5 hunger Flashcards
what causes hunger
Stomach releases ghrelin during food deprivation, and acts on hypothalamus to increase* appetite
What does the quantity of food taken in depend on?
How is body weight regulated?
Why do diets stop working after a while?
digestion and energy: what 3 ways is energy delivered in?
Lipid (fats)
Amino acid (breakdown product of protein)
Glucose (breakdown of sugar, from carbohydrate)
digestion and energy: what 3 ways is energy stored in?
Fat (most preferred way of storing: stores more energy)
Glycogen
Proteins
short summary of 3 phases of metabolism
Cephalic Phase: happens before you eat (e.g. thinking) -> high insulin, low glucagon
Absorptive Phase: when you start eating and absorb energy -> high insulin, low glucagon
Fasting Phase: happens after eating and stored energy is consumed -> low insulin, high glucagon
phase 1 of metabolism: cephalic phase
preparatory phase, which is initiated by the sight, smell, or expectation of food.
insulin levels high
glucagon levels low
phase 2 of metabolism: absorptive phase
nutrients from a meal meeting the body’s immediate energy requirements, with the excess being stored
insulin levels high
glucagon levels low
phase 3 of metabolism: fasting phase
energy being withdrawn from stores to meet the bodys immediate needs
glucagon levels high
insulin levels low
in metabolism, the cephalic phase and absorptive phase promote….. and inhibit…..
promote
- using blood glucose as a source of energy
- conversion of excess glucose to glycogen and fat
- converting amino acids to proteins
- store glycogen in liver and muscle, fat in adipose tissue, and protein in muscle
inhibit
- conversion of glycogen, fat and protein into directly utilizable fuels (glucose, free fatty acids and ketones
The last phase of metabolism (fasting phase), promotes…. and inhibits….
promotes
- conversion of fats to free fatty acids and using free fatty acids as a source of energy
- converting glycogen into glucose, free fatty acids to ketones and protein to glucose
inhibits
- the use of glucose by the body but not by the brain
- the conversion of glucose to glycogen and fat, and amino acids to protein
- storage of fat in adipose tissue
2 pancreatic hormones
Insulin:
High during cephalic and absorptive phase
Glucagon:
High during fasting phase
set point theory and its 3 components
Assumes that there is a set-point (optimal point) for hunger
Has 3 components:
a set point mechanism → defines the set point
a detector mechanism → detects deviations from the set point
an effector mechanism → eliminates the deviations
glucostatic theory
a set point for glucose
glucose levels “set point.” short term regulation because glucose levels change often
lipostatic theory
a set-point for body fat
et point about weight. When weight deviates from set point, the assumption is you continue coming back to that point. Long term regulation about weight.
problems with set point theory
Does not take into account other factors
Unconfirmed research
Inconsistent with evolutionary reasons to eat (having a set-point does not make sense – why do people get obese?)
leaking barrel theory / settling point theory
Implies that body weight fluctuates around a certain settling point
Body weight remains stable as long as there aren’t long term factors that influence body weight
This model claims that the body weight tends to drift around a certain point, i.e. the level at
which the factors that influence weight achieve an equilibrium.
glucostatic theory 1
This theory claims that everybody has a set point for blood level of glucose; a short-term system.
glucose levels “set point.” short term regulation because glucose levels change often
2 cholecystokinin
This chemical stimulates ‘satiety’‐neurons.
3 paraventricular nucleus
Activation of the neurons in this nucleus (in the brain) leads to increased feelings of satiety.
4 positive incentive theory
This theory claims that the quantity of food consumed depends on the pleasure and positive
feelings that eating brings.
5 leptin
This chemical stimulates ‘satiety’‐neurons and at the same time it inhibits ‘hunger’‐neurons.
6 arcuate nucleus
In this nucleus (in the brain) we find 2 types of neurons: one group stimulate the feeling of
hunger, and the other group stimulates the feeling of satiety
7 lateral hypothalamus
activation of the neurons in this nucleus (in the brain) facilitates feeding in many ways.
8 lipostatic theory
This theory claims that everybody has a set point for body fat; this is a long-term system.
10 gherlin
This chemical stimulates ‘hunger’‐neurons.
sham eating
food swallowed wouldn’t reach stomach, so chewing and swallowing but not adding to fullness. Rats with familiar foods eat normal portion size, rats with unfamiliar foods ate more.
what chemical stimulates satiety and which chemical stimulates hunger
insulin
helps to lower blood glucose levels - these insulin levels can differ between people
glucagon
promotes using free fatty acids for energy. When insulin is high, glucagon is low. When insulin is low, glucagon is high
hunger
satiety
hunger related hormone
The Arcuate nucleus: 2 diff type of neurons: appetite stimulating neurons (NPY and AGRP peptides), and appetite suppressing neurons (POMC peptide). Projects to PVN to help with controlling energy intake and expenditure.
Norm is satiety feeling, hunger neurons inhibit the satiety feeling. This is done in 2 ways: the hunger neurons inhibiting satiety, and the neurons inhibiting pvn which also gets info about satiety.
Stomach releases ghrelin during food deprivation, and acts on hypothalamus to increase* appetite
Paraventricular hypothalamus: gathers all the information and provides it to the lateral nucleus. This is an inhibitory effect (can be low/high effect)
satiety=inhibiting your lateral nucleus. So by inhibiting the inhibitory effect, there’s no inhibitory effect on satiety….so you’re hungry
Lateral hypothalamus: releases orexin, which makes you seek food. Controls the insulin secretion and alters taste responsiveness, enhances taste of food (bc of axons from LH to NTS.) facilitates ingestion and swallowing.
satiety related hormone
Leptin - produced in fat cells, decreases appetite and increases fat metabolism. (Inhibits hunger, stimulates satiety.) Leptin is in proportion to your fat tissue, signals satiety/no need to continue eating because enough fatty tissue is present
Glucose - stimulates satiety
CCK (Cholecystokinin)- promotes satiety. Peptide released from gastrointestinal tract to vagus nerve → arcuate nucleus to tell brain you’re satiated
hormone related to body fat
sensory specific satiety
adaptive consequence to not eat the same food continuously to prevent malnutrition. Feeling satisfied with food/flavors you already consumed but if there’s a variety of different foods, you’ll still want that “new” flavor
appetizer effect
eating appetizers or small things before an actual meal makes you more hungry
Role of blood glucose levels in hunger and satiety:
Role of blood glucose levels in hunger and satiety:
Vagus nerve: conveys info about stretching of stomach walls (how full stomach is), the basis for satiety. This is the first signal given about how full your stomach is.
-After a small delay, then the chemical signals arrive to give longer-lasting feeling of satiety. Then the inhibitory effects can occur
Splanchnic nerve: Nerve that tells brain about nutrient contents of the stomach. This in combo with vagus nerve will convey satiety to brain.
causes of obesity
2 causes for obesity: lifestyle and genetic
-Leptin is in proportion to your fat tissue, signals satiety/no need to continue eating because enough fatty tissue is present
-A genetic example: Lack of leptin: (very rare in humans) ob/ob mice:
-Lifestyle cause: poor diet can provoke inflammatory response which leads to less sensitivity to leptin
Negative feedback systems:
Homeostasis: balance in body
Positive-incentive theory: drinking and feeding are motivated by anticipated pleasurable effects. (reward iss motivating factor)
Positive-incentive value: value of the food/drink about to be consumed. Value of the reward. Great value=more incentive
Factors that determine what we eat
learned taste preference and aversions, seeking vitamins and minerals (dietary deficiencies), appetizer effect of satiety, social influences
Factors that influence when we eat:
pre meal hunger, pavlovian conditioning of hunger
Factors that influence how much we eat:
serving sizes (smaller plate=eat less bc eyes believe the plate is quite full), social (when with people, you’ll eat more) (random addition: blue and green may make people eat less, red and yellow might influence eating more)
satiety signal
satiety signal: signal that depends on volume as well as nutritive density, tells us to terminate eating or keep going. Stomach is releasing peptides in the blood which can bind to hypothalamus (ex -melanocortin to inhibit food intake) (like CCK –which helps to reduce food intake per meal)g
-chewing also helps us feel satiated
