Introduction
The control of energy balance requires an understanding of the terms hunger, appetite and satiety. Hunger
is the craving for food that is associated with objective sensations and is a general sensation localized to the
stomach region; it appears when the stomach is empty and coincides with contractions detected by
mechanoreceptors in the stomach wall. Appetite by contrast is the desire for specific types and quantity of
food and satiety is the opposite of hunger resulting from a filling meal. The latter can be divided be divided
into two components, pre and post absorptive. As in drinking, food consumption ceases before absorption
of food from the gastrointestinal tract (GIT) has corrected any energy imbalance. In addition, a post
absorptive component prevents hunger.
For the body to be in energy balance the energy content of food must correspond to energy expenditure of
muscular work, growth, reconstruction and loss of heat from the body. Although these notes will be limited
to control of food intake we do have appetites for minerals if they are lacking. For example you can show a
preference for saline to water if you lack adrenal glands or calcium to water if you lack parathyroid
function.
What are the factors influencing food intake?
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increased plasma glucose concentration (-)
increased production of hormones such as insulin and glucagon and the GIT hormones (-)
increased body temperature (-)
increased palatability of food (+)
stress (+/-)
conditioned responses (+/-)
activation of stomach/ duodenal receptors, stretch receptors and chemo receptors (-)
Physiological control mechanisms.
The physiological control mechanisms can be broadly divided into short or long term regulation. There are
two theories that are reported to be important in the short term regulation:
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glucostatic theory of hunger
plasma amino acid levels
In the first, the glucostatic hypothesis suggests that the availability of glucose appears to play a crucial role
in eliciting hunger. There is ample evidence for glucoreceptors in the CNS. In addition the hypothalamus is
known to receive afferent information from the liver, stomach & small intestine via the vagus. It has also
been shown that depletion of glucoreceptors causes severe disturbances of feeding but there is some
question as to whether glucose is the only regulator. In contrast there is only one theory that is reported to
be important in long term regulation, the lipostatic hypothesis.
Lipostatic hypothesis:
Fat (adipose tissue) of mammals represents an organ which is widely distributed throughout the body and
fluctuates according to metabolic energy demands. Mature adipocyte tissue communicates with the central
nervous system via a hormone circuit that controls satiety. Excessive food intake leads to the deposition of
fat, insufficient food intake decreases fat deposits. One can therefore assume that the body can monitor the
products of fat metabolism. Obesity comprises complex interactions of genetic and environmental factors
and so the mechanism that balances food intake and energy expenditure determines those of us that will be
obese and those that will be lean. One of the molecules that regulates energy balance is the product of the
obese (ob) gene, LEPTIN, a 16kD protein (from the prefix LEPT- or LEPTO- meaning thin and the suffix
-IN commonly given to proteins) which is probably able to function as part of the signalling pathway from
adipose tissue that acts to regulate body fat deposits due to its action on satiety. Leptin, via its action on
metabolism and appetite, is able to;
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lower body weight
lower percentage body fat
reduce food intake
reduce serum concentrations of glucose
reduce serum concentrations of insulin
increase metabolic rate
increase body temperature
increase activity
inhibit neuropeptide Y (NPY) synthesis and release.
The thermostatic hypothesis
The third hypothesis implicated in the control of body weight is the thermostatic hypothesis. It has been
shown that warm-blooded animals consume food in amounts inversely proportional to environmental
temperature. Central thermoreceptors could act as sensors of overall energy balance. This theory is
supported by evidence that local cooling of the CNS can alter feeding behaviour although cooling could, in
theory alter the activity of any neurones and may not be specific. The main evidence for this hypothesis
involves the reaction to fever when there is a reduction in food intake. This is more likely to be the result of
the action of cytokines - cf cytokines later in this account.
Sensory mecahnisms involved in the control of food intake
The sensory mechanisms involved in control of food intake include those from olfactory, taste and
mechanoreceptors in the mouth, throat & esophagus. Evidence from animals with esophageal fistulae show
that they have more meals but do spontaneously stop eating. Much of the sensory information from the
thorax and abdomen travels via the Xth cranial nerve (vague) which is able to detect gastrointestinal filling
by use of mechanoreceptors in the stomach wall and chemoreceptors in stomach, upper small intestine &
hepatic portal bed. We all know that the effect of a "full" stomach gives us the feeling of satiety therefore
we can assume that gastric mechanoreceptors are involved. We also know that if we tube feed animals
before their mealtimes then there is a reduction in subsequent meals. This is due not only to stretching of
mechanoreceptors but also chemoreceptors sensitive to glucose or amino acids. The arrival of nutrients in
the GIT supresses intake. It is therefore highly probable that vagal coeliac afferents are critical for
preabsorptive detection of food.
HYPOTHALAMIC CENTRES.
The hypothalamus is thought to be the most important central relay and integration centre for both the sense
of hunger and satiety but is not involved in the basic mechanical features of the feeding process i.e.
salivation, preparation of food and swallowing. These are all controlled by the brainstem. The involvement
of the hypothalamus results from studies where regions have been either electrically stimulated or
destroyed and the effect on eating observed. Evidence has also been provided from experiments where the
activity of neurones has been recorded whilst sensory systems associated with food consumption have been
activated. Two main areas have been proposed;
SATIETY CENTRE (ventromedial hypothalamus)
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bilaterally destroy the ventromedial hypothalamus, rise in plasma insulin concentration, inhibition
of lipolysis, overeating
electrical stimulation increases sympathetic outflow, inhibits pancreatic insulin secretion,
stimulates lipolysis in adipose tissue and stops eating.
HUNGER CENTRE (lateral hypothalamus)
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receives olfactory, gustatory & visual inputs
senses changes in glucose concentration
bilaterally destroy the lateral hypothalamus, refusal to eat. If you stimulate it you overeat.
inhibited by glucose, insulin, CCK and vagal afferents
Neuropeptides as satiety factors;
Many peptides have been shown to modulate nutrient intake. Broadly speaking these can be divided into
hormones from the pancreas, GIT or the pituitary.
Gastrointestinal hormones
- all decrease food intake.
Cholecystokinin (CCK) is a prototypic satiety agent which decreases feeding. Although CCK is a GIT
hormone it is extensively distributed within the central nervous system (CNS). The role of CCK is complex
since there is evidence that it interacts with dopamine and opiate systems to also modulate psychoses and
anxiety.
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GIT hormone CCK (cholecystokinin) which is released mainly in response to fat entering the
duodenum plays an important role in satiety
released by duodenal mucosa when food is present in it
CCK injected into hungry animals causes them to stop eating
cutting the vagus nerves block the action of CCK.
although there are other peptides, including gastrin-releasing peptide and bombesin, known to be
"satiety factors" CCK appears to be the most important.
Pancreatic hormones
- all decrease food intake
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insulin (unless accompanied by hypoglycaemia) appears to play a role in the physiological control
of feeding.
glucagon and glucagon-like peptide amide (GLP-1), the latter, when injected
intracereboventicularly (ICV) inhibits feeding and GLP-1 receptors are present in the
hypothalamus, particularly PVN and parts of the amygdala
AMYLIN (also known as Islet amyloid polypeptide - IAPP) is a hormone co-stored and coreleased with insulin. It interferes with glucose metabolism and may act as a "satiety" factor.
pancreatic polypeptide
enterostatin.
Pituitary hormones
The evidence for the normal involvement of pituitary hormones in the control of food intake is limited and
is based on observations of eating habits when there is excessive hormonal production. Vasopressin and
thyrotropin-releasing hormone (TRH) decrease food intake. Melanocyte stimulating hormone (dMSH),
growth hormone and prolactin have all been shown to increase food intake.
The Cytokines
The cytokines are released from activated cells during acute and chronic pathological conditions of
infection and malignancy. Most of us have experienced the former with its accompanying suppression of
feeding. This suppression is also a familiar problem in the latter. The intracerebroventricular (ICV)
injection of interleukin 1 (IL-1) decreases short and long term food intake, interferon has a similar
influence. The cytokines bring about their action via the hypothalamus by acting directly on glucosesensitive neurones in the ventromedial hypothalamus (the "satiety" centre) and the lateral hypothalamus
(the "hunger" centre).
Methods of Measuring Body Composition.
BMI- Body Mass Index is measure of body fat based on height and weight that applies to both adult men
and woman.
BMI = weight (kg)/ (height*height)
Underweight < 18.5
Normal weight = 18.5-24.9
Overweight = 25-29.9
Obesity = or greater 30
Functions of fat.
1.
stored energy
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structural ( cell membrane)
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involve in nerve conduction
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critical for absorption of fat-soluble vitamins
5.
backbone for steroids