Hunger, Thirst and Control of Food Intake Flashcards

1
Q

State three triggers of thirst. Which is most potent?

A

Increase in plasma osmolality (most potent)
Decrease in blood volume
Decrease in blood pressure

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2
Q

Where are the osmoreceptors that trigger ADH release located?

A

OVLT - organum vasculosum
SFO - subfornical organ
These are found in the hypothalamus

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3
Q

How do the circumventricular organs detect changes in plasma osmolality?

A

They have an incomplete blood brain barrier so they can detect the changes taking place in the periphery - they are NOT isolated by the BBB.
The changes in plasma osmolality make the cells shrink or swell which signals to the ADH producing cells in the hypothalamus to change ADH release.

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4
Q

How come thirst is temporarily relieved when you drink water but before it has any effect on plasma osmolality?

A

There are receptors in the mouth, pharynx and oesophagus that are involved in this temporary relief of thirst.

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5
Q

What major hormone is involved in regulating thirst? What does it do?

A

Angiotensin II - it stimulates fluid retention

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6
Q

What neural and hormonal components have an effect on the hypothalamus in regulating hunger?

A

Neural - Vagal afferents

Hormonal - Ghrelin, PYY, Leptin

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7
Q

Which part of the brain is heavily involved in regulating hunger and what does it communicate with?

A

Arcuate nucleus

It is located beneath the 3rd ventricle and communicates with the paraventricular nucleus (above the 3rd ventricle)

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8
Q

What are the two groups of neuronal populations in this part of the brain and what effect does this have on hunger?

A

Stimulatory - NPY/Agrp

Inhibitory – POMC

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9
Q

What feature of the arcuate nucleus makes this good for regulating hunger?

A

It has an incomplete blood-brain barrier thus allowing access to peripheral hormones. It integrates peripheral and central feeding controls.

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10
Q

Describe the melanocortin system and how it regulates hunger.

A

POMC can be broken down to produce an anorectic hormone called alpha-MSH that agonises the melanocortin-4 receptor and suppresses food intake.
Agrp, also produced in the arcuate nucleus, can antagonise the MC4R receptor and make you feel hungry.

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11
Q

What mutations or deficiencies within this system can cause obesity?

A

MC4R deficiency and POMC mutation

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12
Q

Where is leptin produced and what are its two roles?

A

Leptin is produced by adipocytes in white adipose tissue

Leptin tells the brain how much fat is stored and hence regulate food intake and regulates thermogenesis.

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13
Q

State three possible mechanisms that would make leptin responsible for obesity.

A

Absence of leptin
Inability of the leptin stores to increase proportionally with increasing fat
Leptin resistance - partially responsible for obesity

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14
Q

What determines the amount of PYY secreted?

A

The size of the meal

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15
Q

Describe the action of PYY.

A

PYY travels to the arcuate nucleus and inhibits NPY release and stimulates POMC neurons so you DECREASE APPETITE.

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16
Q

What structure in Ghrelin is necessary for its receptor activity?

A

Ghrelin has a fatty acid in the 3rd position which is required for receptor activity and it helps it to slip across membranes.

17
Q

Describe the action of Ghrelin.

Ghrelin has the opposite action to PYY.

A

It stimulates NPY/Agrp and inhibits POMC thus INCREASING APPETITE

18
Q

What is the thrifty gene hypothesis?

A

It was evolutionarily sensible to put on some extra fat for use later on when food availability wasn’t guaranteed. So populations that are historically prone to starvation are the most obese.

19
Q

What is the adaptive drift hypothesis?

A

Weight use to show a normal distribution curve with the heaviest people being preyed on. As we became smarter we stopped being preyed on so extra weight became a neutral change.