5 hunger

Question 1

what causes hunger

Answer 1

Stomach releases ghrelin during food deprivation, and acts on hypothalamus to increase* appetite

Question 2

What does the quantity of food taken in depend on?

Question 3

How is body weight regulated?

Question 4

Why do diets stop working after a while?

Question 5

digestion and energy: what 3 ways is energy delivered in?

Answer 5

Lipid (fats)
Amino acid (breakdown product of protein)
Glucose (breakdown of sugar, from carbohydrate)

Question 6

digestion and energy: what 3 ways is energy stored in?

Answer 6

Fat (most preferred way of storing: stores more energy)
Glycogen
Proteins

Question 7

short summary of 3 phases of metabolism

Answer 7

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

Question 8

phase 1 of metabolism: cephalic phase

Answer 8

preparatory phase, which is initiated by the sight, smell, or expectation of food.
insulin levels high
glucagon levels low

Question 9

phase 2 of metabolism: absorptive phase

Answer 9

nutrients from a meal meeting the body’s immediate energy requirements, with the excess being stored
insulin levels high
glucagon levels low

Question 10

phase 3 of metabolism: fasting phase

Answer 10

energy being withdrawn from stores to meet the bodys immediate needs
glucagon levels high
insulin levels low

Question 11

in metabolism, the cephalic phase and absorptive phase promote….. and inhibit…..

Answer 11

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

Question 12

The last phase of metabolism (fasting phase), promotes…. and inhibits….

Answer 12

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

Question 13

2 pancreatic hormones

Answer 13

Insulin:
High during cephalic and absorptive phase
Glucagon:
High during fasting phase

Question 14

set point theory and its 3 components

Answer 14

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

Question 15

glucostatic theory

Answer 15

a set point for glucose
glucose levels “set point.” short term regulation because glucose levels change often

Question 16

lipostatic theory

Answer 16

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.

Question 17

problems with set point theory

Answer 17

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?)

Question 18

leaking barrel theory / settling point theory

Answer 18

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.

Question 19

glucostatic theory 1

Answer 19

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

Question 20

2 cholecystokinin

Answer 20

This chemical stimulates ‘satiety’‐neurons.

Question 21

3 paraventricular nucleus

Answer 21

Activation of the neurons in this nucleus (in the brain) leads to increased feelings of satiety.

Question 22

4 positive incentive theory

Answer 22

This theory claims that the quantity of food consumed depends on the pleasure and positive
feelings that eating brings.

Question 23

5 leptin

Answer 23

This chemical stimulates ‘satiety’‐neurons and at the same time it inhibits ‘hunger’‐neurons.

Question 24

6 arcuate nucleus

Answer 24

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

Question 25

7 lateral hypothalamus

Answer 25

activation of the neurons in this nucleus (in the brain) facilitates feeding in many ways.

Question 26

8 lipostatic theory

Answer 26

This theory claims that everybody has a set point for body fat; this is a long-term system.

Question 27

10 gherlin

Answer 27

This chemical stimulates ‘hunger’‐neurons.

Question 28

sham eating

Answer 28

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.

Question 29

what chemical stimulates satiety and which chemical stimulates hunger

Question 30

insulin

Answer 30

helps to lower blood glucose levels - these insulin levels can differ between people

Question 31

glucagon

Answer 31

promotes using free fatty acids for energy. When insulin is high, glucagon is low. When insulin is low, glucagon is high

Question 32

hunger

Question 33

satiety

Question 34

hunger related hormone

Answer 34

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.

Question 35

satiety related hormone

Answer 35

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

Question 36

hormone related to body fat

Question 37

sensory specific satiety

Answer 37

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

Question 38

appetizer effect

Answer 38

eating appetizers or small things before an actual meal makes you more hungry

Question 39

Role of blood glucose levels in hunger and satiety:

Answer 39

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.

Question 40

causes of obesity

Answer 40

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

Question 41

Factors that determine what we eat

Answer 41

learned taste preference and aversions, seeking vitamins and minerals (dietary deficiencies), appetizer effect of satiety, social influences

Question 42

Factors that influence when we eat:

Answer 42

pre meal hunger, pavlovian conditioning of hunger

Question 43

Factors that influence how much we eat:

Answer 43

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)

Question 44

satiety signal

Answer 44

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