Hypothalamic control of eating Flashcards Preview

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Flashcards in Hypothalamic control of eating Deck (21)
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1
Q

Short term satiety factor from the GI tract?

A

Cholecystokinin (CCK)

signal goes on to brainstem via vagus nerve

2
Q

Long term satiety factor from adipose tissue?

A

Leptin

3
Q

Effect of gastric stretch on food intake?

A

decrease

4
Q

effect of gastric nutrients (sucrose) on food intake if stomach is already stretched?

A

none

5
Q

Effect of intestinal nutrients (sucrose) on food intake?

A

decrease

6
Q

Post absorptive satiety factors from sensors in portal vein of the liver to decrease food intake? (two of them)

A

glucose

free fatty acids

7
Q

Pathway for gastric distention signal:

A

activation of mechanoreceptors—>vagal afferents–> solitary nucleus (medulla) –> decreased food intake

8
Q

Effect on afferent vagal firing rate from leptin?

A

none

9
Q

effect on Solitary nucleus (NTS) firing rate from leptin?

A

increased

10
Q

Satiety factor from duodenum in response to eating?

A

CCK

11
Q

Effects of CCK? (3)

A
  1. gallbladder contraction–> bile –> fat digestion
  2. pyloric constriction –> increased stomach activity, digestion
  3. gastric constrictions –> increased stomach activity, digestion
12
Q

Orexigenic satiety factor from stomach increased by fasting that increases appetite?

A

Ghrelin

13
Q

Leptin is from which gene?

A

OB gene

14
Q

Site of action of leptin?

A

brainstem- solitary nucleus (NTS)

15
Q

fetal hypotonia

mental retardation

hypogonadotropic hypogonadism (decreased FSH, LH)

obesity

hyperphagia

hyperghrelinemia

are sx of:

A

Prader Willi Syndrome

deletion on chromosome 15

16
Q

Three hypothalamic nuclei involved in food intake regulation:

A
  1. lateral hypothalamic area (LHA)
  2. Paraventricular nucleus (PVN)
  3. arcuate nucleus (ARC)
17
Q

Two causes of aphagia with LHA lesion:

A
  1. damage to medial forebrain bundle–>reduced motivation to eat (mesolimbic system, dopaminergic)
  2. loss of neurons that synthesize Orexin
18
Q

Activation of LHA causes?

A

release of “anabolic” NT in brainstem –> increased eating and growth

19
Q

Activation of PVN causes?

A

release of “catabolic” NT in brainstem (corticotropin) –> decreased eating and growth

20
Q

Two populations of ARC neurons?

A
  1. neuropeptide Y (NPY) –> project to PVN, LHA –> increase eating
    - leptin acts on ARC to inhibit NPY and decrease food intake
  2. melanocortin (ProOpioMelanoCortico derived peptide) –> project to PVN and LHA to decrease eating
    - leptin acts on ARC to activate melanocortin (decreasing food intake)
21
Q

Ghrelin site of action in hypothalamus?

A

ARC –> increases NPY activity to increase food intake