Metabolism 2 > Appetite regulation > Flashcards

Appetite regulation Flashcards

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1
Q

what is the main centre for appetite regulation in the brain

A

arcuate nucleus

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2
Q

what is the arcuate nucleus next to

A

The arcuate nucleus is adjacent to the 3 rd ventricle.

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3
Q

what are the 2 main systems in the arcuate nucleus

A

 There are 2 main systems in the ARC, one for inhibiting food and intake and the
other for increasing food intake.

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4
Q

what is an orexigen

A
  • this is a substance that can increase food intake

- it activates specific neurological pathways to increase hunger and food intake

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5
Q

what can an orexigen be

A
  • can be hormones or drugs
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6
Q

what can be an side effect of an oxreigen medication

A

increased weight gain

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7
Q

what is a desirable outcome of orexigen therapy

A
  • cachexia Treatment

- AIDS/cancer

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8
Q

what neurones does the orexigenic pathway involve

A

It involves the NPY/AgRP neurones.

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9
Q

what is an anorexigen

A
  • this is a substance that inhibits food intake

- activates specific pathways to reduce eating

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10
Q

what can an anorexigen be

A
  • hormones or drugs

- there are currently no drugs to target this pathway

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11
Q

what neurones does anorexigen use

A

It involves the POMC/CART neurones.

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12
Q

How does nutrient sensation occur in the GI tract

A
  • Food is broken down into nutrients in the GI tract - this happens by stomach acid, enzymes, gastric contractions and. mastication
  • the nutrients pass into the duodenum and are broken down further
  • these nutrients are then sensed by receptors in the GI tract
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13
Q

how do enteroendocrine cells sense the environment

A
  • have receptors on their apical surface which sense the environment
  • then they have vesicles which they release containing endocrine hormones
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14
Q

How Is the vagus nerve involved in appetite regulation

A
  • has chemoreceptora nd mechanoreceptors

chemoreceptors

  • these are activated by mediates released by the enteroendorcirne cells
  • responds to nutrients, hormones, pH, osmolality

mechanoreceptors

  • stimulated by stretch caused by …
  • meal size
  • gastric distentions hick causes satiety
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15
Q

is the vagus involved in long term or short term control of appetite

A

short term

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16
Q

how is the vagus linked to the arcuate nucleus

A
  • arcuate nucleus connects with the dorsal vagus complex via the nucleus of tracts solitaires
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17
Q

what type of hormone is leptin

A

adipokine

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18
Q

where is leptin made

A

adipose tissue

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19
Q

is leptin anorexgien or an orexigen

A

anorexigne

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20
Q

is leptin long term or short term

A

Does not respond over short term but over longer term

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21
Q

what neurones does leptin activate and inhibit

A

Leptin is a satiety signal

  • Inhibits NPY/AgRP neurones
  • Activates POMC/CART neurones
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22
Q

what does a deficiency inception result in

A

A defect in leptin production or leptin receptors cause marked increases in AgRP
levels.

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23
Q

where is CCK synthesised

A

duodenum

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24
Q

what is CCK released in response to

A

fat and protein

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25
what does CCK do
slows gastric emptying, releases bile and pancreatic enzymes
26
is CCK anorexigenic or orexigen
anorexigenic
27
what is PY released from and to
PYY is released from L cells in the GI tract Released in response to high fat/protein
28
what does PYY do and what neurones does it activate and inhibit
Infusions lead to enhanced satiety Directly inhibits NPY neurones and activates POMC neurones Decrease food intake
29
is PYY short term or long term
Long term negative regulator of body weight
30
how does PYY work
Y1-5 receptors expressed peripheral/vagal/central | Y2 is specifically reported as primary receptor mediating effects
31
Is PYY anorexigenic or orexigenic
anorexigenic
32
what is insulin released due to
Insulin is released in response to increase plasma glucose levels Released following meals
33
what does insulin inhibit and activate
Insulin is an acute satiety signal - Insulin inhibits NPY/AgRP neurones - Insulin activates αMSH/CART
34
is insulin anorexigenic or orexigenic
anorexigenic
35
what type of protein is glucagon like peptide -1
Most powerful known incretin in humans
36
what does GLP-1 do
Released in response to food intake Decrease blood glucose Decreases food intake
37
what is GLP-1 released by
L intestinal cell
38
what does GLP-1 activate and inhibit
 GLP1 inhibits NPY neurones. |  GLP1 also stimulates POMC neurones.
39
Is GLP-1 anorexigenic or orexigenic
anorexigenic
40
describe pancreatic polypeptide
Released in response to food intake, proportional to calories Decreases appetite - anorexigenic Long term energy balance
41
describe oxontymodulin
Anorectic peptide product of preproglucagon Decreases ghrelin levels in plasma May also increase energy expenditure Effective weight loss
42
what is the only orexigen
Ghrelin
43
where is gherkin synthesised
Predominantly synthesised in the stomach - it can also act via the vagus
44
what inhibits gherkin
Inhibited by food intake Ghrelin is suppressed in proportion to the calories ingested
45
where are ghrelin receptors found
Ghrelin receptors found on NPY neurones.  Ghrelin stimulates NPY neurones to increase food intake directly.
46
Ghrelin follows a...
 Follows a Circadian rhythm.
47
what are the short term and long term actions of gherlin
- short term contributes to hunger chronic administration leads to hyperplagia (excessive eating) malignant ghrelinoma causes persevered obesity
48
what are the problems with using Gherkin as a drug target
In obese subjects, ghrelin is low Reducing ghrelin further may not assist with obesity - Safety concerns on regulation of growth - Also, prevent beneficial effect of ghrelin on cardiovascular system and inflammation Ghrelin mimetics may be better suited to anorexia/cachexia Infuse ghrelin increase food intake
49
name some other orexigenic peptides
- neuropeptide Y - agouti related peptide - melanin concentration hormone - orexin - galanin
50
there are different ...
gut micrbiomes between obese and lean mice therefore there may be differences in humans
51
where is the hypothalamus located
below the thalamus
52
what are the 2 neuroendocrine functions of the hypothalamus
Direct neuronal connection to anterior pituitary Hypophyseal portal system
53
what part of the hypothalamus controls food intake
Food intake is controlled by the lateral part of the ventromedial nucleus of the hypothalamus - Known as the arcuate nucleus
54
what are the 2 groups of neuroendocrine neurones that are released from the hypothalamus
Neuropeptide Y (NPY) and Agouti related peptide (AgRP)- orexigens Cocaine and Amphetamine related transcript (CART) and pro-opiomelanocortin (POMC)- anorexigens - these have reciprocal inhibition
55
what is the primary role of the central orexigenic pathway
increase food intake
56
what neurones make up the central orexigenic pathway and what activates it and inhibits it
AGRP/NPY neurones in arcuate nucleus of hypothalamus Activated by ghrelin Inhibited by insulin and leptin
57
what does the central orexigenic pathway release
Releases NPY which activates Y1 receptors Increase food intake by activating second order neurones Inhibits POMC/CART neurones
58
what is AgRP
AgRP is a melanocortin receptor antagonist | - by blocking this receptor it increases food intake and decreased food inhibition intake
59
what neurones are released by the central anorexigeic pathway and what activates and inhibits it
POMC/CART neurones in arcuate nucleus of hypothalamus Activated by insulin and leptin
60
what is the primary role of the central anorexigenic pathway
Decrease food intake by releasing melanocortins
61
how does the central anorexigenic pathway work
- it decreased food intake by releasing melanocortins - main mealnocortin that it releases is α-melanocortin-stimulating hormone (α-MSH) this works by .. - activating second order neurones (MCR4 receptors) - Inhibits NYY/AgRP neurones (MCR3 receptors)
62
what does deficiets in the anorexigenic pathway lead to
Defects lead to Hyperphagia and obesity. Genetic deletion of MC4R in both humans and mice has been linked to severe, hyperphagic obesity.
63
what causes an increase in fatty acid synthesis by malonyl CoA
 Insulin and excess glucose increase fatty acid synthesis via Malonyl CoA.
64
what is malonyl CoA important in
 Malonyl CoA is important in the synthesis of fatty acids. |  Malonyl CoA also inhibits CPT1 to prevent Beta oxidation of FAs.
65
what is malonyl CoA controlled by
 Malonyl CoA levels are controlled by AMPK.  Decreased energy (high AMP/ATP levels) increases AMPK levels.  When there is less energy more Malonyl CoA is activated so more FAs are made
66
what does serotonin do
An Anorexigenic molecule, decreases food intake. | - depletion of this promotes weight gain
67
how does serotonin decrease food intake
 HTr2C increase POMC signalling (Anorexigenic).  HTr1B decreases AgRP signalling (Orexigenic).
68
what was a previous obesity treatment and why was it withdrawn
CB1 antagonist was used as an obesity treatment | - causes suicidal thoughts so it was withdrawn
69
what are the current obesity treatments recommended by NICE
Lifestyle/Behavioural modification Fat absorption inhibition- orlistat Bariatric surgery
70
what were the drug treatments used for obesity but withdrawn
Amphetamines- withdrawn CB1 antagonists- withdrawn GLP-1 agonists- type 2 diabetes but no clear effect on weight loss 5HT drugs- mixed with SSRIs, 5-HT2C effect modest, only in USA
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