Obesity and Omega-3s Reduce Appetite

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Appetite, by definition, is a term used to describe ones natural desire for food. It differs from hunger and satiety, and it is affected by a host of neural, hormonal and physical factors that may vary between individuals. This essay sets out to explain how these factors affect the appetite. In doing so the essay will explore the different regions of the brain (and the body) involved in its regulation and control, and the ways in which these areas may be pharmacologically and surgically manipulated to control the appetite itself.

Appetite can be described as ones instinctual desire for food. The smell and sight of food can trigger thoughts that lead to an increased flow of gastric juices in both the mouth and stomach. Sometimes however, the physical sensations aroused by appetite can be confused with feelings of hunger. Whereas hunger arises when the body requires and craves certain nutrients and calories, appetite arises only as a result of specific psychological triggers (such as memory and smell). Both appetite and hunger ensure the body is fed with food, leading to feeling of fullness and the desire to stop eating again. This full feeling and desire to discontinue eating is known as satiety.

Physiologically, appetite is controlled primarily by three parts of the brain. These include the orbitofrontal cortex of the limbic system, the arcuate nucleus within the appetite centre of the hypothalamus, and brainstem.

Neurons found in the orbitofrontal cortex of the brain’s limbic system are the first to be stimulated and respond to sensory signals that are generated in the presence of food[1]. It is here that the sensory inputs produced by food interact with hunger/satiety signals, allowing us to decipher how pleasant the food is and whether or not we have an appetite for it. It is proposed that hypothalamic neurons (that respond to hunger/satiety signals) send connections to the orbitofrontal cortex to inform it of these signals. It is also suggested that the source of these hypothalamus-orientated signals cause hypothalamic neurons only to respond to the sensory properties of food if hunger exists in the orbitofrontal cortex.

The Hypothalamus is the part of the brain that connects the central nervous system to the endocrine system via the pituitary gland[2]. Through vagus nerves stimulation, it controls the anterior side of the pituitary gland and consequently many of the body’s organs. Located above the brainstem and below the thalamus, the hypothalamus contains clusters of neurons known as nuclei that each carries their own function. These nuclei and other areas of the brain are connected via small neuronal projections, which allow the hypothalamus to regulate appetite and energy intake by coordinating signals between the gastrointestinal tract, peripheral circulation and brain[3].

Recent scientific research has revealed that one of these nuclei, the arcuate nucleus, houses a centralized area dedicated to appetite control. This is commonly referred to as the ‘appetite centre’ [4]. It comprises of many neuronal cell bodies that have sensors known to oversee many of the hormones and neuropeptides that regulate appetite. These sensors are able to monitor these metabolites, and are able to adjust the activity levels of individual organs accordingly to allow the hypothalamus to suppress or stimulate the appetite (in accordance with the changes in energy expenditure).

The appetite centre itself comprises of two different types of neurons, primary and secondary neurons[5]. Primary neurons measure metabolite levels and may regulate appetite effecting neuropeptides such as NPY, POMC and AgRP. Secondary neurons found in the appetite centre use vagal signaling to synchronize information form the primary neurons and coordinate bodily functions accordingly.

The brainstem indirectly affects appetite by providing a pathway for satiety signals to reach the hypothalamus, which is ultimately in charge of appetite...
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