Feeding Behaviour Flashcards
(101 cards)
1
Q
What are appetitive components of feeding?
A
- Preparatory
- Thinking about eating
2
Q
What do the appetitive components of feeding consist of?
A
- Seeking out food/foraging
(detection and identification of food, approaching food and latency to eat, handling and subjugation) - Cost-benefit Analysis
(dangers, predators, trade-off, hedonic value, prior history, experience) - Choose appropriate diet (macro/micronutrients)
3
Q
What are consummatory components of feeding?
A
- Act of eating itself
4
Q
What are some examples of the consummatory components of feeding?
A
- Consumption of food
- Licking, chewing, swallowing
- Act of ingestions
5
Q
What is digestion?
A
Food -> Constituent elements -> Nutrient absorption
6
Q
What are the 3 sources of energy?
A
- Lipids (from fats)
- Glucose (from carbohydrates; complex starch/sugars)
- Amino acids (from proteins)
7
Q
What are 3 forms of energy storage?
A
- Body fat: most of the body’s energy stores, very efficient
- Glycogen: the most utilized; in the liver/muscles
- Muscle Proteins: less utilized as energy store
8
Q
What would your body look like if you did not store any energy as adipose tissue?
A
HUGE
9
Q
What are the 8 steps in digestion?
A
1 - Chewing
2 - Saliva lubricates food
3 - Swallowing
4 - Stomach = storage reservoir; HCl breaks down food; pepsin begins to break down proteins
5 - Stomach empties into duodenum (where most absorption happens)
6 - Digestive elements in duodenum break down protein/starches
7 - Fats are emulsified
8 - Remaining water/electrolytes are absorbed in large intestine; remainder is ejected from anus
10
Q
What are the 3 phases of energy metabolism?
A
1 - Cephalic phase (in head)
2 - Absorptive phase (nutrients)
3 - Fasting phase (no food processed)
11
Q
What are the 2 pancreatic hormones released from islets of Langerhans that control energy metabolism?
A
1 - insulin (beta cells)
2 - glucagon (alpha cells)
12
Q
During what phases is insulin present?
A
- Cephalic phase
- Absorptive phase
13
Q
What are 3 functions of insulin?
A
1 - Promotes glucose use (cell uptake)
2 - Energy conversions (to forms that can be stored)
3 - Promotes storage (in liver, brain, adipose tissue)
14
Q
During what phase is glucagon present?
A
- Fasting phase
15
Q
What are 2 functions of glucagon?
A
1 - Adipose tissue -> free fatty acids
2 - Fatty acids -> ketones (in brain)
16
Q
What happens when insulin is low?
A
Glycogen/protein -> glucose (use in brain; gluconeogenesis)
17
Q
What is the brain’s main source of energy?
A
- Brain uses glucose; it is not good at using ketones
18
Q
What 2 functions need to be regulated for energy maintenance?
A
- Regulation of eating (daily)
- Regulation of body weight (larger time scale)
19
Q
What are the 2 theories of hunger/eating?
A
- Set-point theories
- Positive incentive perspective
20
Q
What are the 3 components of set-point theories?
A
- Set-point mechanisms
- Detector mechanisms (senses)
- Effector mechanisms (triggers hunger/eating)
21
Q
What type of system is a set-point theory?
A
- Negative feedback system
- Maintains homeostasis
(optimal range)
22
Q
What are the 2 main set point theories?
A
- Glucostatic theory
- Lipostatic theory
23
Q
Describe the glucostatic theory?
A
- Short-term regulation of eating
- Daily triggers
- Maintain glucose levels
24
Q
Describe the lipostatic theory?
A
- Long-term regulation of eating
- Maintain lipid levels
- Animals/humans eat more during cold season
25
What are 3 weaknesses of set-point theories?
1 - Evolutionary pressures not considered
- Food supply not constant (set-point assumes food is always available)
- Need to PREVENT energy deficits, not respond
2 - Major predictions not confirmed
- Glucose drops as preparation of feeding (no food necessary)
3 - Do not incorporate taste, learning, social factors or reward mechanisms (NOT just putting in energy)
26
Does a high calorie drink before a meal reduce consumption?
- NO
| - But, the idea that a premeal drink is high in calories does reduce eating
27
What is the positive incentive perspective?
- No internal energy deficits
| - Anticipated pleasure of eating
28
What is positive-incentive (hedonic) value?
- Anticipated pleasure of a behaviour
29
What are some factors which affect the positive incentive value of food?
- Intrinsic (flavour)
- Previous experience (learning)
- Social context
- Time since last meal
- Blood glucose (physiological)
30
How do the set-point theories and positive incentive perspective interact?
- Physiological motivators can override behavioural motivators
(Cannot finish b/c too full)
- Behavioural motivators can override physiological motivators
(snacks in front of TV, eating in a group)
31
What are 3 groups of factors influencing eating?
WHAT: diet selection, preferences, aversions
WHEN: what initiates a meal
HOW MUCH: what ends a meal
32
What are 2 sets of factors influencing what we eat?
- Innate
| - Learned
33
How do innate factors influence what we eat?
```
- Species specific preferences/aversions
Ex. Humans:
Sweet/fat = high energy
Salty = high sodium
Bitter = can be toxic
Sour = can have gone bad
```
34
How do learned factors influence what we eat?
- Preferences/aversions
Individual learning:
- Conditioned preferences/aversions
- Based on post-ingestions consequences of eating
- Restore deficit of vitamin
Social learning:
- Eat what others eat
- Rats/mice prefer food on others' breath
- Humans = culturally defined
35
How do we know if we are getting enough sodium?
- Distinctive flavour (salty)
- Mineral
- Too much = hypertension
36
What are vitamins and minerals?
- Micronutrients (do not need high amounts)
37
How do we know if we are getting enough vitamins/other minerals?
- No distinctive flavour (learn to associate with food/nutrients)
- Post-ingestion consequences of certain foods
38
What happens when rats are fed a thiamine-deficient diet?
- Get sick
- Develop an aversion for that diet
- Learn to prefer a diet that makes them recover from the deficiency (diet w/ vit. B1)
- NOT based on taste
39
If all these mechanisms for selecting the appropriate diet exist, why are there so many people who do not eat a correct diet?
- Variety of food is too complex, so it is hard to make associations
- Food industry exploits innate preferences (food low in nutrients is made to taste good)
40
When do most mammals eat?
- Small meals rather than continuous eating
- 2 peaks of high feeding per day in rats
- Eat during inactive time
- Humans tend to eat few bigger meals per day
41
How does premeal hunger occur?
- Regular meals
- Decrease in glucose as preparation
- Learned mechanism
- Conditioned response to upcoming meal
- Stress coping
42
What is Wood's theory?
- Meal is a stressor which disrupts homeostasis (spikes in nutrient levels)
43
What begins the cephalic phase of eating?
- Premeal hunger
- Insulin release
- Increased glucose consumption
- Homeostasis is imbalanced
44
What are 2 categories influencing when we eat?
Environmental
- Cues that become conditioned; can regulate pre-meal hunger
- Sensory stimuli from food
- Food-related stimuli
- Time of day
- Social (eat w/ friends/family)
Physiological
- Glicoprivic hunger (decrease in blood glucose)
- Lipoprivic hunger (decrease in body fat)
- Biological clock (tells us time of day)
45
What can hunger be stimulated by physiologically?
Hypoglycemia -> glucoprivation -> glucoprivic hunger
| Low lipids/fatty acids -> lipoprivation -> lipoprivic hunger
46
What are the 2 sets of physiological hunger detectors?
Brain -> glucoprivation sensitive
- Brain stem: area postrema or nucleus of solitary tract
Liver -> glucoprivation and lipoprivation sensitive
- Vagus nerve
47
What is satiety? What does it influence?
- Motivational state that makes us stop eating when food is still available
- Influences how much we eat (stop eating)
48
What are satiety signals?
- Act of eating (maybe)
- Previous experiences with the food
- Short term -> stop a meal: GI tract -> brain
- Long term -> body weight: adipose tissue -> brain
49
What are 5 short term satiety signals?
- Head factors (learning)
- Gastric factors
- Duodenum factors
- Intestinal factors
- Liver factors
50
Where do long term satiety signals originate?
- Adipose tissue
51
Describe head factors for satiety signals?
- Short term
- Eyes, nose, tongue, throat
- Mostly learned
52
What happens when a rat's esophagus is changed so food does not reach its stomach?
- Stop eating after usual amount
- Does not decrease for unfamiliar food
- Stomach increases glucose production without being supplied food
- HEAD FACTORS
53
What are 3 psychological/behavioural factors influencing how much we eat?
Serving size: bigger the portion, more we eat
Appetizer effect: eating tasty appetizer increases hunger (trigger for additional eating)
Social influences: lab rats eat more in a group (social facilitation)
54
Do rats eat more on a cafeteria diet vs. rodent chow?
- Eat more on cafeteria diet
| - Choose between different levels of nutrients
55
Describe sensory-specific satiety?
- Taste signals from a food reduce its own incentive value much more than that of other food
- Postingestive consequences of eating reduce the incentive value of all tastes eventually
56
What value does sensory-specific satiety have?
- Evolutionarily adaptive
- A varied diet (resume eating when new is presented; new food will satisfy needs)
- Eating more in times of abundance (store energy for periods of food shortage)
57
What gastric factors influence satiety signals?
- Short term
- Volume (regulates satiety; Cannon and Washburn inflate balloon)
- Nutritive density of food (rats w/ pyloric cuff/additional stomach)
58
Describe the Cannon/Washburn experiment?
1 - Washburn swallowed balloon and thin tube connected to a water filled glass U-tube
2 - Cannon pumped air into the balloon
3 - Washburn's stomach contractions produced an increase in water level in the U-tube
4 - Washburn reported a pang of hunger each time a large stomach contraction was recorded
59
What was the conclusion of the Cannon/Washburn experiment?
- Hunger is the feeling of contractions caused by an empty stomach
- Volume of stomach plays a factor in hunger
60
What did the Cannon/Washburn experiment wrongly suggest?
- Volume matters less than this study suggests
61
What did rats with a pyloric cuff show?
- Prevents stomach emptying
- Rats that receive an extra infusion of saline still eat the same
* Nutritive content matters more than volume
62
What did experiments using rats with a transplanted stomach show?
- Filling of additional stomach still induces satiety, with no nutrient absorption
* A blood factor
- Not transmitted to brain via nervous system
- Body is receiving nutrients without filling original stomach
63
What is a gastric factor influencing when we eat?
- Ghrelin
64
What is ghrelin?
- Blood factor
- Released when there are no nutrients; stomach is empty
- A feeding enhancing hormone
- It also affects metabolism, growth hormones, etc.
- Produced and released by the stomach (small amounts by small intestine, pancreas, brain)
- Blood levels rise just before eating and decline after a meal
65
What is a duodenal factor influencing how much we eat?
- Cholecystokinin (CCK)
66
Describe cholecystokinin?
- Use pyloric cuff
- Found before ghrelin
- Synthesized by endocrine cells in the duodenum
- Gallbladder contraction
- Stimulates pancreatic enzyme secretion (insulin, glucagon)
- Inhibits stomach emptying
- Signals to the brain
67
How does CCK affect how much we eat?
- Decreases food intake and induces food aversions
| - Might mediate learning of food rather than just eating less
68
What are 2 receptors through which CCK acts?
- CCK-A
| - CCK-B
69
What is an intestinal factor influencing how much we eat? How does it do this?
- Peptide YY
- Inhibitor of eating
- Interrupts a meal
- Released in proportion to calories
- Detect nutrient 'richness' of a meal
70
Describe liver factors which influence how much we eat?
- Post absorption signals via vagus nerve
| - Knows if we have eaten contains what we needed
71
What did studies with portal veins infusions show about satiety signals?
- Intestine to liver portal veins
- Collects nutrients from intestine; blood stream takes nutrients to liver
* Liver has inhibitory feedback mechanisms to tell us to stop eating
Infusion of glucose/fructose -> reduced feeding
Fructose is metabolized mostly in liver -> liver causes reduction in feeding
72
How does adipose tissue influence how much we eat?
Long term signals -> Body weight regulation
- Feed rats through canula; eat more than normal and increase adipose tissue
Factors released by body fats (ex. leptin released by adipocytes)
- Leptin = decreased eating and decreased weight
73
Summarize 3 factors which initiate eating?
1 - Liver and vagus nerve: glucoprivic and lipoprivic hunger
2 - Brain: glucodetectors
3 - Stomach: ghrelin
74
Summarize 4 factors which inhibit eating?
1 - Stomach volume (nutrient content)
2 - Duodenum: CCK
3 - Intestine: PYY
4 - Adipose tissue: leptin
75
How does the brain stem impact hunger/satiety?
- Decerebrated rats show fairly normal eating
| - Brain alone can drive eating
76
How does the hypothalamus influence hunger/satiety?
- Old lesion/stimulation studies
- Effect of lesions suggests:
1 - Lateral hypothalamus = feeding center
2 - Ventromedial hypothalamus = satiety center
77
Describe LH syndrome?
Lesions -> Aphagia (cessation of eating) and Adipsia (cessation of drinking)
- Motor impairment
- Melanin-concentrating hormone
- Orexin A/B
- Shows that hypothalamus is essential for eating
78
Describe VMH syndrome? What are the 2 phases?
Lesions -> Hyperphagia (excessive eating) with preference for palatable food
Dynamic phase: excessive eating -> rapid weight gain
Static phase: stabilized (still high) eating -> new obese weight becomes stable
79
What are afferent and efferent signals of the hypothalamus?
```
Afferent signals:
- Nutrients
- Hormones
- Hedonic signals (odours, reward)
Efferent signals:
- Hunger/satiety
- Feeding
- Energy expenditure
- Hormonal milieu
- Reproduction
- Growth
- Lifespan
```
80
What is the shape of the paraventricular nucleus?
- heart
| - It takes oxytocin
81
Describe arcuate NPY neurons?
Neuropeptide Y: feeding enhancer
| Agouti-related peptide: feeding enhancer (antagonism at MC4R)
82
Describe arcuate POMC neurons?
Melanocortins (agonists of MC4R): feeding inhibitors
83
Describe hormones of the lateral hypothalamus?
Melanin-concentrating hormone: feeding enhancer
| Orexins (A/B)/hypocretins: feeding enhancers
84
Describe the paraventricular hypothalamic nucleus effects of hunger/satiety?
- Feeding inhibitor
| - Metabolism enhancer
85
How does leptin impact satiety?
- Inhibits NPY neurons
- Stimulates POMC neurons
* Eat less, burn more
86
Describe the effects of VMH syndrome?
- Metabolism
- Unwanted lesions
- Induces obesity (increase eating)
- Insulin levels increase
- Lipogenesis increased
- Lipolysis decreased
- Most energy stored of fat (body is starved of energy)
- Rat needs to eat to get more energy
* Fat before eating started
87
What other lesions can be caused by VMH lesions?
- Paraventricular nucleus of the hypothalamus
| - Noradrenergic bundle
88
Where are peptides related to hunger/satiety secreted?
GI tract -> blood stream -> brain
| Brain -> in response to blood signals
89
What are some feeding inhibitors?
- Cholecystokinin
- Leptin
- Melanocortins
- Peptide YY
90
What are some feeding enhancers?
- Neuropeptide Y
- Orexin-A
- Ghrelin
91
What is a critical player in the regulation of body weight?
- Leptin
92
How does food restriction affect health/lifespan?
- Enhancement of health
| - Prolonged life span
93
What are 2 hypotheses regarding improved health as a result of food restriction?
1 - accumulation of by-products (free radicals) of energy consumption accelerates aging
2 - activation of conservation/survival mechanisms that protect cells from damage; prolongs cell's lives and slows aging
94
What are 3 forms of daily energy consumption?
- Basal metabolic rate (keep body alive)
- Diet-induced thermogenesis
- Physical activity (move/do things)
95
What is diet-induced thermogenesis?
- Energy expenditure about resting metabolic rate due to processing food
- Increase in energy expenditure above fasting level divided by energy content of food ingested
96
How do changes in body fat affect fat utilization?
Decrease in body fat -> more efficient fat utilization
Increase in body fat -> less efficient fat utilization
97
How do changes in body fat affect diet-induced thermogenesis?
Decrease in body fat -> decrease in body temperature
Increase in body fat -> increase in body temperature
98
Why are weight-loss/weight-gain programs more effective in initial phase?
- Changes in efficiency of energy utilization
99
What is the settling-points theory?
- 'loose' concept of homeostasis
- Long-term changes in various factors -> body weight changes
- Feedback mechanisms limit impact of changes
100
What is the most widely used model of the settling-points theory?
- Leaky barrel model
101
Describe the leaky barrel model?
1 - Water entering hose = available food
2 - Nozzle water pressure = food incentive value
3 - Water entering barrel = ingested energy
4 - Water level = body fat level
5 - Water leaking = energy expenditure
6 - Weight of the barrel on hose = strength of satiety signals
