucose causes L cells to release a glucagon like peptide one or GLP one, all three hormones can cause the arcuate nucleus to increase stimulation of the satiety center and inhibit the feeding center.
In addition, these hormones also have other functions. For example, CK triggers gallbladder, contraction and gut motility.
Peptide yy inhibits ghrelin secretion and glucagon like peptide increases insulin secretion from the pancreas. Insulin is also secreted when the blood glucose level is high, like when you eat a big meal full of carbohydrates.
And its main role is to cause cells to increase glucose uptake. Insulin also acts directly on the hypothalamus to stimulate satiety and inhibit hunger.
CCK peptide Yy and Glucagon, like peptide one and insulin are all short term or acute satiety hormones. Since they fluctuate throughout the day, depending on the food you've eaten.
Another hormone called leptin is considered the long term satiety hormone because its level in the blood remains relatively stable throughout the day.
Leptin levels increase slightly at night, which is responsible for the lack of hunger. When you're sleeping.
Leptin acts on the hypothalamus directly to reduce hunger and increase satiety. Leptin is produced by the adipose cells or fat cells in the body.
So the more adipose tissue you have, the more leptin you produce and it works to try to prevent overeating and obesity. All right.

Review4:45–5:19

As a quick recap, the arcuate nucleus is a switchboard that sends orexigenic neurons to the feeding center and anorexigenic neurons to the satiety center.
The arcuate nucleus receives information from the mckanna receptors through the vagus nerve, as well as various hormones.
Ghrelin is the hormone that stimulates hunger. While the hormones call a cytokinin peptide yy glucagon, like peptide one and insulin cause short term satiety.
And finally, there's leptin which causes long term satiety.