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Physiology 1 > Control Of Food Intake > Flashcards

Control Of Food Intake Flashcards

1
Q

What controls the size of the stomach

A

The size of the stomach is controlled by the

autonomic nervous system with expansion occurring to the fundic area of the stomach first.

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2
Q

What facilitates stomach enlargement- accommodation

A

Stomach
enlargement known as accommodation is facilitated by vasoactive intestinal peptide (VIP) and nitric
oxide (NO).

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3
Q

What causes decreased gut motility and when does this occur

A

When satiety is reached (fullness), satiety factors like peptide YY (PYY) are released to
decrease gut motility.

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4
Q

What hormone gives individual sense of hunger

A

Following this, emptying of the stomach occurs and a sense of hunger is felt
initiated by gut hormones like ghrelin.

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5
Q

What region of the stomach is responsible for emptying- and what mediated the contraction movement

A

The region of the stomach mainly involved in its emptying is
the antrum region and the contractile movement around the antrum is mainly mediated by
acetylcholine.

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6
Q

How does receptive and adaptive relaxation lead to accommodation of stomach

A 
Mechanical stimulation (swallowing) in the pharynx causes receptive relaxation that leads to 
accommodation. Accommodation can also occur in response to adaptive relaxation, a stimulus 
triggered by food being in the stomach interacting with tension receptors.
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7
Q

What does adaptive and receptive relaxation initiate and how

A

Both these mechanisms
initiate accommodation through inhibitory vagal fibres that release acetylcholine to activate
inhibitory enteric pathways

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8
Q

What is inhibitory enteric pathways in the stomach that are activated my acetylcholine - what is the effect

A

Inhibited enteric pathways of the stomach that release VIP, NO, PACAP and/or ATP that relax the
muscles in the stomach.

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9
Q

How can relaxation if the stomach also be achieved ( food )

A

This relaxation can also be achieved by feedback from nutrients in the food.

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10
Q

How is the nutrient feedback loop initiated

A

This feedback loop is initiated when some of the nutrients from food in the stomach reach the
duodenum.

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11
Q

Describe the nutrient feedback loop

A

These nutrients, particularly fats, cause the release of a mediator (CCK in the case of fats)
that initiates a feedback loop to cause the vagal centre to relax the stomach. Vagotomy reduces
accommodation and emptying to cause early satiety in some patients however, not by much. This is
because other sensor factors are involved in controlling the amount of food we eat and therefore the
amount by which the stomach expands.

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12
Q

What is the definition of hunger

A

Hunger is defined as discomfort caused by lack of food and the desire to eat. It is a strong
physiological craving, and a sensation of emptiness in the stomach.

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13
Q

What is the definition of appetite

A

Appetite is defined as the
psychological desire to satisfy the body’s need for food and is stimulated by hunger. One can still
have an appetite without the need to eat.

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14
Q

What is satiety

A

Satiety is the state of being full after eating food. It is a
joyous moment and there is no longer the need to continue eating.

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15
Q

What is aphagia

A

Aphagia is the inability to

swallow and

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16
Q

What is hyperphagia or polyphagia

A

hyperphagia or polyphagia is an abnormal desire for food (indulgence).

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17
Q

What are the three cues to tell you when to stop eating

A

Hunger,

satiation and satiety are cues that tell you when to start and stop eating.

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18
Q

What governs the control of food intake

A

The control of food intake is
governed by the hypothalamus that controls when a person feels full and when a person feels
hungry.

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19
Q

What causes the hypothalamus to variate eg bmi

A

The hypothalamus contributes to variations in BMI with 70% of how the
hypothalamus works dictated by genes. Other factors that influence BMI include family gatherings,
emotions, habitats and food palatability.

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20
Q

How does the hypothalamus control hunger

A

The hypothalamus controls hunger through several nuclei at

its base that regulate energy homeostasis.

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21
Q

What does the prefrontal cortex do

A

The prefrontal cortex is an area of the brain involved in food seeking behaviour. It integrates sensory
information from inside and outside the body as well as emotional and cognitive information from
the limbic system. It translates homeostatic and environmental information into adaptive
behavioural response.

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22
Q

What is the lambic system

A

The limbic system is a complex system of nerves and networks in the brain
that are concerned with instinct and mood. It contributes to emotions and emotional control.
Feeding behaviour in general is associated with motor planning and execution with the cortico-limbic
mechanisms influencing this decision.

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23
Q

What is the hungry thirst centre

A

The lateral hypothalamus (LH) is the hunger and thirst centre. Stimulation of it increases feeding
whilst legion of this region causes aphagia (difficulty in swallowing).

24
Q

What centre is the satiety centre

A

The ventromedial nucleus (VMN)
is the satiety centre. The combination of both nuclei mentioned is able to control feeding (e.g.
problems with the VMN increases appetite).

25
Q

What does the DMN do

A

The dorsomedial nucleus (DMN) modulates energy

intake and is another hunger centre.

26
Q

How is feeding increased due to appetite

A

Release of neuropeptide Y (NPY) into the DMN increases

feeding as appetite is increased.

27
Q

What does the pvn modulate

A

The paraventricular nucleus (PVN) modulates feeding behaviour (i.e.
time of meal and helpings taken). The PVN is also sensitive to NPY as well as opioids.

28
Q

What effects does gaba have

A

GABA is a

mediator that promotes feeding in some instances and inhibits feeding in others.

29
Q

What is the effect of leptin

A

Leptin influences

the PVN by decreasing food intake.

30
Q

What does the accurate nucleus consist of and what does it produce

A

The arcuate nucleus consists of a collection of neurons that
produce orexigenic signals (appetite stimulants) like NPY, opioids, dynorphin, beta-endorphin, POMC,
galanin, some amino acids, GABA and glutamate.

31
Q

Where is the human body clock located

A

The human body clock is located in the
suprachiasmatic nucleus. It can be responsible for different drives of appetite at different times
based on the light-dark cycle. It has been suggested that the medial amygdaloid nucleus plays a role
in feeding behaviour.

32
Q

What ligands are associated with comtroll9jg appetite

A

There are particular ligands associated with controlling appetite (e.g. 5-HT) that
act on this sub-region of the amygdaloid complex.

33
Q

How is appetite regulated in the hypothalamus

A

The way appetite is regulated in the hypothalamus can be analysed using 5-HT2C agonist. There is
usually an appetite stimulating pathway and an appetite suppressing pathway in the different regions
of the hypothalamus involved in food intake control.

34
Q

Describe the appetite stimulating pathway

A

When a signal stimulates the appetite
stimulating pathway, factors like NPY and AgRP are released that increase appetite. The 5HT2C has a
receptor on the axon of the appetite supressing pathway. When 5-HT2C or a 5-HT2C agonist like
meta-chlorphenylpiperazine (mCPP) binds to the 5-HT2C receptor, it stimulates this pathway to
release alpha-MSH by breaking down POMC. Alpha-MSH binds to its receptor, MC4R, with this
interaction causing decreased appetite.

35
Q

How can the appetite stimulating pathway be demonstrated

A

This relationship can be demonstrated experimentally trough
administering animals different doses of Zimelidine. This is a drug that allows 5-HT to persist in the
synaptic cleft (by inhibiting re-uptake) and this increases the length of time it interacts with its
receptor on the appetite suppressing pathway. It was found that in fed animals, the food intake
remained roughly the same when they were given different doses. This would make sense since the
body is already indicating to the brain it does not require food (reduces appetite). However, in fasted
animals, there was a relationship between food intake and the amount of drug administered with
these results emphasising the role 5-HT has on decreasing appetite. 5-HT is termed an anorexigenic
factor with other factors including GABA (although this has more mixed effects on feeding
behaviour).

Appetite in general is regulated by the balance between how much the appetite
stimulating pathway is stimulated and how much the appetite supressing pathway is stimulated.
There is diurnal variation (fluctuations occurring during each day) in food intake.

36
Q

What types of metabolism occur during the day

A

Carbohydrate
metabolism occurs during the day whilst fats are metabolised at night. The hypothalamus is sensitive
to the switch between carbohydrate and fat metabolism.

37
Q

Where is the switch between carbo and fat metabolism located

A

This switch is at the satiety centre located

at the ventromedial wall of the paraventricular nuclei hypothalamus.

38
Q

What happens when the para ventricular nuclei of hypothalamus are stimulated and lesions in this area

A

Stimulation of this region

results in aphagia (difficulty in swallowing) whilst lesions of this region results in hyperphagia

39
Q

Where is the hunger and thirst centre

A

The hunger and thirst centre is the lateral hypothalamus.

40
Q

What increases appetite and decreases pleasure of food - how do these drugs work

A

Opioids and growth
hormones increase appetite whilst opioid antagonists like naltrexone reduce appetite (reduce
hedonic valence or pleasure sensation associated with
food). These drugs work by affecting the balance between
the stimulation of VMN and the LH.

41
Q

What does the level of stretching in stomach effect

A

The level of stretching

of the stomach also affects appetite as well as the level of fat deposition.

42
Q

When are hormones and gut hormones released

A

Gut hormones are hormones and factors released during a meal and these play a role in regulating
food intake.

43
Q

What does fat ingestion cause

A

Fat ingestion causes the release of CCK and slowing of gastric emptying. This gives a
sensation of fullness thus reducing appetite. CCK itself released by I cells or nerves of the intestine is
a satiety factor that when injected into the brain, reduces appetite.

44
Q

What effect do pancreatic hormones play in food intake

A

Pancreatic hormones also play a role in food intake. A small amount of these hormones (e.g. insulin)
are transported to the brain where they act on receptors that cause net anabolic (increased food
intake and body fat through increased production of NPY/AgRP) or catabolic (reduced food intake
and body fat through increased stimulation of POMC/CART neurons) activity facilitated by regions
like the arcuate nucleus in the hypothalamus. This activity influences energy homeostasis and
ultimately the amount of fat stored in the body.

45
Q

What is the overall effect of insulin

A

Insulin itself initially has an anabolic affect but can
also have a catabolic effect as well. Insulin acts at the forebrain (nucleus of the solitary tract) as well
as the liver.

46
Q

What is glucagon secretion associated with

A

Glucagon secretion is associated with satiety and mainly acts at the liver to increase
glucose production. It also generates a signal that is relayed to the hindbrain to reduce energy intake.

47
Q

What does amylin act on

A

Amylin acts directly at the hindbrain (area postrema that primarily controls vomiting as well as some
autonomic functions) to reduce energy intake.

48
Q

Where is lepton expressed and what does jot do

A

Leptin is mainly expressed in adipocytes and affects food intake by decreasing it through inducing
weight loss and increasing energy expenditure. Leptin and ghrelin have antagonistic effects on food
intake. Leptin is secreted by white adipose tissue and acts as a lipostat of the fat stores in adipose
tissue.

49
Q

What does increased leptin mean

A

Leptin operates a feedback mechanism between adipose tissue and the brain with increased
leptin indicating increased adipose tissue size. Leptin then increases the expression of anorexigenic
factors, stimulates metabolic rate and inhibits NPY release.

50
Q

What happens if someone is resistant to leptin - what diseases

A

One can be resistant to the effects of
leptin leading to binge eating. Hyperphagia and severe obesity are associated with leptin deficiency
or leptin receptor defects.

51
Q

What is a quicker way that leptin is released - what is the effect

A

Leptin can also be released by gastric cells that release it at a much faster
rate than adipocytes. This is because the release of leptin by gastric cells is meant to have a short
term effect regulating digestion (delaying gastric emptying, secreting gastric, pancreatic and
intestinal hormones and promoting absorption of nutrients by the intestinal walls) whilst its release
from adipocytes has a more long term effect on food intake.

52
Q

What is ghrelin how is it released and effect

A

Ghrelin is a fast-acting hormone that induces appetite. It is released from the stomach (secreted by
P/D1 cells in the upper stomach), pancreas and adrenals in response to nutritional status.

53
Q

How does ghrelin work

A

It works by
increasing the levels of central orexins (AgRP and NPY) and achieves this by acting on the arcuate
nucleus of the hypothalamus (ARC) activating the expression of the orexins. It also suppresses the
ability of leptin to stimulate anorexigenic factors. The levels of glucose affects the expression of
ghrelin in P/D1 cells.

54
Q

What inhibits secretion of ghrelin

A

The secretion of ghrelin is also inhibited by leptin.
Obestatin is a mediator produced by the epithelial cells of the stomach that is encoded for by the
ghrelin gene but opposes the effects of ghrelin on food intake. It suppresses food intake by
suppressing appetite to decrease body weight gain. It also antagonises ghrelin induced growth
hormone secretion. Obestatin mediates its effects via different receptors to ghrelin despite it
producing antagonistic effects to ghrelin.

55
Q

What controls food intake

A

Food intake control involves the integration of many signals both from the GI tract and from the
brain.

Physiology 1 (67 decks)

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