Week 6- Neural Control of Food Intake

Question 1

How many appetite stimulators are ther?

Answer 1

ghrelin only

Question 2

Name some appetite inhibtiors?

Answer 2

leptin, insulin, GLP-1, CCK, PYY

Question 3

Metabolites, appetite stimulators and inhibitors act where to control feeding?

Answer 3

within the hyptohalamus and/or brianstem

Question 4

What is NPY?

Answer 4

Neuropeptide Y, most potenent oxigen

increases food intake via Y1 and Y5

released by NPY/ArGP/GABA neuron

Question 5

POMC

Answer 5

Neuron that produces melanocortins(alpha-SMH) which acts within the PVN to REDUCES food intake via the MC4R

Question 6

The arcuate nucleus contains which 2 neurons and what do they produce?

Answer 6

orexegenic neuron-NPY,AgRP,GABA

satiety/POMC neuron-alphaMSH

Question 7

AgRP

Answer 7

Question 8

What is the most common monogenetic cuase of obesity?

Answer 8

a mutation on MC4R which on the PVN. This is because if POMC aMSH cannot signal to the receptors then AgRP can continually act and stimulate hunger

Question 9

How do the NPY cells talk to the POMC cells?

Answer 9

communicate via GABA. Activ of NPY/AgRP will lead to inhib of POMC as inhibitory GABA will be produced

Question 10

RAPID signals to control food intake?

Answer 10

NPY and GABA from AgRP neuron stimulate food intake and glutamate from POMC activates satiety cells to decrease food intake

Question 11

slower signals to control food intake

Answer 11

AgRP release from AgRP neuron binds to MC4R on satiety cells in PVN and blocks aMSH activation to therefore stimulates food intake

this is longer term control of feeding

Question 12

are AgRP neurons essential fro survival?

Answer 12

yes, genetic albation of the neurons found that mice starved to death. There was rapid decline in food intake and body weight which shows the important of this neuron in hunger stimulation.

Question 13

How are POMC cells involved in obesity and diabete?

Answer 13

they actually aren’t, they prevent these 2 diseases.

ablation of these neurons sees the dev of obesity and T2DM

Question 14

What is the state of the BBB of the arcuate nucleus and what are the implications?

Answer 14

these neurons have access to blood borne factors( from capillaries but also CSF and ventricles) as the BBB is leaky. the blood borne factors have access due to fenestrated capillaries from the median eminence and tanycytes from glial cells.

Question 15

First order neurons are …

Answer 15

our POMC and AgRP neurons

Question 16

ceond order neruons are our…

Answer 16

PVN cells

Question 17

Leptin and Insulins affect on the NPY/AgRP neurons and POMC cells?

Answer 17

leptin and insulin inhibit NPY/AGRP but activate POMC. This increases alphaMSH which increases MCR4 activation and then increased energy expenditure

Question 18

The functions of ghrelin

Answer 18

increases FI, increases adiposity, increases BGL, increases GH

Question 19

ghrelin is increased in plasma during…

Answer 19

negative energy balance (fasting)

Question 20

ghrelin is decreased in plasma during…

Answer 20

positive energy balance( obesity)

Question 21

role of ghrelin

Answer 21

designed to shift negative to neutral energy balance to ensure survival

Question 22

Where does ghrelin act?

Answer 22

at the NPY/AGRP neurons. this is the only place where ghrelin receptors are located.

They directly activate it which indirectly inhibits POMC

Question 23

Lesions in the ventromedial hypothalamus cause..

Answer 23

obesity, this shows VMH is a satiety centre

Question 24

lesions in the lateral hypothalamus cause..

Answer 24

LH is a hunger centre

Question 25

Lesions in VMH followed by subsequent lesions in LH showed…

Answer 25

1) VMH lesions caused obesity but lesions in LH after reversed obesity and caused stravation

It is thought that if there lesion order were reversed the would not be seen.

Question 26

What si the dual centre hypothesis?

Answer 26

Question 27

Leptins action in the VMH

Answer 27

Leptin can cross the BBB via active transport to act directly on the VMH neurons, within the VMH are where leptin receptors are found. here they alter BNDF level to reduce food intake

leptin also acts at the ARC neurons( which also project to the VMH)

Question 28

LHA action in food intake?

Answer 28

ARC neurons project to the LHA

here LHA cells produce orexin and melanin-concentrating hormone to increase food intake

melanocortins inhibit these neurons to reduce food intake

Question 29

What the gut peptides?

Answer 29

ghrelin, PYY,GLP-1,CCK

Question 30

How does ghrelin regulate food intake

Answer 30

receptors on NPY/AgRP allow for acitvation of this neyron and inhibition via GABA of POMC. drives increase in food intake

Question 31

How do PYY and GLP1 regulate food intake

Answer 31

PYY and GLP-1 reduce food intake via brain stem(vagal afferents, in small intestine sensory neurons when activates signal the release of gut peptides and signal satiety via afferents), area postrema and via the ARC nucleus

Question 32

How does CCK regulate food intake

Answer 32

cck is unique as it is secreted via the intestine and only causes satiety via vagal afferents in the brianstem only

Question 33

GLP-1 in the ARC nuclues

Answer 33

acts at the GLP1-R which is on the POMC. this indirectly inhibits NPY/AGRP via GABA

Question 34

PYY action in the ARC nucleus

Answer 34

inhibits food intake via Y2 receptors on the NPY/AGRP neruons only.

PYY inhibits these neruons to reduce food intake

Question 35

which 2 meal signals only provide long term feedback signals regarding adiposity

Answer 35

leptin and insulin