Now that we’ve all had our fill of that ‘oh-so-good’ holiday homemade cooking, and that we all feel a little bit guilty (I know I feel a little bit guilty); its time for the much anticipated post on how hunger is regulated.

Keep in mind that this information is what little understanding we have on the subject so far; how hunger is regulated is a very, very, veeeery complex system so bear with us. 

Lets get this party started

To simplify this let’s bring back our imaginary pal “John”.
John  is feeling kind of hungry, he ate his breakfast at 8am and its already noon. So he decides to go for a nice grilled chicken sandwich. Why did he feel hungry in the first place?

When he ate his nutritious breakfast, John’s body quickly secreted insulin to store any excess carbohydrates (carbs) into fat cells (adipocytes) which in turn were then full of lovely fat molecules. After a proper blood sugar level was obtained, insulin secretion started dropping; and after adipocytes have had their fill of fats, they started secreting leptin, which told John’s brain “hey man start feeling full already!”. All this is great but it still doesn’t tell us why he felt HUNGRY. We’re getting to that don’t you worry child (obvious SHM reference).

After his blood sugar levels begin to drop (due to constant usage by resting muscle, brain and red blood cells) and insulin levels reach very low concentrations, leptin is then downregulated (fancy way of saying the hormone was told to quit acting on its receptors).  Low blood sugar induces the release of two important hormones: Glucagon and Cortisol, to help maintain a proper quantity of sugar for important tissues. All of which then permits other molecules to bind to John’s neurons: Ghrelin, Neuropeptide Y, plus nervous signaling coming from the Vagal nerve (it innervates the stomach), all of these contribute to stimulate the feeling of hunger in a beautiful ballet of cellular signaling.

Glucagon and Cortisol are two hormones that function to release sugar from storage so that an adequate level is maintained in blood. Additionally they induce the synthesis of glucose from other sources (called gluconeogenesis).

Ghrelin, as was discussed in an earlier post, comes from the antrum of the stomach, it is released in pulses, with the highest peak of blood concentration occurring just before a meal, this has reinforced the notion that it plays a very important role in appetite regulation.

Neuropeptide Y (NPY), as its name states it is a neuronal peptide that binds to certain neurons in the hypothalamus (the place where appetite is regulated in the brain) and very potently stimulates appetite. NPY release is inhibited by high levels of insulin/leptin and when these inhibitory signals are no longer present, NPY is liberated thus hunger ensues.

Serotonin, another neuronal signal (neurotransmitter) acts directly on the hypothalamus via the vagal nerve stimulation: as the stomach stretches after food ingestion, vagal neurons fire their signals directly into the hypothalamus, stimulating serotonin release and acts directly on the neurons that both release NPY and causes an increase in appetite.

The recap !

Food ingestion → Insulin and Leptin spike, stomach distends and vagal nerve is stimulated → Insulin/Leptin/Vagal nerve inhibit NPY and Ghrelin → Appetite is inhibited.

Blood sugar diminishes → Cortisol and Glucagon are secreted → there is no inhibitory stimulation from Insulin/Leptin/Vagal nerve anymore → Appetite is stimulated.

All of this reading really got me hungry…

Or rather your NPY and Ghrelin are acting up???

Either way its nice to be back from the holidays and we wish you all a very prosperous 2013!

-LIMARP Staff