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Metabolism 2 > Appetite regulation > Flashcards

Appetite regulation Flashcards

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
Q

what does CCK do

A

slows gastric emptying, releases bile and pancreatic enzymes

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26
Q

is CCK anorexigenic or orexigen

A

anorexigenic

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27
Q

what is PY released from and to

A

PYY is released from L cells in the GI tract

Released in response to high fat/protein

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28
Q

what does PYY do and what neurones does it activate and inhibit

A

Infusions lead to enhanced satiety

Directly inhibits NPY neurones and activates POMC neurones

Decrease food intake

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29
Q

is PYY short term or long term

A

Long term negative regulator of body weight

30
Q

how does PYY work

A

Y1-5 receptors expressed peripheral/vagal/central

Y2 is specifically reported as primary receptor mediating effects

31
Q

Is PYY anorexigenic or orexigenic

A

anorexigenic

32
Q

what is insulin released due to

A

Insulin is released in response to increase plasma glucose levels

Released following meals

33
Q

what does insulin inhibit and activate

A

Insulin is an acute satiety signal

  • Insulin inhibits NPY/AgRP neurones
  • Insulin activates αMSH/CART
34
Q

is insulin anorexigenic or orexigenic

A

anorexigenic

35
Q

what type of protein is glucagon like peptide -1

A

Most powerful known incretin in humans

36
Q

what does GLP-1 do

A

Released in response to food intake
Decrease blood glucose
Decreases food intake

37
Q

what is GLP-1 released by

A

L intestinal cell

38
Q

what does GLP-1 activate and inhibit

A

 GLP1 inhibits NPY neurones.

 GLP1 also stimulates POMC neurones.

39
Q

Is GLP-1 anorexigenic or orexigenic

A

anorexigenic

40
Q

describe pancreatic polypeptide

A

Released in response to food intake, proportional to calories

Decreases appetite - anorexigenic

Long term energy balance

41
Q

describe oxontymodulin

A

Anorectic peptide product of preproglucagon

Decreases ghrelin levels in plasma

May also increase energy expenditure

Effective weight loss

42
Q

what is the only orexigen

A

Ghrelin

43
Q

where is gherkin synthesised

A

Predominantly synthesised in the stomach

  • it can also act via the vagus
44
Q

what inhibits gherkin

A

Inhibited by food intake

Ghrelin is suppressed in proportion to the calories ingested

45
Q

where are ghrelin receptors found

A

Ghrelin receptors found on NPY neurones.

 Ghrelin stimulates NPY neurones to increase food intake directly.

46
Q

Ghrelin follows a…

A

 Follows a Circadian rhythm.

47
Q

what are the short term and long term actions of gherlin

A
  • short term contributes to hunger

chronic administration leads to hyperplagia (excessive eating)

malignant ghrelinoma causes persevered obesity

48
Q

what are the problems with using Gherkin as a drug target

A

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
Q

name some other orexigenic peptides

A
  • neuropeptide Y
  • agouti related peptide
  • melanin concentration hormone
  • orexin
  • galanin
50
Q

there are different …

A

gut micrbiomes between obese and lean mice therefore there may be differences in humans

51
Q

where is the hypothalamus located

A

below the thalamus

52
Q

what are the 2 neuroendocrine functions of the hypothalamus

A

Direct neuronal connection to anterior pituitary

Hypophyseal portal system

53
Q

what part of the hypothalamus controls food intake

A

Food intake is controlled by the lateral part of the ventromedial nucleus of the hypothalamus
- Known as the arcuate nucleus

54
Q

what are the 2 groups of neuroendocrine neurones that are released from the hypothalamus

A

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
Q

what is the primary role of the central orexigenic pathway

A

increase food intake

56
Q

what neurones make up the central orexigenic pathway and what activates it and inhibits it

A

AGRP/NPY neurones in arcuate nucleus of hypothalamus

Activated by ghrelin

Inhibited by insulin and leptin

57
Q

what does the central orexigenic pathway release

A

Releases NPY which activates Y1 receptors

Increase food intake by activating second order neurones

Inhibits POMC/CART neurones

58
Q

what is AgRP

A

AgRP is a melanocortin receptor antagonist

- by blocking this receptor it increases food intake and decreased food inhibition intake

59
Q

what neurones are released by the central anorexigeic pathway and what activates and inhibits it

A

POMC/CART neurones in arcuate nucleus of hypothalamus

Activated by insulin and leptin

60
Q

what is the primary role of the central anorexigenic pathway

A

Decrease food intake by releasing melanocortins

61
Q

how does the central anorexigenic pathway work

A
  • 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
Q

what does deficiets in the anorexigenic pathway lead to

A

Defects lead to Hyperphagia and obesity.

Genetic deletion of MC4R in both humans and mice has been linked to severe,
hyperphagic obesity.

63
Q

what causes an increase in fatty acid synthesis by malonyl CoA

A

 Insulin and excess glucose increase fatty acid synthesis via Malonyl CoA.

64
Q

what is malonyl CoA important in

A

 Malonyl CoA is important in the synthesis of fatty acids.

 Malonyl CoA also inhibits CPT1 to prevent Beta oxidation of FAs.

65
Q

what is malonyl CoA controlled by

A

 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
Q

what does serotonin do

A

An Anorexigenic molecule, decreases food intake.

- depletion of this promotes weight gain

67
Q

how does serotonin decrease food intake

A

 HTr2C increase POMC signalling (Anorexigenic).

 HTr1B decreases AgRP signalling (Orexigenic).

68
Q

what was a previous obesity treatment and why was it withdrawn

A

CB1 antagonist was used as an obesity treatment

- causes suicidal thoughts so it was withdrawn

69
Q

what are the current obesity treatments recommended by NICE

A

Lifestyle/Behavioural modification
Fat absorption inhibition- orlistat
Bariatric surgery

70
Q

what were the drug treatments used for obesity but withdrawn

A

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

Metabolism 2 (40 decks)

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