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PSYC 304 - SEM 2 > Feeding Lecture 2 till slide 8 > Flashcards

Feeding Lecture 2 till slide 8 Flashcards

1
Q

what are the three ways that the body uses energy?

A
  1. basal metabolism - 60% of energy usage maintains body heat and other resting functions
  2. active behavioural processes - 25% is for behaviours other than rest
  3. digestion of food - 15% of energy is for processing food and breaking it down into molecules to be used by the body
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2
Q

what are the basic nutrients that we need and where do they come from?

A
  1. carbohydrates (4kcal) - gets converted to glucose
  2. amino acids (4kcal) - comes from proteins, is the basic building blocks for all cells
  3. lipids, fats (9kcal) - gets converted to free fatty acids for alternate energy, long term energy source
  4. vitamins, minerals - needed to assist in bodily functions (digestion, cell building, homeostasis)
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3
Q

what types of energy do we get from carbs?

A
  • glucose is the primary fuel of the body
  • glycogen is the storable form of carbs, stored in the liver and muscles
  • complex carbs are broken down to glucose before the body can use it
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4
Q

what are essential amino acids and where do we get them?

A
  • there are 20 amino acids, and 9 of them cannot be produced by the body (essential amino acids)
  • complete protein - source of protein with all 20 amino acids, usually animal protein
  • amino acids can also be converted to glucose
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5
Q

what types of energy do we get from fats?

A
  • long term energy source, can be converted to free fatty acids as alternate energy source
  • if we have low glucose, the body uses free fatty acids
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6
Q

what are the steps of digestion?

A

process takes 18-24 hours
1. chewing - mastication
2. saliva - lubrication
3. swallowing
4. stomach - storage and breakdown
5. duodenum - absorption
6. gall bladder and pancreas - break down proteins into amino acids, starch into simple sugars
7. bile from liver breaks down fats
8. water and electrolytes absorbed by large intestine or ejected

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7
Q

how is glucose regulated in the body?

A

the pancreas regulates blood glucose levels in the bloodstream using two hormones: glucagon and insulin
- glucagon - converts glycogen (stored carbs) into glucose
- insulin allows glucose inside cells to reduce excess blood sugar levels

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8
Q

how exactly does glucagon work to convert glycogen into glucose?

A

when there is too little blood glucose…
- alpha cells of islets of Langerhans signal glucagon to be released
- the liver converts glycogen into glucose and releases into bloodstream
- result: blood glucose levels increase

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9
Q

what is the process of insulin release in the body?

A

when there is too much blood glucose…
- beta cells of islets of Langerhans signal insulin release
- insulin allows excess glucose to go inside the cells instead of in the bloodstream
- the liver stores blood glucose as glycogen, other cells increase consumption of glucose
- result: blood glucose levels decrease

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10
Q

what are the two primary actions of insulin?

A
  1. promotes use of glucose as primary energy source for body
    - most cells of the body need insulin to get glucose in cells
    - except the brain can use glucose without insulin because glucose is it;s only energt source
  2. converts bloodborne fuels to storable forms
    - glucose –> glycogen
    - glucose and fatty acids –> adipose tissue (body fat)
    - amino acids –. protein (muscles)
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11
Q

what are the mechanisms that control insulin release?

A
  • negative feedback mechanisms that keep track of blood glucose levels
  • cephalic phase - the brain (vagus nerve) triggers insulin through the sight/smell/taste/thought of food
  • digestive phase - hormones released by the gut can reach the pancreas and trigger insulin
  • absorptive phase - nutrients entering blood stream can trigger insulin
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12
Q

what is diabetes mellitus?

A

Type 1 Diabietes - juvenile onset
- pancreas stops producing insulin
- excess glucose in the bloodstream
- brain cannot use it all, and cells of the body can’t use glucose without insulin
- the body starts using fatty acids for energy

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13
Q

how does diabetes mellitus affect eating?

A
  • can lead to more eating that doesn’t satisfy hunger and weight loss
  • glucose is in the blood but not in the cells, so we feel we are hungry
  • there is no insulin to put glucose in storable form so we lose weight
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14
Q

is insulin a satiety signal?

A
  • if we lower animal’s insulin level, it becomes hungry and eats a large meal
  • if we give a moderate level of insulin, it eats much less
  • not a satiety signal because if we give large amounts of insulin that convert most glucose to fat, less glucose in the bloodstream…
  • the brain detects glucose deficit and initiates hunger, animals now eat a large meal
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15
Q

is glucose a satiety signal?

A

not exactly
- untreated diabetes leaves a lot of glucose in the bloodstream, but also increases hunger
- under normal conditions, blood glucose can stay stable for hours-days but we still get hungry
- multiple signals in addition to glucose and insulin regulate hunger and satiety

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16
Q

what are the theories on why we get hungry?

A
  1. set-point theory
  2. positive-incentive theory
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17
Q

what is the set-point theory?

A
  • attributes hunger as an energy deficit, low energy = hunger
  • negative feedback system maintains homeostasis
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18
Q

what determines a person’s set point?

A

genetics establish the set point

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19
Q

what are the two basic types of set point theories?

A

eating is controlled by deviations from…
1. glucostatic theory - blood glucose set points
2. lipostatic - body fat set-points (amount of energy in storage)

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20
Q

what are the main problems with set-point theories?

A

1. evolution argues against it
- didn’t just eat when hungry, ate in large quantities when food was available
2. major predictions of set-point theories when tested
- drinking high glucose drinks before meals doesn’t reduce eating
- reducing blood glucose or body fat levels doesn’t happen normally
- glucose stays relatively stable
- body doesn’t want to get rid of fat (energy reserves)
3. set-point theories ignore factors that stimulate eating
- taste of food, social factors

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21
Q

what is the positive incentive theory?

A
  • anticipated pleasure of eating is main factor controlling feeding
  • evolved to crave food because we like it, not because we are in energy deficit
  • if we evolved to eat when in deficit, we wouldn’t survive very long (need to eat when food available)
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22
Q

what factors determine what we eat?

A
  1. taste preferences - some tastes have innate high incentive values, and others are learned from experience or social situations
  2. learning to eat vitamins/minerals - animals learn to choose foods that contain vitamins they lack
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23
Q

then why do we eat junk food when it has no vitamins?

A
  • junk foods have lots of flavours to make us think we are getting more vitamins
  • if we need vitamin D, some people have orange crush to satisfy cravings
24
Q

what factors influence when we eat?

A
  1. pavlovian conditioning
  2. pre-meal hunger
24
Q
A
25
Q

how does pavlovian conditioning influence when we eat?

A
  • environmental cues associated with eating can elicit hunger
  • hunger can be caused by expectation of food
  • ex. rats will eat in response to a tone that has been associated with food, even if they ate recently
  • food/eating is associated with smells, sounds, sights
26
Q

how does pre-meal hunger influence when we eat?

A
  • time of day that one usually eats can trigger hunger
  • a special type of Pavlovian conditioning
  • eating at regular times can condition the brain/body to prepare for incoming food
  • “hunger pangs” are the body getting ready for food, not the body craving food
27
Q

how does blood glucose change around feeding time?

A
  • before a meal is initiated, there is a 10% drop in blood glucose
  • still unlikely that drop in glucose is responsible for feeding because…
  • if there is no meal, glucose levels return to previous levels in 10-15 min, similar to if a meal was consumed
28
Q

why is there a drop in blood glucose before a meal?

A
  • decline may be related to intention to eat
  • insulin increases in the cephalic phase then blood glucose drops in anticipation in feeding
  • increased insulin proves that our body does not have a decline in energy reserves
  • changes in blood glucose may contribute to feeling of hunger, but is not main controller of eating behaviour
29
Q

how to social factors influence satiety?

A
  • humans and animals eat more in groups than alone
  • when two individuals eat together, they tend to take bites together
  • also eat similar amounts of food
30
Q

what is sensory specific satiety?

A
  • satiety can be taste specific, you get full of one taste and move to another
  • humans and animals take in more calories if they are given varied diets
  • encourage consumption of varied diets and to take advantage when different foods are abundant
31
Q

what study was done on sensory specific satiety?

A
  1. humans asked to rate palatability of foods
  2. given one of those foods as a meal
  3. rated foods again, and the one they just ate was rated lower
  4. when given a new meal right after, they ate more
32
Q

what is the physiology of hunger and satiety?

A
  • liver sends signals about whats in the bloodstream via vagus nerve
  • liver receives blood from small intestine, and has detectors for glucose and fatty acids
33
Q

how can we trick the liver to act as if glucose/fat levels are low?

A
  • deoxyglucose (2-DG): binds the glucose receptors but doesn’t activate glucose detectors in liver (glucose antagonist)
  • methyl palmoxirate: disrupts metabolism of fatty acids
  • if we inject these into vein from intestine to liver, there is an immediate increase in feeding
  • if we cut the vagus nerve, it eliminates the effect of the drug injection
  • injecting 2-DG in certain brain ares will also stimulate feeding
34
Q

what hormones does the brain use to suppress hunger?

A
  • stomach: CCK, bombesin, somatostatin
  • liver: detects changes in glucose, input to brain from vagus nerve
  • pancreas: insulin
  • intestine: PYY and GLP-1
  • fat cells: leptin, gives continuous feedback on body’s energy stores
35
Q

what hormone stimulates eating?

A

stomach: ghrelin
- levels remain high during fasting
- drops during a meal (short term)
- levels are high when stomach is empty

36
Q

what brain areas could be responsible for hunger/satiety signalling?

A
  • ventromedial hypothalamus
  • paraventricular nuclei of hypothalamus
  • lateral hypothalamus
  • arcuate nucleus of hypothalamus
37
Q

is the ventromedial hypothalamus responsible for satiety?

A

ventromedial hypothalamus = satiety center?
- if we lesion this area, animals become obese
- starts with massive consumption that achieves new weight (dynamic phase)
- then the maintenance of that weight (static phase)
- animals eventually stop eating, and only gain weight if they like the food given to them
- reinterpretation; VMH regulates energy metabolism, not eating
- VMH lesions increase insulin levels, which increases fat formation, and decreases breakdown of body fat into usable forms

38
Q

what do VMH lesions tell us about hunger and satiety signals in the brain?

A
  • neurons in VMH may not cause effect, lesions also destroy axons from paraventricular nuclei of the hypothalamus
  • lesions of these fibres alone also produce hyperphagia and obesity
39
Q

is the lateral hypothalamus responsible for hunger?

A

lateral hypothalamus = hunger center?
- lesions in this area cause rats to stop eating (aphasia)
- interpretation issues: if we force feed rats for a week, they start eating again
- reinterpretation: LH lesions cause sensory and motor disturbances including decreased appetite
- these animals may have a problem with eating but not lack of hunger

40
Q

so what brain areas are responsible for hunger and satiety?

A
  • control of hunger and satiety is distributed across many brain regions
  • other hypothalamic regions, amygdala, and frontal cortex is also involved
41
Q

what does the arcuate nucleus of the hypothalamus do?

A
  • first-pass appetite control center
  • determines how much we eat based on what is happening in gastrointestinal tract
  • 5 main satiety/hunger hormone signals from body interact with this nucleus to regulate feeding
    1. pancreas = insulin (decrease feeding)
    2. and 3. intestines = GLP1 & PYY (decrease feeding)
    4. fat cells = leptin (decrease feeding)
    5. stomach = ghrelin (increase feeding)
42
Q

how do hormone signals interact with the arcuate nucleus of the hypothalamus to control hunger/satiety?

A
  • they activate different types of neurons in arcuate nucleus
  • Neuropeptide Y (NPY) & agouti-related peptide (AgRP) both increase appetite
  • pro-opiomelanocortin (POMC) & Cocaine/Amphetamine regulated transcript (CART) both decrease appetite
  • competing processes of hunger and satiety, we consider relative values of both
43
Q

how is appetite controlled in the long-term?

A
  • leptin and insulin work as long term modulators of appetite (suppress appetite)
  • they activate POMC/CART neurons and inhibit AgRP/NOY neurons
  • POMC/CART neurons inhibit lateral hypothalamus using a-melanocyte stimulating hormone
  • LH usually increases hunger, but A-MSH inhibits LH
44
Q

how is appetite increased in the short-term?

A
  • ghrelin is released by the stomach when it is empty
  • stimulates AgRP/NPY neurons which have two effects
    1. NPY transmitter inhibits PVN, which usually suppresses hunger
    2. AgRP released in LH blocks a-MSH, which increases LH activity, making us more hungry
45
Q

how is appetite suppressed in the short-term?

A
  • after a meal, the intestines release PYY and GLP1
  • PYY inhibits AgRP/NPY neurons, which disinhibits (increases) PVN activity
  • GLP1 stimulates POMC/CART neurons which inhibits LH activity
46
Q

how can the arcuate nucleus circuitry be bypassed? what brain areas are responsible for this?

A
  • can be bypassed by food-associated cues
  • if we present cues in rats that are full, they still eat more
  • lesions to prefrontal cortex or amygdala or disconnection of the amygdala-LH pathway abolished conditioned increase in feeding
  • but, normal feeding patterns are unaffected, lesions only disrupt cue-induced feeding
  • when there is a food cue, prefrontal cortex and amygdala are activated and excite the LH, causing hunger
47
Q

how does serotonin affect hunger and satiety?

A
  • serotonin is a major brain satiety signal
  • one dose of serotonin agonists in humans can…
    1. reduce feeding, even with a variety of available foods
    2. reduce amount of food consumed per meal, but not number of meals per day
  • increased serotonin shifts food preference away from fatty foods
  • acts as short term satiety signals
48
Q

how does serotonin work to suppress hunger?

A
  • serotonin inhibits release of NPY in the PVN of hypothalamus
  • this then disinhibits PVN neurons, which promotes satiety
49
Q

what is anorexia nervosa?

A
  • obsession with body weight/image and food
  • characterized by self-induced starvation leading to low BW
  • BMI of less than 15
  • intense fear of gaining weight
  • distorted view of one’s body weight or shape
  • persistent lack of recognition of seriousness of low BW
50
Q

how does insulin behave in people with anorexia?

A
  • show higher than normal insulin release in anticipation of food
  • but are often disgusted by a sweet/fatty meal
  • shows that they are obsessed with food
51
Q

what are the potential psychological causes of anorexia?

A
  • positive incentive value for food goes up during starvation
  • meals are a disruptive event on the body, which is intensified during starvation
  • meals forced on anorexic people may lead to conditioned taste aversions
  • even though they think about food, competing factors cause them to avoid it
52
Q

are there any treatments for anorexia?

A
  • very few effective treatments
  • less than 30% show long term recovery
  • about 10% die of starvation or suicide
53
Q

what are the biological mechanisms underlying anorexia?

A
  • information processed by certain brain areas are altered
  • they have abnormal patterns of frontal activation to food-related stimuli
  • palatable tastes can cause abnormal increases in amygdala activity
  • amygdala is involved in the recognition and evaluation of aversive stimuli
  • certain feeding hormone/transmitter levels are reduced (AgRP, NPY, leptin)
  • serotonin abnormalities have also been linked to anorexia
54
Q

what is obesity?

A
  • characterized by excessive adipose tissue
  • more than 25% of fat content in men, and 30% in women
  • 1 in 4 Canadians adults and 1 in 10 children are obese
  • BMI of over 30
55
Q

what are some potential causes of obesity?

A
  • twin studies found that environmental and genetic factors are equally responsible for obesity
  • obese people have larger insulin response to sight, sound, smell of food
56
Q

what are some treatments for obesity?

A
  • exercise and proper diet
  • low calorie diets (often see immediate results, then weight comes back)
  • appetite suppressants, surgical procedures
  • GLP-1 agonists (ozempic)

PSYC 304 - SEM 2 (2 decks)

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