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Chapter 12
Ingestive Behavior
Introduction
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“The constancy of the internal milieu is a necessary component for a
free life.” – Claude Bernard
Animals have evolved from single cell organisms that live in the
ocean. In order to “carry” this environment with us (i.e. water and
solutes), our body and its cells must regulate their fluid balance
This regulation is part of what is called homeostasis – process by
which the body’s substances and characteristics (such as temp and
glucose level) are maintained at their optimal level
Mammals maintain homeostatic control of our body’s fluid and
energy through our ingestive behavior – intake of food, water, and
minerals such as sodium
Physiological regulatory
mechanisms
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A physiological regulatory mechanism is one that maintains the constancy
of some internal characteristic of the organism in the face of external
variability
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Four essential features:
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e.g. keeping body temp constant despite changes in ambient temp
System variable – the characteristic to be regulated; e.g. temp
Set point – the optimal value of the system variable; e.g. 78°
Detector – monitors the value of the system variable; e.g. thermostat
Correctional mechanism – restores the system variable to its set point; e.g. AC or
heater
Negative feedback – a process whereby the effect produced by an action
serves to diminish or terminate that action; when AC or heater is turned on
and successfully changes temp back to set point, the detector senses this
and turns AC/heater off
Satiation mechanism – a brain mechanism that causes cessation of hunger
or thirst, produced by adequate and available supplies of nutrients or water
Drinking
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Fluid balance
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Body contains 4 major fluid compartments:
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Intracellular and intravascular fluid must be kept in tight regulation
Intracellular fluid controlled by conc. of solutes in interstitial fluid
(normally isotonic, or same osmotic pressure, by process of diffusion)
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If ISF loses water (hypertonic), water will be pulled out of the cells
If ISF gains water (hypotonic), water will move into the cells
Blood plasma volume must be regulated in order to pump blood
effectively
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1 of intracellular fluid – 2/3 of body’s water
3 of extracellular fluid (intravascular fluid – blood plasma, cerebrospinal
fluid, interstitial fluid – b/t cells)
If blood volume too low (hypovolemia), lead to heart failure
For 2 different types of regulation, need 2 types of receptors: one
measuring blood volume, the other measuring cell volume
Drinking
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2 types of thirst
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Most times, we ingest more water or solutes than needed; these are
then excreted by kidney
When levels of either water or solutes are too low, corrective
mechanisms are activated: thirst, or salt appetite (rare for modern
humans)
Our bodies lose water continuously, through sweating, breathing,
urination, defecation, and in some circumstances through vomiting
Osmometric (osmotic) thirst – occurs when the tonicity (solute conc.) of
the ISF increases; e.g. when eat salty meal with no water
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Osmoreceptors – neuron that detects changes in the solute conc. of the ISF
that surrounds it
Hypertonicity of blood plasma (where salt is absorbed into) draws water
from ISF, which then causes water to leave cells; when blood volume
increases, the kidneys begin to excrete both water and solutes, allowing the
blood plasma volume to remain constant
Drinking
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2 types of thirst
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Osmotic thirst (con’t)
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Osmoreceptors located in the anterior hypothalamus, one of the
circumventricular organs (CVO’s)
OVLT (organum vasculosum of the lamina terminalis) – CVO located on the
blood side of the BBB, and thus substances dissolved in the blood are able
to pass through to the ISF of this organ
Volumetric thirst
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Produced when blood plasma volume is low
Leads to both thirst and salt appetite
2 types of receptor systems: Renin-angiotensin system & atrial
baroreceptors
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Renin-angiotensin system – hypovolemia activates kidneys to release an enzyme
called renin, which then catalyzes the conversion of a blood protein called
angiotensinogen into a hormone called angiotensin (AngII)
AngII stimulates secretion of hormones by posterior pituitary and adrenal gland
to conserve water and solutes, and stimulates drinking and salt appetite
Drinking
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2 types of thirst
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Volumetric thirst (con’t)
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Atrial baroreceptors
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The atria of the heart contains stretch receptors that detect when blood volume is
low, which then stimulates thirst
Neural mechanisms of thirst
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Sensory info from atria is conferred to the nucleus of the solitary tract
(NTS) in the medulla
AngII crosses weak BBB near CVO’s to provide thirst and salt appetite
signal (esp. via subfornical organ (SFO))
Neurons in SFO project to MnPO (median preoptic nucleus)
Eating
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Some facts about metabolism
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Food ingestive behaviors are more complex than those of water balance
We must obtain adequate amounts of carbohydrates, fats, amino acids,
vitamins, and minerals other than sodium
Absorption, fasting, and the 2 nutrient reservoirs
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Our bodies need food for “building blocks” (i.e. to construct and
maintain our organs and muscles) and “fuel”
Fuel comes from food we have consumed that travels through the
digestive tract, but those nutrients must be able to be stored for when
the gut is empty
2 types of reservoirs: short-term (carbs) and long-term (fats)
Nutrient reservoirs
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Short-term
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Located in cells of liver and muscles
Cells filled with complex, insoluble carb called glycogen
Cells in the liver convert glucose (obtained from diet) into glycogen and
store it; this storage is stimulated by the presence of insulin, a peptide
hormone produced by the pancreas
When glucose enters the body, some is stored as glycogen and some is
used as fuel
When there are low levels of glucose in the blood, the pancreas begins
to secrete glucagon, which stimulates the conversion of glycogen back
into glucose
This reservoir primarily serves to fuel the CNS
Nutrient reservoirs
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Long-term
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Adipose tissue – filed with triglycerides (complex molecules that contain
glycerol, a soluble carb, combined with 3 fatty acids)
Found beneath the skin and in various locations in the abdominal cavity
Cells can expand in size
Reservoir for rest of body besides brain
What keeps us alive when we are fasting; when body starts to use carb
reservoir, fat cells start converting triglycerides into fuel that cells can
use
Fatty acids can be metabolized by cells in all of the body except the
brain; glycerol can be converted to glucose in the liver for use in the
brain
So, why does brain get all the glucose?
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Insulin must be present at a cell in order for it to take up glucose into it
However, neurons and glia do not require insulin to take up glucose
Metabolism
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Fasting phase – the phase of metabolism during which nutrients are
not available to from the digestive system; glucose, amino acids,
and fatty acids are derived from glycogen, protein, and adipose
tissue during this phase
Absorptive phase – the phase of metabolism during which nutrients
are absorbed from the digestive system; glucose, and amino acids
constitute the principle source of energy for cells during this phase,
and excess nutrients are stored
What starts a meal?
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Social and environmental factors
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Often we eat out of habit or because of some stimuli present in our
env’t (e.g. clock, smell food)
Meal schedule very important: rarely adjust times of meals, but can
adjust size of meals
If we have eaten recently or if a previous meal was large, we tend to
eat a smaller meal
However, due to other social factors, such as parental cues (“finish your
plate”) or peer influence, satiety signals can be ignored
DeCastro and DeCastro (1989) found that the amount of food eaten
was directly proportional to the amount of other people who were
present during a meal
What starts a meal?
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Physiological hunger signals
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The amount of food that we eat is inversely related to the amount of
nutrients left over from previous meals
Fall in glucose level (hypoglycemia) is a potent stimulus for hunger
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Glucoprivation – a dramatic fall in the level of glucose available to cells
Hunger can also be caused by lipoprivation ( fall in level of fatty acids
available to cells)
2 sets of detectors for these metabolic fuels: one set located in the
brain (sensitive to glucoprivation) and the other in the liver (sensitive to
both glucoprivation and lipoprivation)
What stops a meal?
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2 types of satiety signals: short-term info from gastrointestinal tract,
long-term from adipose tissue
Head factors
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Receptors located in in head (e.g. eyes, nose, tongue, and throat)
provide info about appearance, odor, taste, texture, and temp of food
Most effects involve learning: taste and odor of foods can serve as
stimuli that permit animals to learn about the caloric density of foods
(e.g. sweet taste = glucose, fuel)
Rats can learn to eat less of a food with a particular flavor when the
eating of that food was paired with caloric infusion
What stops a meal?
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Gastric factors
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Stomach not necessary for feelings of hunger?
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Not completely true: when stomach is empty, a peptide called ghrelin is
secreted which activates a hunger signal
The stomach also contains receptors that can detect the presence of
nutrients
Intestinal factors
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Afferent axons from the duodenum (first portion of small intestine) are
sensitive to the presence of glucose, amino acids, and fatty acids
Entry of food into the duodenum suppresses food intake in rats; rats
fitted with a gastric fistula ( a tube that drains contents out of the
stomach) continue to consume food (this method is called sham
feeding)
The duodenum controls the normal rate of stomach empyting by
secreting a peptide called cholecystokinin (CCK), which also serves a a
satiety signal in the brain
What stops a meal?
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Liver factors
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Metabolic factors present in the blood
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The liver is the first organ to “learn” that food is being received by the
intestines; when it does so it sends a satiety signal to the brain
Insulin receptors in the brain may serve as a satiety signal
Long-term satiety: signals from adipose tissue
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Signals from the long-term nutrient reservoir may either suppress
hunger signals or augment short-term satiety signals
Some variable related to body fat (as opposed to weight) may serve as
the system variable
Leptin – hormone secreted by adipose tissue; decreases food intake
and increases metabolic rate
Genetically obese mice (ob mouse) cannot produce leptin, thus become
grossly obese
Brain mechanisms
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Brain stem
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Ingestive behaviors are evolutionarily old; thus controlled by “older”
parts of the brain (mid- and hindbrain)
Decerebrate animals (animals in which the brain stem has been severed
from the forebrain) can still perform basic ingestive behaviors (e.g.
chewing, swallowing) but not more complex ingestive behaviors (e.g.
foraging)
Hypothalamus
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Lateral hypothalamus (LH) lesions produce anorectic effects (stop
eating)
Ventromedial hypothalamus (VMH) lesions produce increase in food
intake and severe weight gain
Brain mechanisms
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Hypothalamus (con’t)
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Role in hunger
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Two populations of neurons in LH secrete hormones that stimulate hunger
and increase metabolic rate: melanin-concentrating hormone (MCH) and
orexin
Arcuate nucleus of the hypothalamus: secretes a NT called neuropeptide Y
(NPY) and a peptide called agouti-related peptide (AGRP); these both act on
the MCH and orexin neurons of the LH to induce hunger
Also, ghrelin secreted from stomach induces hunger
Role in satiety
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Arcuate nucleus also contains neurons that secrete both CART and α-MSH,
which serve to induce satiety
Eating disorders
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Obesity
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Evolutionarily old bodies living in a modern environment
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i.e. our bodies still act accordingly to possible times of famine; but in
modern industrialized nation, this is obviously unnecessary
Both genetic and environmental factors
Treatments include: pharmacotherapy, behavior therapy, gastric
surgery, combo
Unfortunately very common in modern world
Anorexia nervosa/bulimia nervosa
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Both exaggerated concern of body image
AN is refusal to maintain above certain BMI by not eating
BN concerns cycles of binge eating and purging behaviors (e.g.
vomiting, laxative use)
Not as common as obesity, ~2% of population