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PSY290: Neurochemical Basis for Behaviour > Lecture 7: Eating > Flashcards

Lecture 7: Eating Flashcards

1
Q

Why do we eat? (2)

A
  1. Food is a source of energy (cabs, fatty acids and proteins) and we need energy to survive.
  2. The brain is only about ~2% of B.M but uses up ~20% of glucose
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2
Q

What does BMR/RMR stand for?

A

Basal/resting metabolic rate

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3
Q

What is glucose converted to?

A

glycogen in the liver and muscles

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4
Q

What is extra glucose and fatty acids converted to?

A

fat/adipose

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5
Q

What are the phases of eating behavior?

A
  1. Cephalic/Digestive
  2. Absorptive
  3. Fasting
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6
Q

What does the cephalic stage begin with?

A

Begins with the body sensing or expecting food through internal (e.g. hunger) and external cues (e.g. seeing food)

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7
Q

What does the cephalic stage lead to physiologically?

A

Prepares the body for food consumption by activating the autonomic nervous system (includes enteric).

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8
Q

Which nerve is involved in enabling the parasympathetic NS which regulates the activity of other organs which prepares us to eat and digest food?

A

Cranial Nerve X (Vagus Nerve)

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9
Q

What happens to glucose levels after meal? (4)

A
  1. Rise of glucose in blood plasma (rise in use of glucose)
  2. Rise of insulin
  3. Drop in glucagon
  4. Conversion of excess glucose to glycogen and fat
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10
Q

What does the increase in insulin do after a meal? (3)

A
  1. Glucose uptake from blood
  2. Conversion of glucose + fatty
    Acids to stored energy
  3. Lowers blood glucose
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11
Q

What does the decrease in glucagon do after a meal? (3)

A
  1. Conversion of stored energy (glycogen +fat) to glucose and fatty acids
  2. Increases blood glucose
  3. Process 1 and 2 are inhibited during the cephalic phase
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12
Q

What are the two pancreatic hormones important for the cephalic phase?

A
  1. insulin

2. glucagon

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13
Q

What happens during the absorptive phase? (3)

A
  1. Nutrients (e.g. glucose) are absorbed into the blood stream
  2. These nutrients are first consumed to meet immediate energy needs
  3. Excess nutrients are stored as glycogen, proteins, and fats for later use.
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14
Q

What happens during the fasting phase? (4)

A
  1. Energy is taken from stores to meet needs
  2. Insulin levels drop
  3. Glucagon levels rise
  4. With prolonged fasting, the hormone gherlin is secreted by stomach and increases hunger
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15
Q

What is glucostatic theory?

A

Hunger is moderated by rises and falls of glucose. We try to maintain homeostasis of glucose levels.

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16
Q

What are criticisms levelled at the glucostatic theory? (4)

A
  1. Blood glucose levels rarely drop before eating
  2. Blood glucose levels in the body change with eating, glucose levels for neurons do not (it remains stable)
  3. We will eat if we have eaten recently and our consumption is related to the portion size we’re given (you’ll eat what you’re given rather than what you need to correct a blood glucose level deficit
  4. When we experimentally increase or decrease glucose levels, hunger is not significantly affected
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17
Q

What is the set point or Lipostatic theory? What does it explain?

A

We eat to maintain a lipid store/body weight. In most people, bodyweight changes slowly. Genetic forces keeping bodyweight stable. Explains why >80% of people regain previous weight within 5 years.

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18
Q

What are the heritability scores for bodyweight? Obesity?

A

(h2 = 0.8)

obesity (h2 = 0.4-0.7)

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19
Q

What two things change when we lose weight?

A
  1. metabolism slows

2. fat storage capability increases

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20
Q

According to the lipostatic theory, what are the phases of a diet? (5)

A
  1. Weight loss
  2. Amount of energy leakage is reduced which reduces rate of weight loss
  3. We plateau at a new stable settling point
  4. When diet is terminated, weight gain is rapid because of high incentive value and low level of energy leakage
  5. As weight accumulates, the incentive value of food decreases until a set point is reached.
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21
Q

What are criticisms of set-point theory? (3)

A
  1. Some people gain weight consistently throughout their adult life
  2. Why would this happen if there was a drive to keep fat storage at a constant level?
  3. From an evolutionary perspective, why have a system in place that limits energy storage? After all, food availability is NOT guaranteed
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22
Q

What animal study creates a problem for set point theory?

A

Rodent’s esophagus was disconnected from its stomach so that the rodent could eat but never store it. According to set point theory we expect large meals to maintain weight. But this doesn’t happen immediately.

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23
Q

What is positive incentive value theory? What does it explain?

A

Eating is guided by cravings not deficits
Consumption of nutrients activated the reward centers of the brain (eating is pleasurable). Explains how humans have a strong preference for sweet, fatty and salty foods (calorically dense), avoid bitter foods
No mineral cravings (they don’t have “taste” associated with them).

24
Q

What different structures are responsible for the food as a reward theory? (5)

A
  1. Tongue (sensation of taste)
  2. Insula (recognition of taste)
  3. Amygdala (emotion)
  4. frontal areas (cognitive value)
  5. Striatum (reward and planning future behavior, involved in control)
25
Q

What is the reward system?

A

A group of interconnected neural structures implicated in the attribution of reward to stimuli. The NT involved is dopamine in the mesolimbic pathway which is implicated in habit formation and impulse control. The expectation and taste of food activates the release of dopamine in multiple reward-associated areas.

26
Q

What hypothalamic nuclei are involved in energy metabolism? What hormones are they sensitive to?

A
  1. Ventromedial
  2. Lateral
  3. Paraventricular
  4. Arculate

Leptin, insulin, gherlin and PYY3-36

27
Q

What is the ventromedial hypothalamus important for?

A

VMH plays a role in energy metabolism, that is it is better at increasing fat stores. Lesion of VMH leads to obesity. Used to be thought as a structure that terminated eating behavior (satiety center).

28
Q

What is the lateral hypothalamus responsible for?

A

LH inhibits fat storage, stimulating the LH results in the increase in eating (optogenic study). With lesions to the LH there is weight loss.

29
Q

What is the arculate responsible for?

A

Cells in the ARC are sensitive to leptin and gherlin due to specialized neurons POMC and AgRP that have different effects on the PVH. Depending on which neuron the PVH is getting the signal from either increase or decrease in eating behavior.

30
Q

What is leptin?

A

Hormone associated with anorexia (decrease in eating)

31
Q

What is gherlin?

A

Hormone associated with orexogenesis (increases in eating)

32
Q

What do AgRP neurons do?

A

They express the neuropeptide Y (NPY), agouti-related protein (aAgRP; an antaganist of melanocortin signaling) and GABA. In turn, these neurons stimulate food intake when activated (orexigenic)

33
Q

What are AgRP neurons inhibited by? Activated by?

A

Insulin and Leptin. Gherlin.

34
Q

What do POMC neurons do?

A

Express pro-opiomelanocortin (POMC) and release alpha-melanocyte stimulating hormone which inhibits food intake.

35
Q

What are POMC neurons stimulated by?

A

Leptin.

36
Q

What is satiety signaling?

A

Combination of short-term signals (CCK, GLP1 from the gut) and long term signals (related to adiposity, insulin, leptin)

37
Q

What is leptin?

A

Leptin is a hormone that reduces food intake by signaling satiety, impaired leptin leads to weight gain. It is secreted from adipose stores. The more adipose the more leptin is released. While food is being in taken, the effects of leptin are more significant than insulin.

38
Q

What signaling does leptin augments? What system is it affecting?

A

CCK, mesolimbic dopamine pathway (+ other reward systems)

39
Q

What is the surest way to reduce leptin levels?

A

Restricting calories by fasting/dieting and losing fat stores. However, this in turn associates with increased perceived pleasure of good and amount of work we’re willing to do for it.

40
Q

What does a leptin gene mutation lead to?

A

Increase food intake and reduced energy expenditure.

41
Q

What is leptin’s role in obesity?

A

In obesity, leptin levels are higher (more white adipose tissue in obesity, white adipose tissue makes leptin)
It is suggested that leptin signaling is less effective in obesity (i.e. there is leptin resistance).

42
Q

Which experiment showed the role of satiety peptides?

A

Transferred a 2nd stomach and intestine into a rat that was joined to rat’s blood vessels and filled with foods. But this cannot absorb energy from food (happens in intestine). Changes of behaviour are due to change in stomach content. Rats ate less in proportion to the volume + caloric density of foods in 2nd stomach. Suggests that stomach may release blood-borne signals (satiety peptides - CCK)

43
Q

What are the factors affecting the settling point of weight? (6)

A
  1. Availability of food
  2. Incentive value of food
  3. Amount of food we eat
  4. Body fat stores
  5. Amount of energy we expend (daily activity)
  6. Satiety signals (CCK, leptin, sensitivity)
44
Q

What is the sensory pathway of eating?

A

Taste receptors -> cranial nerves -> thalamus -> primary gustatory cortex -> primary sensory cortex

45
Q

What is anosmia? What does it lead to? Where does it happen?

A

Loss of sense of smell, leads to weight loss and Parkinsons. Damage to areas involved in olfaction such as OFC may have similar anosmia effect (patients with OFC lesions are thin).

46
Q

How does cannabis affect our system?

A

Cannabinoids (such as anandamide and THC) can bind to cannabinoid receptors type 1 (CB1) receptors in the olfactory system which result an increased olfactory sensitivity which is related to increased feeding (the munchies in mice).

47
Q

Obesity epidemic stats. (3)

A

Affects 1/4 adult Canadians, predictor of poor health outcomes, partly genetic (h2 = 30-70%).

48
Q

What is the likely cause of the obesity epidemic?

A

Change in food an access to it.

49
Q

What is different about the reward system in obesity? (4)

A
  1. Reduced dopamine receptor type 2 (DR2)
  2. Reduced glucose metabolism
  3. Increased activity in some areas associated with food salience (need to eat more to achieve pleasure).
  4. Eating is less rewarding in obesity so people eat more
50
Q

What is anorexia? Who is the most affected?

A

Anorexia is the most fatal psychological disorder. No appetite by nervousness. Refusal to consume enough food to maintain weight. Neural representations of their own appearance is different. Often diagnosed during puberty, brain development, hormones, stress, cultural factors. Difficult to treat because people think that they are actually doing a good thing for their body. 75-90% are women.

51
Q

What is different about the nervous system in anorexia? (7)

A
  1. Reduced reward value of food (lowered activation of insula and anteroventral striatum in response to sweet taste)
  2. Increased anxiety towards food
  3. Lack of compensatory response to food restriction
  4. Heightened harm avoidance (more D2, D3 expression in the striatum (e.g caudate) correlates with harm avoidance behavior.
  5. Parietal cortex functions differently, self-perception is skewed.
  6. Overall gray matter may be reduced.
  7. Increased ventricle size and sulci depth before recovery.
52
Q

What are neural correlates of anorexia?

A
  1. Genetic variations in the serotonin system (5-hydroxytryptamine)
  2. Genetic variations in the estrogen system also linked
  3. Genes have weak effects, many are involved and all interact with environmental forces
  4. Changes in the expression of serotonin receptors, serotonin transporter and D2/D3 receptors.
53
Q

What is bulimia nervosa?

A

Recurrent episode of binge eating followed by vomiting to reduce weight gain. Common in women.

54
Q

What are eating disorder myths (4),

A
  1. Lifestyle choice
  2. Not genetics
  3. They only affect young white women of high SES
  4. They are a phase that will resolve easily
55
Q

What are the four influences on eating disorders? (4)

A
  1. Genetic predisposition (serotonin receptor gene mutation)
  2. Nonshared environmental influence (serotonin dysfunction exacerbated by estrogen fluctuations)
  3. Genetic predisposition 2 (estrogen receptor gene mutation increases estrogen effects on serotonin system)
  4. Nonshared environmental influence (choice of career and social groups)

PSY290: Neurochemical Basis for Behaviour (9 decks)

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