Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LCRS Endocrinology > Endocrine control of food intake > Flashcards

Endocrine control of food intake Flashcards

1
Q

What decides whether you should be eating or not?

A

Hypothalalmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the key part of the hypothalamus involved in regulation of food intake?

A

Arcuate nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The arcuate nucleus is a circumventricular organ, what does this mean?

A

It has an incomplete blood-brain barrier so allows access to peripheral hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the two neuronal populations in relation to food intake?

A

Stimulatory- NPY and Agrp neurones

Inhibitory- POMC neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do NPY and Agrp do to appetite?

A

Increase it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Under normal conditions, what is POMC broken down into?

A

alpha-MSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is alpha-MSH?

A

Endogenous agonist for MC4R which decreases food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In relation to MC4R, what is Agrp?

A

Endogenous antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens when you need to eat?

A

You stimulate Agrp activity and block the inhibitory signal of alpha-MSH and stimulates food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Of the three proteins, which one is there a known mutation of associated with appetite?

A

POMC deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is POMC deficiency normally associated with?

A

Red hair and very pale skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does leptin do?

A

Tells the brain how much fat there is in storage so regulates eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where does leptin come from?

A

Fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens in people that are leptin deficient ?

A

They think that they are starving all the time because there isn’t any leptin to tell the brain that there are fat stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What would central or peripheral administration of leptin do?

A

Decrease food intake and increase thermogenesis- it activates POMC and inhibits NPY/Agrp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are leptin levels like in fat people?

A

High- It circulates in plasma in concentrations proportional to fat mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens with leptin in obese people?

A

They develop leptin resistance- ineffective as a weight control drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the effects of no leptin?

A

Hyperphagia, lowered energy expenditure and sterility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens to children with no leptin?

A

They don’t go through puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why don’t children with leptin deficiency go through puberty?

A

The hypothalamus won’t be releasing GnRH because leptin has a permissive effect on its release

21
Q

Why do fat people have more insulin?

A

It circulates at levels proportional to body fat because fat people are more likely to be insulin resistant

22
Q

What is the body’s largest endocrine gland?

A

GI tract

23
Q

What is cholecystokinin involved in?

A

Gall bladder contraction
Gastrointestinal motility
Pancreatic exocrine secretion

24
Q

What is secretin involved in?

A

Pancreatic exocrine secretion

25
Q

What is GIP involved in?

A

Incretin activity

26
Q

What is ghrelin involved in?

A

Hunger

Growth hormone release

27
Q

What is gastrin involved in?

A

Acid secretion

28
Q

What is pancreatic polypeptide involved in?

A

Gastric motility

Satiation

29
Q

What is ghrelin released by?

A

Stomach

30
Q

How many amino acids long is ghrelin?

A

28

31
Q

What converts ghrelin to its active form?

A

Ghrelin O-acetyltransferase (GOAT)

32
Q

How do ghrelin levels change throughout the day?

A

It is high in the morning then goes down after breakfast and rises again until lunch (the pattern repeats for every meal)

33
Q

What effect does ghrelin have on appetite and how?

A

It increases appetite by directly modulating neurones in the arcuate nucleus:
Stimulates Agrp/NPY neurones
Inhibits POMC neurones

34
Q

What is both PYY and GLP-1 secreted by?

A

L-cells

35
Q

What shape are L cells?

A

Distinctive flask shape

36
Q

What is PYY 3-36?

A

Fullness hormone that is released post-prandially

37
Q

How does PYY 3-36 decrease appetite?

A

Directly modulates neurones in the arcuate nucleus:
Inhibits NPY release
Stimulates POMC neurones

38
Q

What is the incretin effect?

A

If you give someone oral glucose you get a much bigger insulin response than when you give same amount of glucose IV

39
Q

Why is there the incretin effect?

A

Glucose travelling in the GI tract stimulates the release of hormones that potentiate the effects of glucose-induced insulin release

40
Q

What is GLP-1?

A

Gut hormone coded for by preproglucagon gene that is released post prandially and has an incretin role and reduces food intake

41
Q

What are GLP-1 based drugs used to treat?

A

Diabetes mellitus

42
Q

Why does GLP-1 not cause hypoglycaemia?

A

It only stimulates glucose-induced insulin release so it only works when it is needed and when there is low glucose, there is no insulin release

43
Q

What is a problem with GLP-1?

A

It is quickly inactivated by DP-4 (dipeptidyl peptidase 4) so drugs have to be altered to have a longer half life

44
Q

What is saxenda?

A

Long acting GLP-1 agonist- structure of GLP-1 has been tweaked so it’s more resistant to degradation, it also has a fatty acid group attached which stops it from being cleared from the circulation
It has recently been approved as a treatment for obesity and diabetes

45
Q

What happens with high levels of PYY 3-36?

A

Nausea

46
Q

What comorbidities is obesity associated with?

A 
Depression
Stroke
Sleep apnoea
Myocardial infarction
Hypertension
Diabetes
Bowel cancer
Osteoarthritis
Peripheral vascular disease
Gout
47
Q

How much of body weight is due to heritability?

A

60-80%

48
Q

What is the thrifty gene hypothesis?

A

Specific genes were selected for to increase metabolic efficiency and fat storage, evolutionarily sensible to put on weight, thin people don’t survive famine so don’t pass on their genes- evolutionary drive to put on weight

49
Q

What is the adaptive drift hypothesis?

A

Used to be normal distribution of body weight:
Thin people will not survive/be able to reproduce
Fat people will be eaten
Eventually, improved at defending against predators so excess bodyweight became a neutral change

LCRS Endocrinology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions