appetite regulation, energy balance

Question 1

hunger

sasiety

satiation

Answer 1

Hunger: Desire to eat due to an uncomfortable emptiness in the abdomen.
Satiation: Sensation of fullness during the meal leading to meal termination.
Satiety: Post-meal period feeling of fullness and determining the timing of the next meal.

Question 2

how is the hypothalamus used in hunger

Answer 2

The hypothalamus picks up neuronal and nutritional signals from the circulation

Role in Hunger:
Arcuate Nucleus (ARC) Activation:

The arcuate nucleus (ARC) IS the major control centre of hunger in the hypothalamus
-it contains neurons that are crucial for hunger regulation. There are two groups of neurons with opposing functions in the ARC.
1. appetite stimulaitng neurons including NPY + AGRP peptides
2. appetite supressing neurons including POMC peptide

Neurons of the ARC porject to other nuclei in hypothalamus, the PVN is the most important one in hunger. PVN neurons further process the information and project to other circuits outside the hypothalamus, thus coordinating a response that controls energy intake and expenditure.

Ghrelin’s Influence:

Ghrelin, a hormone produced in the stomach, acts on the growth hormone secretagogue receptor type 1A in the hypothalamus. This action enhances the activity of NPY and AgRP neurons while suppressing POMC neurons, thereby promoting hunger and meal initiation.

Question 3

short term regulation of hunger and energy

Answer 3

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 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 (fullness) of the stomach is perceived by the brainstem as satiety from stretch signals. 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
(Cholescystokinin: CCK is a potent satiety signal released by stretch receptors in stomach and picked up by brainstem and hypothalamus)

Question 4

long term regulation of hunger and energy

Answer 4

Long-term regulation 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.

Question 5

the role of leptin and ghrelin

Answer 5

-Leptin, produced by adipose tissue in proportion to overall body fat mass. A well fed state means more fat, which means more leptin secretion. Leptin signals energy sufficiency and promotes satiety by acting on receptors in the hypothalamus. Leptin thus increases metabolic rate, activity level, and temperature and inhibits Insulin synthesis and release and decreases food intake.

-Ghrelin, a hormone produced in the stomach, acts on the growth hormone secretagogue receptor type 1A in the hypothalamus. This action enhances the activity of NPY and AgRP neurons while suppressing POMC neurons, thereby promoting hunger and meal initiation.
- Grehlin levels drop shortly after a meal and increase before a meal and during fasting

Question 6

Hormones stimulating fullness (satiety)

Answer 6

LEPTIN- signals to the brain the body has enough stored energy, acts on hypothalamus to supress appetite

CCK- slows down gastric emptying, stimulates digestion, prolonging the sense of satiety

GLP-1- Promotes insulin secretion and slows stomach emptying

PYY- Acts on hypothalamus to reduce hunger and slow gastric motility, maintaining sense of fullness

Oxyntomodulin-

POMC-

insulin can also trigger satiety=

Question 7

hormones stimulating hunger

Answer 7

Ghrelin- stimulates food intake by acting on hypothalamus. Grehlin stimulates NPY AND AgPR.

NPY- most powerful appetite stimulating peptides, activated in low energy states

AgRP- works with NPY, inhibits signals from leptin and other satiety promoting peptides

Question 8

Hunger

Answer 8

Absolutely! With the background knowledge in place, let’s explain what happens when we feel full and what happens when we feel hungry in terms of the peptides, hormones, and neural processes involved.

What Happens When We Are Hungry
Hunger is the body’s way of signaling that it needs more energy. The process involves multiple signals from the stomach, brain, and other tissues:

Ghrelin Secretion:

Ghrelin, often called the “hunger hormone,” is primarily produced by the stomach.
When your stomach is empty (between meals or during fasting), ghrelin levels rise and enter the bloodstream, signaling to the brain that it’s time to eat.
Ghrelin acts on the hypothalamus, particularly stimulating NPY/AgRP neurons, which are hunger-promoting neurons.
These neurons send signals that increase your appetite, making you feel hungry.
Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP):

These are two peptides produced in the hypothalamus that are crucial for stimulating hunger.
NPY: One of the strongest appetite-stimulating signals in the brain. When energy levels are low (such as during fasting), NPY is released to increase food intake.
AgRP: This peptide works alongside NPY to increase hunger and suppress signals that reduce appetite (like those from leptin).
Low Leptin Levels:

When the body has low energy stores (low fat), leptin levels drop because leptin is produced by fat cells.
Low leptin signals to the brain that the body’s energy reserves are low, triggering hunger. It reduces the inhibition on hunger-promoting neurons (like NPY and AgRP).
Gastrointestinal Signals:

The empty stomach triggers the production of ghrelin, but the GI tract is also quiet in terms of fullness signals (like PYY and CCK, which are not produced when the stomach and intestines are empty).
Motivation to Eat:

As these hunger signals (ghrelin, NPY, and AgRP) ramp up, the brain increases cravings for food and activates reward centers. You become more motivated to seek food and eat, often craving high-energy foods to quickly replenish energy reserves.

Question 9

Satiety

Answer 9

What Happens When We Are Full
Feeling full, or experiencing satiety, happens when the body has taken in enough food to meet its immediate energy needs. Several mechanisms come into play to signal fullness and reduce appetite:

Stretch Receptors in the Stomach:

As you eat, your stomach stretches. This sends signals to the brain via the vagus nerve, which communicates that the stomach is getting full.
This mechanical signal starts the process of reducing appetite even before nutrient absorption takes place.
Hormones from the Gut:

Cholecystokinin (CCK): Released by cells in the small intestine in response to the digestion of fats and proteins.
CCK slows down stomach emptying and stimulates the release of digestive enzymes. It also sends signals to the hypothalamus, creating a sense of fullness.
Peptide YY (PYY): Secreted by the ileum and colon after food passes through the intestines.
PYY acts on the brain to reduce hunger and slow gastric motility, helping you feel fuller for longer.
Glucagon-Like Peptide-1 (GLP-1): Also produced in the small intestine after eating, GLP-1 slows down digestion and stimulates insulin release. It acts on the hypothalamus to reduce appetite.
Leptin:

Leptin levels rise when your body has enough energy stored, particularly in fat cells. It is secreted by adipose tissue (fat cells) and acts on the hypothalamus to suppress hunger and promote energy balance.
When leptin levels are high, the brain knows that energy stores are sufficient, reducing the desire to eat.
Leptin primarily activates POMC/CART neurons in the hypothalamus, which promote satiety and inhibit hunger.
Inhibition of Hunger-Promoting Signals:

POMC/CART neurons, activated by leptin and satiety signals like PYY, CCK, and GLP-1, suppress the action of hunger-promoting neurons (like NPY and AgRP).
This reduces the release of hunger-stimulating peptides, keeping appetite low.
Insulin’s Role:

Insulin, produced by the pancreas after eating, also helps reduce appetite.
It works similarly to leptin by acting on the brain to signal that energy is available. Insulin inhibits hunger-promoting pathways and helps glucose from the meal be used or stored.
Motivation to Stop Eating:

As satiety signals increase, the brain’s reward centers become less activated by food, reducing the motivation to eat.
This leads to a feeling of fullness and satisfaction, prompting you to stop eating and allowing your digestive system to process the meal.