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sem 2 Liver and GI > Control of food intake > Flashcards

Control of food intake Flashcards

1
Q

when when we start to eat what happens?

A

enlargement of the fundic area to accommodate for the food entering - controlled by VIP and NO

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2
Q

once accommodation has happened what do you get a feeling of?

A

satiety due to Peptide YY (PYY)

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3
Q

where is PYY secreted from and what does it do?

A
  • secreted by the pancreas

- decreases food intake by inhibiting gut motility

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4
Q

antrum - contractile movement

A

thick muscular region, contractile movement mediated by Ach

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5
Q

receptive relaxation

and adaptive

A

as soon as we see the food or start to swallow (food is travelling down the oesophagus) we have receptive relaxation
- vagal innervation of the nerves that encircle the oesophagus and the stomach, allowing receptive relaxation of the stomach

there are also adaptive relaxing factors that are released when the food is actually in the stomach which allow accommodation to occur (NO, VIP)

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6
Q

why is CCK released?

A

as the food starts to get digested a little bit, there are nutrients within the food that allow a specific hormone called CCK to be secreted which can impact on the relaxant effects, (nutrients eg. fats, lipids).

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7
Q

what is a vagotomy? why do people have it?

A

surgical operation in which one or more branches of the vagus nerve are cut, typically to reduce the rate of gastric secretion
-if they have ulcer disease/malignancy

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8
Q

consequences of a vagotomy

A

reduces accommodation and gastric compliance

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9
Q

what is gastric compliance?

A

accommodation and perception of distention

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10
Q

what is distention?

A

a state of being enlarged or swollen from internal pressure)

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11
Q

side effects of a vagotomy

A
  • 5% of patients develop symptoms of early satiety

- disturbances of fundic and antral contractility

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12
Q

Hunger

A

o Discomfort caused by a lack of food and the desire to eat

- A strong physiological craving/drive for food/sensation of emptiness in the stomach

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13
Q

Appetite

A

o Physiological desire/drive to satisfy the body’s needs of food, stimulated by hunger

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14
Q

Satiety

A

o State of being full after eating food

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15
Q

Aphagia

A

o The inability or refusal to swallow

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16
Q

Hyperphagia/Polyphagia

A

o An abnormal desire for food

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17
Q

Reasons for difference in BMI

A 
o	Genes (70%)
o	How much we eat and its composition
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18
Q

hypothalamus

A

the control centre for appetite, thirst and food intake

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19
Q

how does the hypothalamus control/regulate feeding?

A
  • The balance of stimulating and inhibiting forces in the hypothalamus

• The base of the hypothalamus has several nuclei that regulate energy homeostasis

o Controls the appetite, the size of the helping and our ingestive behaviour

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20
Q

pre-frontal cortex

A

integration of sensory information from inside and outside the body

receive emotional and cognitive information from the limbic system

helps one make choices by translating all of the homeostatic and environmental information into adaptive behavioural response

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21
Q

limbic system

A

complex system of nerves and networks in the brain, areas concerned with instinct and mood. may control emotions (pleasure fear, anger)

the satiation of feeding behaviour is associated with motor planning and execution

cortico-limbic mechanisms of reward appear to be under executive control

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22
Q

name the hypothalamic nuclei that modulate food intake

A
  1. Lateral hypothalamus (LH) = hunger centre
  2. Ventromedial nucleus (VMN) = satiety centre
  3. Dorsomedial nucleus (DMN) = modulates energy intake (hunger centre)
  4. Paraventricular nucleus (PVN) = modulates feeding behaviour
  5. Arcuate nucleus
    • Neurons produce orexigenic signals
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23
Q

ventromedial nucleus and lateral hypothalamus

A
  • have the ability to restrain feeding if required

- hypothalmic lesion can cause an increase in appetite, with weight gain that tends to persist

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24
Q

how does the dorsomedial nucleus (DMN) cause effects

A
  • release NPY into DMN which causes an increase in feeding

- stimulates appetite/food intake

25
Q

neurones in the arcuate nucleus do what?

A

produce orexigenic signals (increase appetite)

-NPY, the opioids, β-endorphin, and glutamate

26
Q

Suprachiasmatic nucleus

A
  • responsible for controlling circadian rhythms

- human body block located here

27
Q

role of medial amygdaloid nucleus

A

sub-region of the amygdaloid complex that participates the regulation of food intake, stimulated by ligands

serotonin (5-HT) regulates appetite and food intake

serotonin 5-HT(2C) and 5-HT(1A) receptors appear to be critical in the regulation of food intake

28
Q

appetite stimulating pathway

A

releases agouti-related peptide (AgRP) and neuropeptide Y (NPY)

29
Q

appetite suppressing pathway

A

a serotonin 5HT2C agonist (eg. mCPP) binds to 5HT2C receptors on POMC neurons in the appetite suppressing pathway, activating POMC neurons leading to production to precursor POMC

POMC is broken down into alpha-melanocyte stimulating hormone (alpha-MSH)

Alpha-MSH binds to melanocortin 4 receptors (MC4R) to suppress appetite.

30
Q

Zimelidine experiment

A

-feeding animals Zimelidine inhibits the reuptake of 5-HT from the synaptic cleft, meaning it persists, suppressing appetite

31
Q

side effects of zimelidine?

A

dry mouth, increased sweating (hyperhidrosis), vertigo, nausea, dryness of nasal membranes

32
Q

diurnal variation in food intake

A

o Carbohydrates are metabolised during the day
o Fats are metabolised at night
o Hypothalamus responds to the switch between carbohydrate and fat metabolism

33
Q

aphagia vs hyperphagia

A
  • Stimulation of ventromedial wall of paraventricular nucleus → aphagia (inability, refusal to swallow)
  • Lesions of ventromedial wall of paraventricular nucleus → hyperphagia (increased appetite or excessive hunger)
34
Q

Brain has glucostat - what is this

A

special receptor neurons that monitor and regulate BG levels and their fluctuations in the bloodstream

35
Q

stimulation of lateral hypothalamus causes what?

A

increased feeding

36
Q

legions in lateral hypothalamus causes what?

A

aphagia (inability/refusal to swallow)

37
Q

role of Orexigenic and Anorexigenic neurotransmitters in the hypothalamus

A

o Orexigenic neurotransmitters
- Increase appetite

o Anorexigenic neurotransmitters
- Decrease appetite

38
Q

factors that affect if food is sought?

A
  • Food preferences
  • Emotions
  • Environment
  • Life style
  • Circadian rhythm
39
Q

how can the concentration of glucose in the blood affect hunger?

A

[glucose]blood: stimulates gluco-receptors in hypothalamus

– ↓ [glucose]blood → up-regulation of hunger

– ↑ [glucose]blood → up-regulation of satiety

40
Q

the deposition of fat may do what?

A

may control appetite through leptin

leptin is a hormone released from fat cells, which will signal to the hypothalamus

acts to inhibit hunger and regulate energy balance

41
Q

temp affects feeding?

may explain why diabetic patients feel hungry despite ↑[glucose]blood

A

cold environments stimulate feeding

hot environments inhibit appetite

42
Q

distention of a full stomach does what?

A

inhibits appetite

contraction of an empty one stimulates appetite

43
Q

role of gut hormones in food intake

A
  • Fat ingestion causes CCK release and the slowing of gastric emptying (sense of fullness)
  • CCK (from I cells in the intestine) and somatostatin inhibit further food intake, satiety factors
  • Injection of CCK in the brain leads to a reduction of appetite
  • Overwhelming evidence that somatostatin decreases appetite
44
Q

role of pancreatic hormones in food intake (insulin)

A
  • Insulin is secreted into the blood from the pancreas in direct proportion to the amount of fat stored in white adipose tissue.

o As it circulates through brain capillaries, a small amount of insulin is transported into the brain where it acts on insulin receptors in the arcuate nucleus of the hypothalamus

o influences energy homeostasis (food intake and energy expenditure) and the amount of fat stored in the body by exerting a net catabolic action

insulin inhibits lipolysis in adipocytes

45
Q

is insulins effect catabolic or anabolic in terms of body fat and food intake? name the substances involved

A

anorexigenic agent

both - at first catabolic, then anabolic

can have 2 possible effects (reduce food intake and body fat, or vice versa)

catabolic - NPY, AgRP
anabolic - POMC/CART neutrons

46
Q

leptin

A

o White adipose tissue releases leptin (lipostat; signals fat stores in adipose tissue)

o Controls fat stores by operating a feedback mechanism between adipose tissue and brain

o increase in adipose tissue size leads to an increase in leptin secretion

  • Increases the expression of anorexigenic factors (POMC, CART, CRH, neurotensin)
  • Stimulates metabolic rate
  • Inhibits NPY, which stimulates feeding
47
Q

can you be resistant to the effects of leptin?

A

Yes, for example with binge eating, despite adequate or growing adipose tissue (obese)

48
Q

leptin deficiency/leptin receptor defects causes what?

A

Hyperphagia and severe obesity

49
Q

Ghrelin

A
  • An appetite-inducing hormone (an orexin)
  • Fast-acting and stimulates food intake
  • Released by stomach, pancreas, adrenals in response to nutritional status

circulating levels of ghrelin:

  • increase just before a meal (preprandially)
  • decrease just after a meal
  • Increases central orexins (NPY and AgRP), generates hunger signals
  • Suppresses the ability of leptin to stimulate anorexigenic factors
50
Q

leptin can inhibit what?

A

secretion of ghrelin

51
Q

Obestatin

A
  • Produced by epithelial cells of stomach
  • Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake
  • Suppresses food intake (suppresses appetite; ↓ body weight gain)
  • Antagonises ghrelin-induced food intake (and growth hormone secretion)

Obestatin mediates its effects via different receptors to ghrelin

52
Q

obesity in women

A

imbalance of ghrelin and obestatin has a role in obesity

– Decreased ghrelin/obestatin ratio characterise obesity in women

53
Q

removal of the lateral hypothalamus vs removal of the ventromedial hypothalamus

A

removal of lateral hypothalamus - hypophagia (decreased feeding), leading to death due to severe weight loss

removal of the ventromedial hypothalamus - hyperphagia (increased feeding), leading to weight gain and severe obesity.

54
Q

feeding is regulated by…

A

a balance of stimulating and inhibiting forces in the hypothalamus

55
Q

PFA (perifornical area)

A

very sensitive hypothalamic site for NPY-induced eating

56
Q

where in NPY found in the brain, and what happens if you inject NPY into the hypothalamus?

A

found in high concentrations within neurons of hypothalamus

if injected into the hypothalamus, it stimulates powerful stimulus to eat

57
Q

FX (fornix)

A
  • C-shaped bundle of nerve fibres in the brain that carries signals from the hippocampus to the mammillary bodies to the anterior nuclei of thalamus.
  • It is part of the limbic system – involved in memory and recall. Has re-collective memory so lets us decide whether we want to eat something again or not
58
Q

ME (median eminence)

A

part of the hypothalamus from which regulatory hormones are released

integral to the hypophyseal portal system (connects the hypothalamus with the pituitary gland)

sem 2 Liver and GI (11 decks)

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