A homeostasis theory of hunger

[ajmemeni_cro]

According to control theories (most having origin in the cybernetics), behavior is produced to maintain a certain sensed variable on a set-point (also called a refference point).

If the sensed variable is below the refference point, the organism will behave in a way that increases the sensed variable. If it is above the refference point, the organism will behave in a way that decreases the sensed variable.

There are many examples in the body - the sugar level (regulated by insulin and glukagon), body temperature (regulated by various means: sweating, shivering, taking clothes on or off, ...).
To sense a variable, the system must have a sensor for it. There are sensors for sugar levels, there are sensors for body temperature and all the other controled variables.

When it comes to hunger, I don't think there is a general explanation of how it works and I'm wondering why is that.
What might be the sensors for hunger?

They apparently don't have a lot to do with calorie intake, that is not measured directly. If it were, no one would be overweight. There seems to be a connection to the protein ratio in diet (protein rich diets beeing more satiating), and there certainly seems to be a conection to spent energy - exercise increases hunger, as well as periods of not taking food (basal metabolism spendig energy).

Comments?

[hankst]

Hunger and satiation are very complex, and several factors influence things.

Satiation:
- sensoric qualities of food (taste, smell, looks)
- GI tract content and filling
- nutrients in the intestines + blood
- metabolites in the liver
- (high) ATP concentration in the liver
- several hormones and peptides (cck, glucagon, ****tostatin, glp, grp, leptin, insulin, estrogens)
- CNS (serotonin, crf)

Hunger:
- sensoric qualities of food (taste, smell, looks)
- (low) ATP concentration in the liver
- sinking body temperature
- hormones (ghrelin, progesteron, glucocorticoids)
- CNS (noradrenaline, dopamin, npy, ghrf)

Edit:
Protein rich diets are only more satiating in the short term, in the long term it evens out - and I have no source of backing that up, except our prof @ uni.

[KLMARB]

I think you might be looking for the hexsosamine biosynthetic pathway, regarding leptin flux.

[ajmemeni_cro]

Hunger and satiation are very complex, and several factors influence things.

Satiation:
- sensoric qualities of food (taste, smell, looks)
- GI tract content and filling
- nutrients in the intestines + blood
- metabolites in the liver
- (high) ATP concentration in the liver
- several hormones and peptides (cck, glucagon, ****tostatin, glp, grp, leptin, insulin, estrogens)
- CNS (serotonin, crf)

Hunger:
- sensoric qualities of food (taste, smell, looks)
- (low) ATP concentration in the liver
- sinking body temperature
- hormones (ghrelin, progesteron, glucocorticoids)
- CNS (noradrenaline, dopamin, npy, ghrf)

Edit:
Protein rich diets are only more satiating in the short term, in the long term it evens out - and I have no source of backing that up, except our prof @ uni.

In control theories, the causal loop is precicely defined. There is a sensor of the controled variable (for example, the sensor for the tendon tension is a special cell in the tendon). there is a comparator that compares the sensed quantity with the refference quantity (usualy a neuron) and there are effectors that work on changing the sensed variable (muscles).

So. The comparators in the loop that controls the energy balance (or something like that) are somewhere in the brain. They might use those neurotransmiters you wrote in communicating with the effector neurons that create the sense of hunger.

The hormones might be communication carriers between the organs that need energy and the the sensors of hunger.

[sensing levels of certain hormones (A)]---->[comparing to a refference value(B)]--->[if A>B, stop eating], [if A<B, eat]--->again to the start of the loop.

[ajmemeni_cro]

I think you might be looking for the hexsosamine biosynthetic pathway, regarding leptin flux.

I don't know much about that, could you write some cliffs?

[MakeABanana]

I don't know much about that, could you write some cliffs?

Cliffs:
- Adipocytes receive glucose and enters glycolysis
- A small percentage of the fructose-6-phosphate produced in glycolysis ends up in the hexosamine pathway
- Fast forward, and you get uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) from the hexosamine pathway
- Leptin release from adipocytes is regulated by UDP-GlcNAc; the more UDP-GlcNAc, the more leptin is released.

[HydroStorm]

There's also leptin resistance that can entirely throw of one's homeostasis of hunger once someone has an impaired endocrine function &/ abnormal amounts of visceral fat.