Lecture 48-49: Eating Flashcards

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
In general, all orexigenic peptides are Gi/Gs-linked? Anorexigenic?
Gi-linked, while anorexigenic peptides are Gs-linked
26
Melanocortin is an/orexigenic? What is a natural antagonist for Melanocortin receptor?
Anorexigenic; AgRP
27
What is the strongest orexigenic factor?
NPY
28
Melanin-Concentrating Hormone is expressed where? An/orexigenic?
Lateral hypothalamus; orexigenic
29
CRF and TRF are expressed where. An/orexigenic?
PVN in medial hypothalamus; anorexigenic
30
CART is expressed where. An/orexigenic?
Arcuate nucleus of hypothalamus and lateral hypothalamus; anorexigenic
31
Orexin produces pro-/anti-feeding effects
Pro-feeding
32
The full action of insulin and glucose require what?
The brain! Via the hypothalamus
33
Describe Ghrelin: where it's secreted, when, an/orexigenic; targets (2)
Stomach; during fasting; orexigenic; NPY/AgRP neurons AND reward neurons
34
Describe Glucagon-like peptide 1 (GLP1): where it's secreted, when, an/orexigenic; target
Intestinal L cells; during feeding; anorexigenic (promotes insulin/reduces glucacon); mainly acts in periphery
35
What hormone has been used in drug development?
GLP1 peptide agonist (Exenatid)
36
What is a surgical treatment for obesity? Name serious adverse events (2)
Bariatric surgery; malabsorption/metabolic syndromes and depression
37
T/F: Feeding peptides innervate VTA-NAc pathway. Explain
True! Via hypothalamic-VTA and NAc pathway
38
Agents that enhance serotonin function do what to appetite? What is the proposed receptor? Knockout mice for this receptor...
Suppression; 5HT2c receptor; develop obesity
39
Cannabinoid-related drugs for obesity would do what? Problems with these drugs.
CB1 antagonist; linked to depression/suicide
40
Is there a role of leptin in anorexia?
No evidence
41
Genetic contribution to anorexia/bulimia (%)
40-60%
42
Eating disorders (4)
Anorexia nervosa, bulimia nervosa, binge eating disorder, eating disorder not otherwise specified
43
Gender disparity in anorexia and bulimia
Aorexia = 10 : 1; bulimia = 5 : 1
44
Core symptoms of eating disorders (3) w/ description
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
Name and define two types of binges
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
Evaluation of shape and weight includes which two behaviors?
1. Avoidance; 2. Checking
47
Three personality/risk factors for eating disorders
1. Picky eating; 2. Perfectionism; 3. Harm avoidance
48
The course of anorexia begins with...what does this cause?
A diet/large loss of weight; stress --> decrease of HPG axis (lower LH, FSH, leptin AND increased Peptide Y, ghrelin, eCB system)
49
Even after re-achieving a healthy weight, what are long-term effects of anorexia?
Continued HPG, serotenergic and eCB system dysregulation
50
Relapse rate for anorexia (%)
70%
51
Mortality for anorexia (%)
10%
52
In anorexia, signals for appetite might be high, so why isn't there an appropriate response?
Sensitization: constantly high appetite signals "burn-out" the receptors (etc), decreasing the appropriate response
53
Harm avoidance is characterized by which two traits and is related to which NT system?
(+) error detection and inhibition in response to uncertainty; Dysregulation of 5HT system
54
How is harm avoidance affected by ovarian hormone surge?
Increase in dysphoric mood, error detection, inhibition in response to uncertainty
55
Initial starvation does what to ovarian hormone surge? This is what stage of anorexia?
Decreases it --> temporary relief; Early State AN
56
Describe late stage AN
Continued decrease in 5HT --> dyphoric mood and stress adaptations
57
Describe problems with re-feeding
Re-feeding leads to more 5-HT (via tryptophan) and very high levels of dysphoria, error detection, inhibition response to uncertainty
58
Prolonged periods of starvation impacts brain volume...
Loss of volume (mostly in gray matter) but it returns post-weight restoration (insula may be one exception)
59
Heritability for anorexia (%)
50%
60
First-line treatment for anorexia
Family based therapy
61
Medications for anorexia?
None outperform placebo
62
Binge-purge cycle for negative reinforcers
Negative emotional state --> over eat (feel better) --> negative appraisal/loss of control --> compensatory behavior (binge) --> dietary control --> hedonia and vulnerability to environmental stress
63
Binge-purge cycle for positive reinforcers
Novelty, pleasure seeking/impulsivity --> overating --> neg appraisal --> neg emotional state --> hedonic drive to increase pleasure
64
Bulimia involves which two personality types
Cluster C: perfectionism, harm avoidant; Cluster B: novelty seeking, impulsive
65
Treatments for bulimia nervosa (4)
1. CBT (most robust); 2. Interpersonal therapy; 3. Guided self-help; 4. Medication (SSRIs)
66
Over all, how effective are bulimia treatments?
About 40% remission/reduction
67
Describe the relationship between serotonin and bulimia and the endocrine contribution
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