Complex Mechanisms of Hunger and Satiety in Humans

The control of food intake in humans involves a complex interplay between different physiological factors and mechanisms. The hypothalamus plays a crucial role with its distinct feeding and satiety centers that regulate eating habits based on signals affecting feelings of hunger or fullness. The glucostatic theory highlights how glucose levels influence these centers, impacting the desire to eat, while the lipostatic theory focuses on body fat's role in modulating food intake to maintain weight balance. Hormones like leptin, secreted by adipocytes and regulated by the gene obese (ob), are key in maintaining body weight, with deficiencies leading to obesity. Additionally, structures such as the nucleus tractus solitaries (NTS) provide taste sensations that affect feeding behavior, while ghrelin produced by the stomach induces hunger when active. Neuropeptide Y acts as a neurotransmitter influencing appetite and fat storage, while melanocortins and corticotropin-releasing hormone (CRH) reduce food intake under stress conditions. Peptide YY antagonizes ghrelin's effects by inhibiting feeding post-meal, with resistance observed in obesity cases. Orexin promotes eating by modulating meal size and is regulated by leptin and ghrelin. Collectively, these mechanisms illustrate the intricate network governing hunger and satiety, emphasizing their interdependence for balanced food intake.

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Running head: ANATOMY AND PHYSIOLOGY
Anatomy and Physiology
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Introduction
The control of food intake in humans is a very complicated process. Hunger as well as
satiety are being affected by different physiological factors and process, each of which has
salient features of its own.
Physiological mechanisms that influence food intake
The hypothalamus has two distinct centers which act during the regulation of food
intake. A feeding center that is tonically active and a satiety center that inhibits the feeding
center thereby stopping food intake. Signals from these centers results in the changes in
feeding habits of an animal and creates their sensation of hunger or fullness (Soria-Gómez et
al., 2014).
The glucostatic theory suggests that if the glucose level is high it inhibits the feeding
center by not suppressing the satiety center and as a result the animal loses its desire to eat.
When blood glucose level decreases due to excess of insulin the satiety center is suppressed
and as a result the feeding center gets activated and hence the animal senses hunger or has the
desire to eat. Hence in case of a diabetic patient whose glucose level is already high that
person will have less desire to eat. The lipostatic theory is another theory that states that the
bodies eating behavior is dependent on the amount of fat present in the body. The body
usually tries to balance its eating behavior by modulating the brain so that it can maintain a
certain amount of body weight. If the fat storage increases then eating decreases and vice
versa. Obesity is the result when this mechanism gets hampered.
A hormone called leptin is also responsible for maintaining the body weight of an
animal. It is secreted from adipocytes and acts as a messenger between the adipose tissue and
the brain. This protein is produced under the control of the gene obese (ob). It has been found

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that the animals lacking the gene leptin as well as animals having a defective leptin gene
tends to become obese (Hall, 2015).
Nucleus tractus solitaries (NTS) are a group of sensory nuclei which form a column
of grey matter which is embedded into the medulla oblongata. One of the main functions of it
is that it provides the sensation of taste from the facial nerve as it makes up around two third
portion of the anterior part of our tongue. If it is active more then it increases the food intake
whereas if it is damaged or less active then the person loses the desire to eat as the food
seems tasteless.
The hormone ghrelin is produced from stomach when the feeding center is active and
this hormone is responsible for the sensation of hunger. When the satiety center is active it
stops the synthesis of this hormone which results in loss of appetite and the desire to eat.
Neuropeptide Y (NPY) is a peptide which is composed of around thirty six amino
acids which acts between the autonomic nervous system and the brain as a neurotransmitter.
It is mainly acts as a vasoconstrictor and also helps in the buildup of fat tissue in the
abdominal region. It also interferes with the production of leptin and makes the gene mutated
at high concentrations which in turn results in excess food intake by the organism and results
in obesity.
Melanocortins are group of peptides which are released from the pituitary gland that
acts as receptors for various corticotropin hormones. Corticotropin-releasing hormone
(CRH) is a forty one amino acid peptide which is involved in stress response. It is released
from the hypothalamus and excess of CRH results in lowering of the NPY peptide and hence
reduces the food intake by the organism (Rizzo, 2015).

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Peptide YY (PYY) or peptide tyrosine-tyrosine is present in humans. It is made up of
thirty-six amino acids and is secreted from the ileum and colon in response to feeding. PYY
secretion inhibits feeding which is an antagonist to the function of ghrelin which induces
feeding by the sensation of hunger. Obese people become resistant to leptin and tend to have
less amount of PYY in their body (Crespo et al., 2014).
Orexin builds the desire to eat food, and associates with the capacity of the
substances that increases its production. Orexin is likewise appeared to increase the size of
the meal by the suppression of postingestive feedback. They are inhibited by the action of
leptin and becomes active by the action of ghrelin and hypoglycaemia (Sherwood, 2015).
Conclusion
From the above discussion, it is indicated that the sensation of hunger and satiety is
not dependent only on one or two factors but is a complex mechanism where various factors
play a crucial role. Each of these mechanisms is interlinked and function in collaboration to
maintain the balance of food intake as required by an individual.

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References
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