Endo 15: Endocrine control of food intake Flashcards

1
Q

What is the input to the hypothalamus

A

GHRELIN, PYY & other gut hormones

Neural input from the periphery and other brain regions

LEPTIN

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2
Q

What are the outputs of hypothalamus

A

Food Intake
and
Energy Expenditure (TRH)

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3
Q

Why is paraventricular nucleus important

A

Releases TRH

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4
Q

Where is arcuate

A

Bottom of hypothalamus next to the 3V

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5
Q

How does arcuate receive hormonal input. What function does arcuate nucleus serve

A

Incomplete blood brain barrier, allows access to peripheral hormones.
(circumventricular)

Integrates peripheral and central feeding signals.

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6
Q

What are the key neuronal populations in the arcuate nucleus

A

Stimulatory (NPY/Agrp neuron)

Inhibitory (POMC neuron)

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7
Q

How is POMC used in different brain areas

A

pituitary cut up to ACTH

Hypothalamus cut up to MSH

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8
Q

What hormone is present in the paraventricular nucleus and the function

A

MC4R…. reduces appetite

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9
Q

How does POMC neuronal bodies affect paraventricular nucleus

A

Releases a-MSH to stimulate PVN to decrease food intake

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10
Q

How to AGRP/NPY affect PVN

A

releases AGRP which inhibits MCR4 so increased appetite

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11
Q

T/F NPY and Agrp mutatuons are responsible for obesity prevalence

A

F!! POMC deficiency and MC4-R mutations cause morbid obesity, but NOT responsle for obesity prevalence

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12
Q

What does the hypothalamus receive signal from

A

From leptin, the gut and brainstem as well as cortical regions

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13
Q

What is the ob gene, what occurs in deficiency

A

Ob gene codes for leptin in ob/ob mouse there is no leptin, nothing to tell the brain that there are adequate fat stores in the adipose tissue

Profoundly obese.
Hyperphagia.
Diabetic.
Decreased body temperature.
Decreased energy expenditure.
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14
Q

What is leptin, where is it released, and where are its receptors

A

Leptin released from WHITE adipose tissue

Leptin receptors in the hypothalamus (Ob-R)

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15
Q

How does leptin work on the hypothalamus

A

Activates POMC and inhibits NPY/AgRP neurons.

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16
Q

What is the effect of central or peripheral administration of leptin in those who have deficiency

A

Central or peripheral administration decreases food intake and increases thermogenesis.

17
Q

What will leptin be when body fat is

a) high
b) low

A

a) high when body fat high

b) low when body fat low

18
Q

With obese humans, what are leptin levels like

A

Most obese humans have high leptin (high fat mass)….

19
Q

Can leptin be used as a weight control drug

A

No, leptin is ineffective as a weight control drug.

the brain is now unresponsive to leptin because it’s been high due to high adiposity

20
Q

What is the role of inslin in food intake.

T/F insulin secretion from the pancreas increases in proportion to body adiposity

A

Insulin circulates at levels proportional to body fat.

Receptors in the hypothalamus.

Central administration reduces food intake.

T! Glucose-induced insulin secretion from the pancreas increases in proportion to body adiposity, owing to the capability of expanding fat stores to induce resistance to insulin’s glucose-lowering effects.

21
Q

What is the body’s largest endocrine organ

A

The gut

22
Q

How many gut hormones are there

A

20+

23
Q

What do gut hormones control

A

gut motility, secretion of other hormones, appetite.

24
Q

Rlease of gut hormone is regulaated by what

A

Release regulated by gut nutrient content.

25
Q

How dows grehlin impact appetite. Where is grehln released

A

Released in stomach

It stimulates NPY/Agrp

Imhibits POMC

INCREASES appetite

26
Q

What type of hormone makes you feel full?

A

PYY (satiety)

27
Q

How does PYY work and where is it released

A

Released from L cells in intestine

Inhibits NPY release.

Stimulates POMC neurons.

Decreases appetite.

28
Q

What is GLP1 and what is the effect on appetite

T/f: GLP1 is made from the same gene as glucagon. PYY also comes from this gene.

A

Gut hormone coded for by the preproglucagon gene and released post-prandially in the L cells by the gut

F: glucagon, glp1 and glp2 from same gene but PYY from elsewhere

29
Q

What type of hormone is GLP1….. explain this hormone type

A

Hormones that
Are released after eating
Augment insulin secretion from b islet cells

30
Q

2 functions of GLP-1

A

Well characterised incretin role and also reduces food intake.

31
Q

Are there therapeutic uses of GLP1

A

GLP-1 agonists are injectable only

or

DPP-4 inhibitors (DPP-4 endogenousl breaks down GLP-1, so these drugs prevent breakdown)

32
Q

Why is it difficult to give injection for GLP-1

How is GLP-1 agonists used in type II diabtetes

A

Very short lives as they’re peptide hormones so are broken down,,,, haf life just 1 minute, so can be modified to saxenda (which is modified GLP so longer lived)

Used in type II diab. because they can cause increased release of insulin to control sugar and also inhiit appetpite

Also have recently been licensed for obesity treatment

33
Q

Coud PYY3-36 be used a as a drug target

A

No because narrow therapeutic window and cause nausea above this, and no efffect below it

34
Q

What is thrify vs drift gene

A

thrifty gene stated that those who had genes that caused storage of fat were selected for as starvation was a big problem in cave men times. This shows as Populations historically prone to starvation become most obese when exposed to Western diet and sedentary life-style (e.g. Pima Indians, Pacific Islanders).

drfity gene says that there is normal distribution of body mass, as if you are too fat you are eaten and if you are too thin then you starve.

BUT then 20,000 years ago people learnt to defend against predators so obesity isn’t selected against…. so body fat was then a neutral change/genetic drift….

In a healthy environment those genetically prone will have same BMI as everyone else but in toxic environment i.e. like the western fat diet one, then these people will put on lots of weight

35
Q

Which gene codes for leptin

A

The Ob gene