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Brain and Behavior > Lecture 48-49: Eating > Flashcards

Lecture 48-49: Eating Flashcards

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1
Q

Diagnostic criteria for anorexia nervosa (4)

A
  1. Body weight
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2
Q

Diagnostic criteria for bulimia (4)

A
  1. Binge eating (loss of control); 2. Purging; 3. Over-concern with body weight; 4. Weight can be normal, high, low
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3
Q

How common are genetic disorders that cause morbid obesity? Name one target for such a mutation

A

Very rare; leptin/leptin receptor

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4
Q

What is genetic component (%) of obesity risk? Health risk what what BMI?

A

70%; 35

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5
Q

What is the best obesity “hit” from GWAS studies?

A

FTO gene (DNA/RNA demethylase); 16% of adults are homozygous for obesity-causing gene

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6
Q

A lesion where causes animals to stop eating (orexigenic region)?

A

Lateral hypothalamus (LH)

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7
Q

A lesion where causes animals to become obese (anorexigenic region)?

A

Medial hypothalamus (MH)

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8
Q

Neural circuits involved in feeding (3)

A
  1. Hypothalamus (physiological need for food); 2. Mesolimbic DA system (desire for food as rewarding); 3. Cerebral cortex (control)
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9
Q

Which neurobiological system mediates hunger?

A

Hypothalamus

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10
Q

Which neurobiological system mediates appetite?

A

Mesolimbic DA system

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11
Q

Which neurobiological system integrates psychological/social factors with feeding behavior?

A

Cerebral cortex

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12
Q

Leptin increases/decreases food intake. What else does it do? (2)

A

Decreases; increases energy use and sympathetic tone

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13
Q

What makes leptin? What kind of molecule?

A

Adipose tissue; small peptide

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14
Q

Leptin does what to orexigenic factors?

A

Decreases them

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15
Q

Where does leptin produce its effect? What kind of receptor does leptin use? Final effect of signal transduction?

A

Hypothalamus; protein kinase; TFs

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16
Q

T/F: Leptin levels explain common obesity? Explain.

A

False! Heavy people DO have higher leptin levels

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17
Q

What is leptin’s primary site of action (structure and nucleus)

A

Hypothalamus: arcuate nucleus

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18
Q

Leptin inhibits…(2)

A

Orexigenic factors: Neuropeptide Y (NPY), Agouti-related peptide (AgRP)

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19
Q

Leptin stimulates…(2)

A

Anorexigenic factors: alpha-Melanocyte-stimulating hormone (a-MSH); CART

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20
Q

Leptin is able to stimulate the hypothalamus because?

A

Lack of BBB

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21
Q

Arcuate nucleus projects to…

A

Lateral and medial hypothalamus

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22
Q

Medial hypothalmus factors

A

Anorexigenic: CRF, TRF

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23
Q

Laterial hypothalmus factors

A

Orexigenic: MCH

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24
Q

Neuropeptide Y does what?

A

Neuropeptide Y neurons in arcuate nucleus project
to medial hypothalamus (PVN), where they inhibit anorexigenic peptides (CRF), and to lateral hypothalamus, where they stimulate orexigenic peptides (MCH)

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25
Q

In general, all orexigenic peptides are Gi/Gs-linked? Anorexigenic?

A

Gi-linked, while anorexigenic peptides are Gs-linked

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26
Q

Melanocortin is an/orexigenic? What is a natural antagonist for Melanocortin receptor?

A

Anorexigenic; AgRP

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27
Q

What is the strongest orexigenic factor?

A

NPY

28
Q

Melanin-Concentrating Hormone is expressed where? An/orexigenic?

A

Lateral hypothalamus; orexigenic

29
Q

CRF and TRF are expressed where. An/orexigenic?

A

PVN in medial hypothalamus; anorexigenic

30
Q

CART is expressed where. An/orexigenic?

A

Arcuate nucleus of hypothalamus and lateral hypothalamus; anorexigenic

31
Q

Orexin produces pro-/anti-feeding effects

A

Pro-feeding

32
Q

The full action of insulin and glucose require what?

A

The brain! Via the hypothalamus

33
Q

Describe Ghrelin: where it’s secreted, when, an/orexigenic; targets (2)

A

Stomach; during fasting; orexigenic; NPY/AgRP neurons AND reward neurons

34
Q

Describe Glucagon-like peptide 1 (GLP1): where it’s secreted, when, an/orexigenic; target

A

Intestinal L cells; during feeding; anorexigenic (promotes insulin/reduces glucacon); mainly acts in periphery

35
Q

What hormone has been used in drug development?

A

GLP1 peptide agonist (Exenatid)

36
Q

What is a surgical treatment for obesity? Name serious adverse events (2)

A

Bariatric surgery; malabsorption/metabolic syndromes and depression

37
Q

T/F: Feeding peptides innervate VTA-NAc pathway. Explain

A

True! Via hypothalamic-VTA and NAc pathway

38
Q

Agents that enhance serotonin function do what to appetite? What is the proposed receptor? Knockout mice for this receptor…

A

Suppression; 5HT2c receptor; develop obesity

39
Q

Cannabinoid-related drugs for obesity would do what? Problems with these drugs.

A

CB1 antagonist; linked to depression/suicide

40
Q

Is there a role of leptin in anorexia?

A

No evidence

41
Q

Genetic contribution to anorexia/bulimia (%)

A

40-60%

42
Q

Eating disorders (4)

A

Anorexia nervosa, bulimia nervosa, binge eating disorder, eating disorder not otherwise specified

43
Q

Gender disparity in anorexia and bulimia

A

Aorexia = 10 : 1; bulimia = 5 : 1

44
Q

Core symptoms of eating disorders (3) w/ description

A
  1. Eating disturbances (PRIMARY symptom = too little, binging, or overeating); 2. Dietary restraint (can be either intention or behavior); 3. Body image disturbance (over-evaluation in shape/weight)
45
Q

Name and define two types of binges

A

Subjective binge: patient may consider “binge” but is normal amount of food; Objective binge: abnormally large amount of food w/ an out of control feeling

46
Q

Evaluation of shape and weight includes which two behaviors?

A
  1. Avoidance; 2. Checking
47
Q

Three personality/risk factors for eating disorders

A
  1. Picky eating; 2. Perfectionism; 3. Harm avoidance
48
Q

The course of anorexia begins with…what does this cause?

A

A diet/large loss of weight; stress –> decrease of HPG axis (lower LH, FSH, leptin AND increased Peptide Y, ghrelin, eCB system)

49
Q

Even after re-achieving a healthy weight, what are long-term effects of anorexia?

A

Continued HPG, serotenergic and eCB system dysregulation

50
Q

Relapse rate for anorexia (%)

A

70%

51
Q

Mortality for anorexia (%)

A

10%

52
Q

In anorexia, signals for appetite might be high, so why isn’t there an appropriate response?

A

Sensitization: constantly high appetite signals “burn-out” the receptors (etc), decreasing the appropriate response

53
Q

Harm avoidance is characterized by which two traits and is related to which NT system?

A

(+) error detection and inhibition in response to uncertainty; Dysregulation of 5HT system

54
Q

How is harm avoidance affected by ovarian hormone surge?

A

Increase in dysphoric mood, error detection, inhibition in response to uncertainty

55
Q

Initial starvation does what to ovarian hormone surge? This is what stage of anorexia?

A

Decreases it –> temporary relief; Early State AN

56
Q

Describe late stage AN

A

Continued decrease in 5HT –> dyphoric mood and stress adaptations

57
Q

Describe problems with re-feeding

A

Re-feeding leads to more 5-HT (via tryptophan) and very high levels of dysphoria, error detection, inhibition response to uncertainty

58
Q

Prolonged periods of starvation impacts brain volume…

A

Loss of volume (mostly in gray matter) but it returns post-weight restoration (insula may be one exception)

59
Q

Heritability for anorexia (%)

A

50%

60
Q

First-line treatment for anorexia

A

Family based therapy

61
Q

Medications for anorexia?

A

None outperform placebo

62
Q

Binge-purge cycle for negative reinforcers

A

Negative emotional state –> over eat (feel better) –> negative appraisal/loss of control –> compensatory behavior (binge) –> dietary control –> hedonia and vulnerability to environmental stress

63
Q

Binge-purge cycle for positive reinforcers

A

Novelty, pleasure seeking/impulsivity –> overating –> neg appraisal –> neg emotional state –> hedonic drive to increase pleasure

64
Q

Bulimia involves which two personality types

A

Cluster C: perfectionism, harm avoidant; Cluster B: novelty seeking, impulsive

65
Q

Treatments for bulimia nervosa (4)

A
  1. CBT (most robust); 2. Interpersonal therapy; 3. Guided self-help; 4. Medication (SSRIs)
66
Q

Over all, how effective are bulimia treatments?

A

About 40% remission/reduction

67
Q

Describe the relationship between serotonin and bulimia and the endocrine contribution

A

Serotonin dysregulation is exacerbated by puberty and leads to difficulty regulating drive to eat; binge-purge cycle leads to endocrine disturbances that delay signals of satiety and fullness

Brain and Behavior (56 decks)

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