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Essay 3- How do hormones regulate satiety in mammals?
INTRO
Satiety is the feeling or state of being fed and full, with the absence of hunger.
The regulation of satiety is important for ensuring that mammals consume an
appropriate amount of food; enough to provide energy for body functions and to
obtain required nutrients, but not so much that obesity results. Control of hunger
is intrinsically linked to satiety; they are essentially opposites and are both
involved in controlling appetite and the amount of food eaten. Additionally their
regulation mechanisms are not distinct from one another; they involve the same
neurotransmitters and are heavily dependent on control by the hypothalamus.
Therefore, hormonal regulation of hunger must also be described when
explaining hormonal regulation of satiety.
THE HYPOTHALAMUS
The hypothalamus is the centre of control of hunger and satiety, regulated itself
by hormones. The arcuate nucleus of the hypothalamus projects to the lateral
hypothalamus, the hunger control centre, and to the ventro-medial nucleus of the
hypothalamus, the satiety control centre. The neurons in the arcuate nucleus
express peptides that increase hunger to stimulate food intake; neuropeptide Y
(NPY) and agouti-related peptide (AgRP). In addition pro-opiomelanocortin
(POMC) and cocaine-and amphetamine-regulated transcript (CART), which
decrease hunger and increase satiety and so inhibit feeding, are synthesised by
the neurones. These neurons and peptides are involved in control of both hunger
and satiety, and the levels of expression of the peptides is controlled by
hormones.
HORMONE 1 –
PROTEIN HORMONE REGULATORS OF HUNGER AND SATIETY
Protein hormone regulators of hunger and satiety include leptin and insulin,
which work in similar ways to decrease hunger levels and food intake. Leptin is a
protein hormone secreted by adipose tissue, and its concentration in the blood is
proportional to the mass of body fat, related to the amount of food that has been
stored. Insulin, another protein hormone, is secreted during digestion, and its
concentration in the blood is proportional to how much food has been or is being
digested and absorbed that day. Leptin and insulin are carried by transporters
across the blood brain barrier in levels proportional to their blood concentration
through the endothelium of capillaries in the brain, or move through
fenestrations in capillaries to enter the brain. They acts on receptors on neurons
in the arcuate nucleus of the hypothalamus, causing altered expression of genes
for neuropeptides and receptors. For example both cause the inhibition of NPY
synthesis and release, and Leptin is believed to stimulate the conversion of POMC
into alpha-melanocyte stimulating hormone in the arcuate nucleus, which acts as
a neurotransmitter. CART production is also stimulated by leptin. The result of
these actions of leptin and insulin is a suppression of appetite, and increased
satiety. During starvation, adipose tissue is used up and leptin levels decrease.
This results in an increase in hunger. Reduced leptin levels also highten the
activity of the rewards systems in the forebrain, such as those controlled in the
nucleus accumbens and amygaloid nuclei, to increase the reward from eating so
that the mammal is more driven to find food. In combination insulin and leptin act
to set the overall daily hunger level and therefore food intake, but the times at
which mammals are driven to eat is variable. Between meals blood glucose levels
fall, and the blood levels of the peptide hormone ghrelin secreted from the
stomach rise. Ghrelin is an appetite stimulant, acting via stimulates synthesis and
secretion of NPY and AgRP in the arcuate nucleus of the hypothalamus. These
changes are thought cause the immediate drive to eat. Peptide hormones other
than gherlin are involved in control of satiety and hunger; these act more quickly
than the protein hormones leptin and insulin.
PEPTIDE HORMONE REGULATORS OF SATIETY
FEED FORWARD CONTROL NOT THE SAME THING!!!!!
Peptide hormone regulators of satiety include cholecystokinin (CCK), and
peptide YY (PYY), that are involved in control mechanisms to regulate food
intake. There is a time lag between when eating starts and when leptin and
insulin act to control the level of food that is consumed, therefore the
hypothalamus requires a warning that a meal has been eaten, will be digested,
and that energy reserves will be replenished soon, in the form of temporary
satiety signaling more immediately after food is eaten, using these peptide
hormones. These are important in ensuring that not too much food is consumed
as it takes time for food to be digested, and so for insulin to signal to the
hypothalamus, and incorporated into energy reserves, and so for leptin to signal
to the hypothalamus. The peptide hormone CCK is released into the blood during
digestion from the duodenum where it is synthesised, and along with being
involved in the control of stomach emptying, stomach secretions, bile secretion,
and stimulating secretion of pancreatic digestive enzymes it is an important
temporary satiety signal. The levels of CCK are proportional to the amount of
food in the gastro-intestinal tract that will be absorbed in due course. The
greater the levels of CCK, the more full the mammal feels. This has been
demonstrated experimentally; injection of mammals with CCK while eating a
meal will cause them to feel full more quickly, resulting in suppression of
appetite and the test subjects eating less. For example; rats injected with CCK
when they feed eat smaller meals due to lack of hunger more quickly after eating
has commenced. However, possibly due to the action of leptin and insulin the
overall level of hunger throughout the day is the same, so the rats ate more
frequently, resulting in the overall daily energy intake being constant. CCK acts
on receptors in the lateral hypothalamus, interacting with CCK-A G-protein
coupled to reduce appetite. Rats deficient in the CCK-A receptor are obese,
illustrating how CCK action is important in reducing food intake.
Another peptide hormone involved in regulation of satiety is peptide YY (PYY),
which acts on Y G protein coupled receptors in the hypothalamus. Produced by
cells in the intestine, it is released into the blood after food is eaten in levels
proportional to the energy content of the meal. It acts on the Y receptors to
inhibit NPY production, and stimulates POMC production to decrease hunger
levels, and increased satiety resulting in a reduction in food intake. There are
many other peptide hormones involved in regulation of satiety, that work in
similar ways to CCK and PPY.
CONCLUSION
In conclusion hormones including leptin, insulin, CCK and PPY regulate satiety by
being secreted in levels proportional to the amount of food that has been stored
in the body, or that is being digested. Although they have different hormone
structures, protein or peptide, and some are involved in more temporary satiety
signaling, all function in very similar ways. They all act in negative feedback
mechanisms that are used to control the amount of food that is consumed, and all
function by action on the hypothalamus.
BIBLIOGRAPHY
Austin, J., & Marks, D. (2009). Hormonal Regulators of Appetite. International
Journal of Pediatric Endocrinology, 2009, 141753. doi:10.1155/2009/141753