ingestive behaviors study guide
Set Point Theory
The primary goal is to achieve homeostasis.
Homeostasis is maintaining a stable internal environment despite external changes. Such as body temperature, glucose levels, pH balance.
Think of a thermostat. It would need detectors to monitor temperature.
Hunger and thirst may operate in the same way.
Digestion In The Mouth
Physical chewing breaks down food.
Saliva moistens food and buffers pH.
Food mass is called a bolus.
Digestion In The Esophagus
Peristalsis is the involuntary, wave-like contractions that push food toward the stomach.
Digestion In The Small Intestine
The small intestine completes the digestion of food by absorbing nutrients through the lining.
Digestion In The Large Intestine
The large intestine absorbs water from indigestible food and sends the rest out of the body as waste.
Digestion In The Stomach
The stomach uses an enzyme, Pepsin, to break down food.
The stomach is highly acidic to kill microorganisms and to help break down food.
Bolus + stomach juices = chyme.
Chyme is an acidic mass of partially digested food and digestive secretions that moves into the small intestine.
Does The Stomach Help Us Feel Full?
Stomach contractions accompany hunger pangs.
Hunger pangs are the growling, crampy feelings when you’re hungry.
An empty stomach contracts rhythmically, stimulating hunger signals.
A stretched stomach from food or water changes the firing rate of hypothalamic cells.
The hypothalamus is a key region for hunger and satiety; therefore, when full, the hypothalamus decreases hunger-promoting neurons and increases satiety-promoting neurons.
When food is removed from the stomach, the absence of stretch leads to eating.
Increased food in the stomach leads to a reduction in eating.
Is the Stomach The Center Of Hunger?
The stomach releases neuropeptides that serve as hunger cues.
HOWEVER, removing the stomach from the body still leads to normal eating behavior.
Therefore, hunger cannot be 100% from the stomach.
In a research study, blood transfusions were made from well-fed rats to food-deprived rats; those rats stopped eating.
So, something in the blood must make one feel hunger and satiety.
Glucostatic Theory
States that glucose levels are the most important hunger cue.
Injecting glucose into hungry animals suppresses eating.
Injecting insulin, which lowers glucose levels, increases eating.
Glucose levels drop 10 minutes before a meal.
Injecting glucose at that time can prevent the meal.
Although if you wait too long and inject it 3-4 minutes before the meal, the meal will still be eaten.
Glucoreceptors
Glucoreceptors detect glucose levels and are found in the brain and liver.
Thioglucose is a fake glucose, but it is damaging to glucoreceptors.
However, injecting glucose into the ventromedial hypothalamus does not suppress hunger.
As a result, animals overate and became obese because their brain couldn’t sense glucose properly.
Sugars such as fructose are processed in the liver and lead to satiety despite being unable to cross the blood-brain barrier.
But, severing the connections between the liver and the brain does not change eating behaviors.
Problems With The Glucostatic Theory
Diabetes patients have little to no insulin levels.
This leads to high glucose levels, causing an increase in appetite.
It may not be about how much glucose is in the blood, but how much of the glucose is utilized for energy.
Therefore, diabetics have high glucose levels, but low utilization of it.
How Leptin Works For Hunger
Leptin-deficient mice were obese.
Leptin injections led to a 30% loss in body weight.
Leptin comes from body fat; therefore, more body fat equals more leptin.
Leptin may work in the hypothalamus and inhibit neuropeptide Y (NPY).
NPY triggers eating behaviors.
Leptin, Genetics, and Human Obesity
Genetic deficiencies of leptin in humans are rare.
8-year-old girl with 57% body fat and 190 lbs.
2-year-old boy with 54% body fat and 64 lbs.
In both circumstances, leptin injections helped them control their weight and eating habits.
Since obese people typically have more leptin, they may have leptin resistance since high leptin levels in normal individuals decrease hunger.
Injecting leptin as a dieting agent for normal obese people has not led to great results.
CCK and Hunger
Cholecystokinin (CCK) is a “fullness hormone“ released in the small intestine when you eat fat and protein.
Tells the brain, “We’ve got enough nutrients, stop eating!“
Injecting CCK stops eating behaviors.
CCK-blocking drugs lead to eating.
CCK receptors are located in the ventromedial hypothalamus.
High CCK levels cause nausea.
This begs the question: Does CCK stop eating because it promotes satiety or because it makes you feel queasy?
NPY and Hunger
Injections of NPY lead to extreme overeating.
Especially carbohydrates.
Since CCK suppresses appetite, CCK suppresses NPY.
NPY is found in the hypothalamus.
Problem: NPY is the most abundant neuropeptide in the brain.
Linked to memory, body temperature, blood pressure, sexual function.
Found all over the brain, as well.
Ghrelin and Hunger
Ghrelin levels increase when fasting and drop after a meal.
Therefore, ghrelin promotes hunger.
Ghrelin binds to receptors in the arcuate nucleus of the hypothalamus.
Ghrelin responds more strongly to low glucose levels than fat/protein levels.
Ghrelin breaks down into obestatin, which reduces appetite.
Ventromedial Hypothalamus (VMH)
Lesions to the VMH lead to overeating.
When lesioned, rats overate and doubled in body weight in a few weeks.
However, the rat gets a new set point and feeds normally at the new weight.
Stimulation of the VMH leads to satiety.
The VMH may control insulin levels.
An increase in insulin levels is seen after lesions.
Increased insulin increases eating.
Damage may change the amount of insulin that is released.
Lateral Hypothalamus (LH)
Lesions to the LH lead to starvation.
When lesioned, rats starved themselves.
But, this can be overcome by force feeding.
Eventually, the force-fed rats ate on their own.
Stimulation of the LH leads to eating.
The LH may be linked to reward systems.
The LH may be linked to attention.
Damage to the LH can lead to sensory neglect.
If pinched (stimulation), rats with LH damage will eat.
Osmometric & Volumetric Thirst
Osmometric thirst detects water movement in and out of cells.
Volumetric thirst detects less volume in the extracellular fluid.
Osmometric & Volumetric Thirst Brain Areas
Lamina terminalis
Borders the ventricles in the brain.
Contains cells outside of the blood-brain barrier.
Able to more easily monitor fluid levels.
Short-Term Hunger
Glucose utilization may be monitored for short-term hunger.
Long Term Hunger
Leptin levels and fat stores may be more important for long-term hunger.