Lecture 48-49: Eating Flashcards Preview

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Flashcards in Lecture 48-49: Eating Deck (67):
1

Diagnostic criteria for anorexia nervosa (4)

1. Body weight

2

Diagnostic criteria for bulimia (4)

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

3

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

Very rare; leptin/leptin receptor

4

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

70%; 35

5

What is the best obesity "hit" from GWAS studies?

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

6

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

Lateral hypothalamus (LH)

7

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

Medial hypothalamus (MH)

8

Neural circuits involved in feeding (3)

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

9

Which neurobiological system mediates hunger?

Hypothalamus

10

Which neurobiological system mediates appetite?

Mesolimbic DA system

11

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

Cerebral cortex

12

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

Decreases; increases energy use and sympathetic tone

13

What makes leptin? What kind of molecule?

Adipose tissue; small peptide

14

Leptin does what to orexigenic factors?

Decreases them

15

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

Hypothalamus; protein kinase; TFs

16

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

False! Heavy people DO have higher leptin levels

17

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

Hypothalamus: arcuate nucleus

18

Leptin inhibits...(2)

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

19

Leptin stimulates...(2)

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

20

Leptin is able to stimulate the hypothalamus because?

Lack of BBB

21

Arcuate nucleus projects to...

Lateral and medial hypothalamus

22

Medial hypothalmus factors

Anorexigenic: CRF, TRF

23

Laterial hypothalmus factors

Orexigenic: MCH

24

Neuropeptide Y does what?

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)

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

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