Hunger, Eating, and Obesity - Engeland

Question 1

What short-term satiety signal comes from the oropharyngeal region?

Answer 1

Taste

• If fed state –> decrease feeding
• If fasted state –> increase feeding

Question 2

What is the result of gastric stretch caused by fluid alone?

Answer 2

Decreased food intake

Question 3

What is the result of gastric stretch due to nutrients?

Answer 3

No additional decrease in food intake

(gastric stretch due to nutrient value in the stomach does not cause amplified effect)

Question 4

What is the result of intestinal stretch due to nutrients?

Answer 4

Decrease in food intake

Question 5

What are the preabsorptive satiety factors?

Answer 5

Gastric stretch + Intestinal nutrient

Question 6

What are the postabsorptive satiety factors?

Answer 6

• Liver factors:
  
  • Portal Vein has sensors for glucose & free fatty acids
  • results in decreased food intake

Question 7

Where does information about gastric distention go? How does it travel to the brain?

Answer 7

• Activity in gastric mechanoreceptors
• Activate Vagus Nerve afferent
• Solitary Nucleus (medulla)
  
  • results in decreased food intake

Question 8

What hormone is released from the duodenum in response to meals (fed state)?

Answer 8

Cholecystokinin (CCK)

Question 9

What effect does CCK have on digestion in the GI tract?

Answer 9

• CCK causes:
  
  • Gallbladder contraction
    
    • secrete bile to digest fats
  • Pyloric constriction
  • Gastric contraction
    
    • hold surplus food in stomach until ready for digestion

Question 10

What pathway does active CCK receptors activate?

Answer 10

• Increased Vagal Nerve afferents
• Increased stimulation in Solitary Nucleus
• Decreased food intake

Question 11

What produces Ghrelin? What effect does it’s release have?

Answer 11

• Produced by the GI tract (stomach)
  
  • increased production during fasted state
• Orexigenic effect
  
  • increases appetite

Question 12

What are the symptoms of Prader-Willi Syndrome (deletion on chromosome 15)?

Answer 12

• Fetal hypotonia (decreased muscle tone)
• Mental retardation
• Hypogonadotropic hypogonadism
  
  • decreased gonadal fxn due to decreased FSH & LH
• Obesity
  
  • Primary Mechanism: Hyperphagia (excessive eating)

Question 13

What does hyperghrelinemia in Prader-Willi Syndrome cause?

Answer 13

• Increased ghrelin secretion into the blood causes orexigenia
  
  • makes them feel like they need to eat more

Question 14

What is leptin? What does it do?

Answer 14

• Ob gene product
  
  • released by adipocytes
• Leads to decreased food intake

Question 15

People who are obese actually have low levels of leptin, so where must the problem be with long-term satiety signals?

Answer 15

Receptor for leptin

Question 16

What effect does adding leptin have on the neuronal firing rate in the Solitary Nucleus due to gastric distention?

Answer 16

Increased responsiveness to gastric stretch

(but why?!?)

Question 17

Where is the site of action for leptin?

Answer 17

Arcuate nucleus in the Hypothalamus

Question 18

What does activation of the Lateral hypothalamic area result in?

Answer 18

Release of “anabolic” neurotransmitter in brainstem

-Orexin –> Increased eating

Question 19

What is the result of a lesion in the Lateral hypothalamic area (LHA)?

Answer 19

Aphagia

• cessation of eating
• due to damage of the medial forebrain bundle
  
  • loss of neurons that synthesize “orexigenic” peptide
    
    • reduced motivation to eat
      
      • involves dopaminergic Meso-limbic system
    • reduced motor function
      
      • not eating more because you can’t move

Question 20

What does activation of the Paraventricular nucleus (PVN) result in?

Answer 20

• Release of “catabolic” neurotransmittor(s) in brainstem
  
  • Corticotropin Releasing Hormone
  • Decreased eating

Question 21

What two types of neurons are projected from the Arcuate nucleus?

Answer 21

• Neuropeptide Y (NPY) neurons
  
  • increased eating
• Melanocortin (POMC-derived peptide) neurons
  
  • decreased eating

***Both project to Paraventricular & Lateral Hypothalamic Nuclei (PVN & LHA)

Question 22

How does NPY effect the PVN?

Answer 22

• Activates GABAnergic inhibitory interneuron
• Inhibitory neuron –> inhibits release of CRH (which normally decreases eating)
• No release of CRH –> INCREASED EATING!

Question 23

How does Melanocortin (MSH) effect the PVN?

Answer 23

• MSH inhibits GABAnergic inhibitory interneuron
• PVN is able to release CRH –> DECREASED EATING!

Question 24

How does Leptin effect the Arcuate Nucleus?

Answer 24

• Inhibits Neuropeptide Y activity
  
  • decreased food intake
• Activates Melanocortin activity
  
  • decreased food intake

Question 25

How does Ghrelin affect the Arcuate Nucleus?

Answer 25

• Increase Neuropeptide Y activity
  
  • increased food intake

Question 26

Where do the three efferents from the Solitary Nucleus go to in order to stop/decrease food intake?

Answer 26

• Motor Nucleus of Trigeminal (CN V)
  
  • stop mastication
• Nucleus Ambiguus
  
  • stop swallowing
• Facial Nucleus
  
  • stop chewing

Question 27

What effect does release of CRH from the PVN have on the Solitary Nucleus?

Answer 27

Excitatory

(wants Solitary Nucleus to fire inhibitory efferents to stop/decrease food intake)

Question 28

What effect does Orexin release from the LHA have on the Solitary Nucleus?

Answer 28

Inhibitory

(does NOT want Solitary Nucleus to fire inhibitory efferents to stop/decrease food intake)