In order to ensure that we continue to eat food to fuel our bodies, we experience the sensation of hunger.
In this article, we will look at the key signals involved in the control of appetite, including those that promote hunger and those that cause satiety.
Appetite Control Centre
The appetite control centre is located in the hypothalamus. Within in hypothalamus lies the arcuate nucleus, which plays a key role in the control of appetite.
The appetite centre contains both primary and secondary neurones. The primary neurones process external signals, be it neuronal, hormonal or nutritional. The secondary neurones are then responsible for co-ordinating the inputs received via the primary neurone.
These primary neurones are either excitatory or inhibitory. The neurotransmitters released by excitatory and inhibitory neurones are:
- Excitatory: Neuropeptide Y (NPY) and Agouti-related peptide (AgRP). These promote hunger.
- Inhibitory: POMC and CART. POMC can be cleaved into other neurotransmitters such as α-MSH and β-endorphin. These suppress hunger.
From the Gut
Ghrelin is a peptide hormone produced in the pancreas and released from the stomach wall when the stomach is empty. This stimulates the excitatory primary neurones, and therefore stimulates appetite. When the stomach is full, ghrelin release is inhibited, thus the appetite stimulus is also inhibited.
PYY (full name – peptide tyrosine tyrosine) is a short peptide hormone released by cells in the ileum and colon in response to feeding. It inhibits the excitatory primary neurones of the arcuate nucleus. This causes appetite suppression.
From the Body
Leptin is a peptide hormone released into the blood by adipocytes (fat cells). Leptin stimulates the inhibitory neurones and inhibits the excitatory neurones in the arcuate nucleus to cause suppression of appetite.
Insulin is a hormone released from beta cells in the islets of Langerhans of the pancreas. This suppresses appetite in a similar way to leptin.
Clinical Relevance – Leptin Deficiency
Leptin deficiency may arise from deletion of the leptin gene causing severe obesity, hyperphagia (excessive eating) and a reduced metabolic rate. However, this is incredibly rare.
Leptin deficiency can also be found in conditions and syndromes where there is significant lipodystrophy. The effects of leptin deficiency can be reversed with the use of exogenous leptin.