Hunger, Satiety and the Brain Flashcards

1
Q

What did early studies of hunger show when they decerebrated the Brain Stem in rats?

A

The rats showed fairly normal eating

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2
Q

What early studies were done on the hypothalamus?

A

Old lesion and stimulation studies

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3
Q

What were the findings of the early studies on the Hypothalamus?

A

1.) Lateral Hypothalamus: feeding centre

2.) Ventromedial Hypothalamus: satiety centre

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4
Q

What happened when they lesioned the VMH?

A

The rats developed “VMH syndrome”

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5
Q

What does VMH syndrome cause?

A

Hyperphagia

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6
Q

What is hyperphagia?

A

Excessive Eating

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7
Q

What did the rats develop a preference for?

A

Palpable Food

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8
Q

What is Palpable food?

A

Any food that is reading to the palate

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9
Q

What happened when rats were in their dynamic phase?

A

Excessively Eating which lead to rapid weight gain

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10
Q

What happened when rats were in their stable phase?

A

Stabilized (but still high) eating which lead to a new stable weight

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11
Q

What happen when you lesion the LH?

A

“LH syndrome”

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12
Q

What does “LH syndrome” consist of?

A

Aphagia: stop eating

Adipsia: stop drinking

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13
Q

What did they also notice when they lesioned the LH?

A

Motor deficits and the lack of responsiveness to sensory inputs

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14
Q

What did new researchers look at when studying the hypothalamus in regards to hunger?

A

Paraventricular Nucleus of the Hypothalamus

Arcuate Hypothalamus Nuclei

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15
Q

What does the Lateral Hypothalamus produce?

A

Melanin Concentrating Hormone and Orexins/Hypocretins (Orexin A and B)

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16
Q

What do the Orexins/Hypocretins do?

A

Enhance your appetite which enhances your feeding

17
Q

What are Accurate NPY Neurons?

A

Feeding enhancers (NPY and Agouti Related Peptide)

18
Q

What are your Arcuate POMC Neurons

A

Feeding Inhibitors (Melanocortins - MCR-4)

19
Q

What is your PVN?

A

Feeding Inhibitor (MCR-4)

20
Q

What is your Lateral Nucleus?

A

Feeding Enhancer (MCH and Orexin A + B/Hypocretins)

21
Q

What is the role of the Hypothalamic nuclei?

A

Regulating food intake, energy expenditure, glucose and lipid metabolism in the peripheral tissues by leptin

22
Q

What does Leptin do?

A

Decrease your appetite

23
Q

What happens when Leptin acts on the POMC neurons of the Arcuate Nucleus?

A

It signals to the PVN to reduce food intake

24
Q

What happens when Leptin isn’t present?

A

It signals to the Arcuate nucleus to increase food intake at other sites

25
What did new discover discover about VMH syndrome?
Most effects are due to changes in metabolism nit feeding behaviour
26
What effects did they find in VMH syndrome?
- Insulin levels increased - Lipogenesis: formation of fat increased - Lipolysis: breakdown of fat decreased Most energy was stored as fat Rats needed more energy, therefore they ate more
27
Where is Leptin released from?
Adipose Tissue
28
What does Leptin control?
Long Term Satiety signals
29
What does leptin Regulate?
Body Fat/Composition
30
What does Leptin inhibit?
NPY of the Arcuate Nucleus
31
What does Leptin stimulate?
POMC Neurons of the Arcuate Nucleus
32
What is the net effect of leptin?
Eat less, burn more calories
33
How do signals travel from the GI tract?
Gi tract --> bloodstream --> brain
34
What does your brain respond to?
Signals from the blood stream
35
What are some feeding enhancers?
Catecholamines, NPY, Orexin A and B, Ghrelin
36
What are some feeding inhibitors?
CCK, PYY, Melanocortins (MCR-4, Glucagon