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METABOLISM 2 > Appetite Regulation > Flashcards

Flashcards in Appetite Regulation Deck (30):
1

Define 'anorexigen'

Molecules which cause the inhibition of appetite e.g. by activating POMC or CART

2

Define 'orexigen'

Molecules which stimulate appetite e.g. by stimulating NPY, AgRP and MCH

3

Which hypothalamic nucleus is involved in appetite regulation?

Arcuate nucleus

4

Which neurone systems are involved in increasing appetite and decreasing energy expenditure when stimulated?

NPY and AgRP

5

Which neurone systems are involved in decreasing appetite and increasing energy expenditure when stimulated?

POMC and CART

6

Describe the neuropeptide Y (NPY) neurone system in the hypothalamus

These neurones express NPY and activation causes increased food intake and decreased energy expenditure

7

Describe the agouti-related peptide hormone (AgRP) neurone system in the hypothalamus

AgRP is found on some of the neurones that present NPY also, and this peptide acts as a MC4R antagonist to inhibit appetite reduction

8

What happens if an individual has a genetic deletion of the genes coding for the MC4R receptors?

The melanocortin molecules produced by the post-translational modification of POMC will be unable to bind to their MC4R target receptor, and therefore unable to exert its effects, and therefore appetite is not inhibited, leading to hyperplasia and subsequent obesity

9

What happens if an individual has a genetic deletion of the genes coding for the MC4R receptors?

The melanocortin molecules produced by the post-translational modification of POMC will be unable to bind to their MC4R target receptor, and therefore unable to exert its effects, and therefore appetite is not inhibited, leading to hyperplasia and subsequent obesity

10

How does insulin affect AgRP levels?

Insulin reduces the levels of AgRP as AgRP is involved in increasing appetite and reducing energy expenditure, which is counter-intuitive to the action of insulin.

11

Name 7 anorexigenic molecules

Serotonin, PYY 3-36, POMC, GLP-1, CCK, leptin, elevated malonyl-CoA

12

Explain how serotonin acts to decrease appetite and increase energy expenditure (anorexigen)

Serotonin production leads to serotonin binding to receptors in the arcuate nucleus of the hypothalamus:

At HTr2c serotonin binding increases POMC signalling to reduce appetite

At HTr1b serotonin causes decreased AgRP signalling to inhibit appetite increase

13

Explain how PYY (3-36) acts to decrease appetite and increase energy expenditure (anorexigen)

PYY is secreted by the gut cells (enterocytes) in response to food and then travels in the blood to the hypothalamus where it inhibits the NPY neurones via the Y2 receptor, and stimulates the POMC neurones in order to decrease appetite and increase energy expenditure

14

Explain how GLP-1 acts to decrease appetite and increase energy expenditure (anorexigen)

GLP-1 is secreted by L-intestinal cells in response to food, and thereafter it travels in the blood to the hypothalamus where it inhibits NPY and stimulates POMC

15

Where is PYY produced?

Enterocytes (in response to food)

16

Where is GLP-1 produced?

L cells in the intestine in response food

17

Where is cholecystokinin (CCK) produced?

I type intestinal cells (enteroendocrine cells) in the duodenum and small intestine

18

Explain how CCK acts to decrease appetite and increase energy expenditure (anorexigen)

CCK is secreted from I-type enteroendocrine cells in the duodenum and small intestine in response to food and it acts to suppress appetite via stimulation of the vagus nerve

19

Explain how leptin acts to decrease appetite and increase energy expenditure (anorexigen)

High leptin levels cause AgRP levels to drop in order to inhibit appetite promotion

20

Where is leptin produced?

Adipocytes, therefore if someone has more fat, they will secrete more leptin (which should reduce appetite)

21

On which pathway does leptin primarily act?

AgRP; high leptin levels inhibit AgRP, low levels stimulate AgRP (to increase appetite)

22

Name three orexigenic molecules/factors

Ghrelin, low leptin levels, low malonyl CoA

23

Explain how ghrelin acts to increase appetite and decrease energy expenditure (anorexigen)

Ghrelin is secreted by the stomach in the absence of food, and binds to ghrelin receptors on NPY neurones and via the vagus nerve to increase appetite and decrease energy expenditure

24

Explain how ghrelin acts to increase appetite and decrease energy expenditure (anorexigen)

Ghrelin is secreted by the stomach in the absence of food, and binds to ghrelin receptors on NPY neurones and via the vagus nerve to increase appetite and decrease energy expenditure

25

Outline the role of malonyl CoA in decreasing appetite

Appetite is decreased where there is increase of LCFA CoA and malonyl-CoA as these molecules inhibit AgRP/NPY neurones and increased LCFA-CoA stimulates CART/POMC to decrease appetite

26

Outline the role of malonyl-CoA in increasing appetite

A reduced malonyl CoA level increases AgRP/NPY activity and decreases POMC/CART pathways in order to increase appetite and decrease energy expenditure

27

What causes an increase in malonyl-CoA levels?

There is glucose availability which leads to an increase in glycolysis which creates an elevated ATP:AMP ratio in the mitochondria which inactivates AMP-kinase (AMPK) which leads to the activation of ACC and inactivation of MCD (malonyl-CoA dehydrogenase) so more malonyl-CoA is formed and less is broken down.

28

What causes a decrease in malonyl CoA levels?

There is a reduction in glucose availability which increases the AMP:ATP ratio in the mitochondria which leads to the activation of AMPK which activates MCD and inactivates ACC which leads to greater malonyl CoA breakdown and reduced synthesis, hence the reduced levels

29

What drug may be given in order to increase appetite?

A form of cannabinoid; these act on CB1 receptors in the hypothalamus to increase appetite

30

What drug may be given in order to decrease appetite?

- Amphetamine derivatives for 5HT (serotonin) and noradrenaline
- SSRI derivatives, mostly 5HT
- Cannibinoid antagonists
- Leptin
- GLP-1 agonists